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Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I
Open accessAbstract
Oxidative damage from elevated production of reactive oxygen species (ROS) contributes to ischemia-reperfusion injury in myocardial infarction and stroke. The mechanism by which the increase in ROS occurs is not known, and it is unclear how this increase can be prevented. A wide variety of nitric oxide donors and S-nitrosating agents protect the ischemic myocardium from infarction, but the responsible mechanisms are unclear. Here we used a mitochondria-selective S-nitrosating agent, MitoSNO, to determine how mitochondrial S-nitrosation at the reperfusion phase of myocardial infarction is cardioprotective in vivo in mice. We found that protection is due to the S-nitrosation of mitochondrial complex I, which is the entry point for electrons from NADH into the respiratory chain. Reversible S-nitrosation of complex I slows the reactivation of mitochondria during the crucial first minutes of the reperfusion of ischemic tissue, thereby decreasing ROS production, oxidative damage and tissue necrosis. Inhibition of complex I is afforded by the selective S-nitrosation of Cys39 on the ND3 subunit, which becomes susceptible to modification only after ischemia. Our results identify rapid complex I reactivation as a central pathological feature of ischemia-reperfusion injury and show that preventing this reactivation by modification of a cysteine switch is a robust cardioprotective mechanism and hence a rational therapeutic strategy.
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“Conversely, S-nitrosation of the other three cysteines was unaffected by changes in complex I activity (Fig. 2d and Supplementary Figs. 8–10).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO reproducibly S-nitrosated three subunits: the 75 kDa, B8 and ND3 subunits (Fig. 2b,c, Supplementary Fig. 7b and Supplementary Table 2).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Notably, MitoSNO treatment did not inhibit complex I in the normoxic myocardium in vivo (Fig. 1g)”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO administered at reperfusion significantly decreased infarct size (Fig. 1b and Supplementary Fig. 2).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“we identified four cysteines that were S-nitrosated by MitoSNO: two on the 75 kDa subunit and one each on the ND3 and B8 subunits (Fig. 2c,d and Supplementary Table 3).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Using this method, we found that only respiratory complex I and the FoF1-ATP synthase were detectably S-nitrosated within mitochondria in vivo (Fig. 1f, Supplementary Fig. 6a and Supplementary Table 1).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“In the MitoSNO-treated mice, complex I activity returned to its initial levels after 30 min”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Although S-nitrosation did not affect FoF1-ATP synthase activity (Supplementary Fig. 6b)”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO did not alter hemodynamics (Supplementary Fig. 4).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“S-nitrosation of ND3 Cys39 was negligible under conditions of high activity but increased markedly under conditions of low activity (Fig. 2d).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Neither SNAP nor the MitoSNO-targeting moiety (MitoNAP)11 had this effect (Fig. 1b).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“In contrast, in the absence of MitoSNO treatment in vivo, complex I was not affected after 5 min of reperfusion, but its activity then decreased by ~50% during 30 min of reperfusion and could not be restored ex vivo by reductants”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Within the intact, ischemic heart perfused ex vivo in a Langendorff system, there was substantial (~40%) S-nitrosation of ND3 by MitoSNO that was not present in normoxic hearts; in contrast, the amount of S-nitrosation of the 75 kDa subunit cysteines was similar under normoxia and ischemia (Fig. 3a, Supplementary Table 4 and Supplementary Fig. 11).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO administered at reperfusion blocked this rise in the amount of hydrogen peroxide, whereas administration of SNAP did not (Fig. 1c).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“This led to the selective S-nitrosation of mitochondrial proteins in the reperfused heart (Fig. 1a), as visualized by labeling with a red fluorescent probe15–17. In contrast, equal doses of the untargeted precursor S-nitrosating compound S-nitroso-N-acetylpenicillamine (SNAP) S-nitrosated only nonmitochondrial myocardial and plasma proteins (Fig. 1a).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Intravenous injection of MitoSNO into mice also resulted in S-nitrosation of the ND3 cysteine in vivo during reperfusion of the ischemic heart, whereas MitoSNO injection did not have this effect in normoxic hearts (Fig. 3b).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Complex I activity was lower in heart mitochondria from MitoSNO-treated mice compared to untreated mice, and this decreased activity was normalized by selective S-nitrosothiol reduction using copper and ascorbate15–17 (Fig. 1g).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Moreover, ND3 Cys39 was extensively S-nitrosated (>50%) by MitoSNO in isolated rat heart mitochondria during anoxia but was negligibly modified under normoxic conditions (Fig. 2e,f).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO was protective only during reperfusion: injection 10 min after reperfusion was ineffective (Supplementary Fig. 3).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Using MitoB we found that the amount of mitochondrial hydrogen peroxide remained low during ischemia and increased only after reperfusion in vivo (Fig. 1c).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“The rise in the amount of mitochondrial hydrogen peroxide was associated with increased protein carbonylation (Fig. 1d), a marker of oxidative damage, as well as necrotic (Fig. 1b) and apoptotic (Fig. 1e) cell death, and these effects were all prevented by MitoSNO.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO protected control cardiomyocytes treated with a scrambled RNAi construct from ischemia-reperfusion injury, but decreasing complex I activity by NDUFAF1-targeted RNAi completely abolished MitoSNO protection (Fig. 4a).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Copper and ascorbate treatment restored complex I activity, indicating that the inhibition of activity was due to S-nitrosation of ND3 Cys39 (Fig. 3d).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“Exposure of isolated bovine heart mitochondrial membranes to MitoSNO under conditions in which complex I is in a high activity state led to S-nitrosation of the 75 kDa and B8 subunit cysteines but not of the ND3 subunit, and this exposure did not affect complex I activity (Fig. 3d).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“We selectively knocked down expression of the complex I assembly factor NDUFAF1 (ref. 36) by RNAi, which decreased protein amounts by 80% (Supplementary Fig. 16a–c) and lowered complex I activity (Supplementary Fig. 16d) while leaving the amount of complex II unaffected (Supplementary Fig. 16a,e).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [36] Mimaki, M. et al. Understanding mitochondrial complex I assembly in health and disease. Biochim. Biophys. Acta 1817, 851–862 (2012). source
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“Our model shows that Cys39 is located at the hinge region of complex I facing the mitochondrial matrix. Furthermore, Cys39 is adjacent to the half-channel element of one of the four proposed proton translocation pathways of complex I and is close to the ubiquinone binding pocket, where ubiquinone receives electrons from the N2 iron-sulfur center (Fig. 3g)34.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [34] Baradaran, R., Berrisford, J.M., Minhas, G.S. & Sazanov, L.A. Crystal structure of the entire respiratory complex I. Nature 494, 443–448 (2013). source
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- Rests on an assumption: The prokaryotic complex I structures used for modeling are sufficiently homologous to mammalian complex I to locate ND3 Cys39 accurately.
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In the paper
“Nitrite infusion during prolonged ischemia resulted in substantial S-nitrosation of this cysteine, which was negligibly modified by nitrite under normoxic conditions (Fig. 4b,c and Supplementary Table 5).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“In contrast, incubation with MitoSNO under conditions in which complex I is in a low activity state led to S-nitrosation of ND3 Cys39, as well as of the other three cysteines, and inhibited complex I activity (Fig. 3d).”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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In the paper
“Together these data indicate that cardioprotection by MitoSNO acts through mitochondrial S-nitrosation, which inhibits mitochondrial hydrogen peroxide production at reperfusion.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“As complex I was the only S-nitrosation target identified in our proteomic analysis whose activity was affected by this modification, we consider it to constitute a probable node for cardioprotection.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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“MitoSNO has been reported to be protective in mice with cardiomyocyte deficiency of protein kinase G18, indicating that the cardio-protection conferred by MitoSNO is not due to nonmitochondrial pathways that operate through cyclic GMP–protein kinase G signaling3,6”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [18] Methner, C., Lukowski, R., Hofman, F., Murphy, M.P. & Krieg, T. Protection through postconditioning or a mitochondria-targeted S-nitrosothiol is unaffected by cardiomyocyte-selective ablation of protein kinase G. Basic Res. Cardiol. 108, 337 (2013). source
- Not checked yetcites [3] Lundberg, J.O., Weitzberg, E. & Gladwin, M.T. The nitrate-nitrite–nitric oxide pathway in physiology and therapeutics. Nat. Rev. Drug Discov. 7, 156–167 (2008). source
- Not checked yetcites [6] Costa, A.D. et al. Protein kinase G transmits the cardioprotective signal from cytosol to mitochondria. Circ. Res. 97, 329–336 (2005). source
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In the paper
“previous work has shown that complex I is inhibited by various nitric oxide donors in vitro and that this inhibition is associated with S-nitrosation2,10,11,21–24.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [2] Shiva, S. et al. Nitrite augments tolerance to ischemia/reperfusion injury via the modulation of mitochondrial electron transfer. J. Exp. Med. 204, 2089–2102 (2007). source
- Not checked yetcites [10] Sun, J., Morgan, M., Shen, R.F., Steenbergen, C. & Murphy, E. Preconditioning results in S-nitrosylation of proteins involved in regulation of mitochondrial energetics and calcium transport. Circ. Res. 101, 1155–1163 (2007). source
- Not checked yetcites [11] Prime, T.A. et al. A mitochondria-targeted S-nitrosothiol modulates respiration, nitrosates thiols, and protects against ischemia-reperfusion injury. Proc. Natl. Acad. Sci. USA 106, 10764–10769 (2009). source
- Not checked yetcites [21] Clementi, E., Brown, G.C., Feelisch, M. & Moncada, S. Persistent inhibition of cell respiration by nitric oxide: crucial role of S-nitrosylation of mitochondrial complex I and protective action of glutathione. Proc. Natl. Acad. Sci. USA 95, 7631–7636 (1998). source
- Not checked yetcites [22] Burwell, L.S., Nadtochiy, S.M., Tompkins, A.J., Young, S. & Brookes, P.S. Direct evidence for S-nitrosation of mitochondrial complex I. Biochem. J. 394, 627–634 (2006). source
- Not checked yetcites [23] Dahm, C.C., Moore, K. & Murphy, M.P. Persistent S-nitrosation of complex I and other mitochondrial membrane proteins by S-nitrosothiols but not nitric oxide or peroxynitrite. J. Biol. Chem. 281, 10056–10065 (2006). source
- Not checked yetcites [24] Galkin, A. & Moncada, S. S-nitrosation of mitochondrial complex I depends on its structural conformation. J. Biol. Chem. 282, 37448–37453 (2007). source
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In the paper
“These data suggest that complex I ND3 Cys39 is the crucial functional S-nitrosation target and that other interactions of MitoSNO with mitochondria do not contribute to protection.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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In the paper
“This mechanism probably contributes to cardioprotection by untargeted nitric oxide donors and alterations to nitric oxide metabolism in general, although nonmitochondrial pathways may also contribute.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
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In the paper
“We assessed infarct size after 120 min of reperfusion using triphenyltetrazolium chloride staining and expressed it as a percentage of the risk zone as described recently40.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > In vivo treatments
What the sources say
- Not checked yetcites [40] Nadtochiy, S.M., Redman, E., Rahman, I. & Brookes, P.S. Lysine deacetylation in ischaemic preconditioning: the role of SIRT1. Cardiovasc. Res. 89, 643–649 (2011). source
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In the paper
“We used an open-chest, in situ mouse (C57BL/6) heart model as recently described41.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > In vivo treatments
What the sources say
- Not checked yetcites [41] Schmidt, K. et al. Cardioprotective effects of mineralocorticoid receptor antagonists at reperfusion. Eur. Heart J. 31, 1655–1662 (2010). source
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In the paper
“The nitrite (NO2−) anion protects from ischemia-reperfusion injury in vivo1–3,37 and is thought to act as an S-nitrosating agent in the ischemic myocardium2.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [1] Duranski, M.R. et al. Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver. J. Clin. Invest. 115, 1232–1240 (2005). source
- Not checked yetcites [2] Shiva, S. et al. Nitrite augments tolerance to ischemia/reperfusion injury via the modulation of mitochondrial electron transfer. J. Exp. Med. 204, 2089–2102 (2007). source
- Not checked yetcites [3] Lundberg, J.O., Weitzberg, E. & Gladwin, M.T. The nitrate-nitrite–nitric oxide pathway in physiology and therapeutics. Nat. Rev. Drug Discov. 7, 156–167 (2008). source
- Not checked yetcites [37] Shiva, S. & Gladwin, M.T. Nitrite mediates cytoprotection after ischemia/reperfusion by modulating mitochondrial function. Basic Res. Cardiol. 104, 113–119 (2009). source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As the S-nitrosation of the ND3 subunit only occurs after anaerobic incubation, these findings suggest that MitoSNO decreases ROS production by S-nitrosating the ND3 subunit.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
hedgeddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“To assess differences in protein fluorescence using two-dimensional DIGE, we used an experimental design that included biological variance analysis (BVA)12. In each DIGE experiment, we used four biological replicates, where a biological replicate is an independently prepared heart tissue subjected to the CyDye sample preparations described above.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > SNO-DIGE experimental design
What the sources say
- Not checked yetcites [12] Chouchani, E.T. et al. Identification of S-nitrosated mitochondrial proteins by S-nitrosothiol difference in gel electrophoresis (SNO-DIGE): implications for the regulation of mitochondrial function by reversible S-nitrosation. Biochem. J. 430, 49–59 (2010). source
plainn = 4- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one. The quote only partly states this claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We scanned all gels at 100- to 200-μm pixel size, and the photomultiplier tube was set to ensure a maximum pixel intensity within the linear acquisition range for the region of the gel being analyzed (most commonly the sub–20 kDa region of gels containing the complex I ND3 subunit) and thereby ensuring that fluorescent signal intensities were in the linear range.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Gel imaging and analysis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All samples were shielded from light throughout the experiment to preserve S-nitrosothiols.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Mitochondrial preparations and incubations
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Reperfusion of the ischemic tissue rapidly reactivates complex I and generates hydrogen peroxide, which causes oxidative damage that leads to the cell death underlying ischemia-reperfusion injury.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“All animal experiments described here were carried out in accordance with the UK Home Office Guide on the Operation of Animal (Scientific Procedures) Act of 1986 and the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication 85–23, revised 1996). All procedures were approved under the Project License number PPL 80/2393.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > In vivo treatments
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“As the ND3 subunit is encoded by mitochondrial DNA, its cysteine cannot be replaced genetically, and there are no known natural mutations or polymorphisms in the gene encoding this subunit (MT-ND3)31.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
What the sources say
- Not checked yetcites [31] Bridges, H.R., Birrell, J.A. & Hirst, J. The mitochondrial-encoded subunits of respiratory complex I (NADH:ubiquinone oxidoreductase): identifying residues important in mechanism and disease. Biochem. Soc. Trans. 39, 799–806 (2011). source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Together these data suggest that ischemia exposes ND3 Cys39 for S-nitrosation and that this modification specifically mediates the reversible inhibition of complex I in vivo.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This result indicates that S-nitrosation of ND3 Cys39 does not disrupt complex I function by affecting the interaction of NADH with the flavin mononucleotide site and that the S-nitrosation of other residues in complex I does not affect its activity.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We incubated mitochondria or mitochondrial membranes from both the in vitro and in vivo treatment groups in 100 mM NEM to quench unreacted thiols.”
- Also stated in: § Differential labeling of respiratory complex I S-nitrosothiols · plain
“Mitochondria from mice treated in vivo with an S-nitrosating agent were isolated as described above in buffer supplemented with 100 mM NEM before differential labeling.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Differential labeling of respiratory complex I S-nitrosothiols
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
- Also stated in: § Differential labeling of respiratory complex I S-nitrosothiols · plain
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“When protein S-nitrosothiols were to be assessed in mitochondria isolated from hearts that had been subjected to in vivo treatments, 100 mM NEM was included in the isolation buffers.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Mitochondrial preparations and incubations
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“When S-nitrosating species are present during reperfusion, the exposed ND3 cysteine becomes S-nitrosated, locking complex I in a low activity state and decreasing ROS production during the reperfusion phase.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Pelleted samples were washed three times in Chelex 100–treated PBS before resuspension in 100 μl of the same buffer containing 1 mM ascorbate and 10 μM CuSO4”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Differential labeling of respiratory complex I S-nitrosothiols
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Error bars represent the s.e.m. from at least three replicates unless otherwise stated.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Statistical analyses
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“For analysis, we spiked the tissues with deuterated internal standards, extracted the MitoB and its product MitoP from the reaction with hydrogen peroxide and determined the amounts of MitoB and MitoP present in the tissue by liquid chromatography and tandem mass spectrometry as described previously20.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Measurement of mitochondrial hydrogen peroxide flux in vivo
What the sources say
- Not checked yetcites [20] Cochemé, H.M. et al. Measurement of H2O2 within living Drosophila during aging using a ratiometric mass spectrometry probe targeted to the mitochondrial matrix. Cell Metab. 13, 340–350 (2011). source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“MitoSNO stability was assessed before use from its absorbance at 340 nm.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Chemical syntheses
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“NO2− and control saline infusions began 15 min before ischemia and continued throughout the ischemic phase so that a constant final concentration of NO2− was maintained in the heart.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Ex vivo heart treatment with nitrite
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“We measured mitochondrial hydrogen peroxide in vivo using the MitoB mass spectro-metric probe as described previously20.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Measurement of mitochondrial hydrogen peroxide flux in vivo
What the sources say
- Not checked yetcites [20] Cochemé, H.M. et al. Measurement of H2O2 within living Drosophila during aging using a ratiometric mass spectrometry probe targeted to the mitochondrial matrix. Cell Metab. 13, 340–350 (2011). source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“We treated mouse hearts with nitrite using previously established protocols known to elicit cardioprotection38.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Ex vivo heart treatment with nitrite
What the sources say
- Not checked yetcites [38] Webb, A. et al. Reduction of nitrite to nitric oxide during ischemia protects against myocardial ischemia-reperfusion damage. Proc. Natl. Acad. Sci. USA 101, 13683–13688 (2004). source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“In parallel, we determined the citrate synthase activity of each sample46. We then normalized the complex I rate to the citrate synthase rate and expressed it as a percentage of the appropriate control.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Measurement of complex I activity
What the sources say
- Not checked yetcites [46] Srere, P.A. Citrate synthase. Methods Enzymol. 13, 3–10 (1969). source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“When administering NO2− or saline solutions to ischemic hearts, we deoxygenated the solutions during preparation by bubbling with 95% N2 and 5% CO2.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > Ex vivo heart treatment with nitrite
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We protected cells from light during hypoxia (2 h) and reperfusion (1.5 h) and measured cell death using a lactate dehydrogenase (LDH) release assay (Cytotoxicity Detection, Roche Applied Science) according to the manufacturer's instructions.”
§ Cardioprotection by S-nitrosation of a cysteine switch on mitochondrial complex I > ONLINE METHODS > In vitro ischemia reperfusion injury to cells
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper relies on this without support.
Before this study, the existence and physiological importance of S-nitrosation of complex I in vivo had not been demonstrated.
“However, to our knowledge, the existence and physiological importance of S-nitrosation of complex I in vivo has not previously been demonstrated.”
The paper relies on this without support.
The conservation of ND3 Cys39 across metazoans implies that this residue has a physiological role.
“Cys39 in ND3 is conserved throughout metazoans, consistent with a physiological role for this residue.”
The paper relies on this without support.
The prokaryotic complex I structures used for modeling are sufficiently homologous to mammalian complex I to locate ND3 Cys39 accurately.
“We modeled the location of ND3 Cys39 using structures of prokaryotic complex I (refs. 32–34). This modeling led to an orthologous mammalian core structure containing ND3 Cys39”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Mechanistically, this protection is dependent on MitoSNO transnitrosating a critical cysteine in the active site of complex I.”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [170]
In the citing paper
“This S-nitrosation of Cys39 in the ND3 subunit of complex I inhibits its catalytic activity and, hence, attenuates reverse electron transport and ROS production (170).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [170]
In the citing paper
“For example, MitoSNO (FIGURE 14), a mitochondrially targeted S-nitrosothiol, was shown in rodent models to significantly attenuate infarct size after MI (170).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [170]
In the citing paper
“Murphy and coworkers used a mitochondria-selective S-nitrosating agent to demonstrate that nitrosation of Complex I serves a protective role during ischemia/reperfusion by reducing oxidative damage and tissue necrosis [212, 213].”
From Signaling and stress: The redox landscape in NOS2 biology (2015) · cites this paper as [213]
Citations
Cites
Perkins, D. N., Pappin, D., Creasy, D. M., & Cottrell, J. S. (1999) · Electrophoresis · doi:10.1002/(sici)1522-2683(19991201)20:18 · Cited by 8,264
Yellon, D. M., & Hausenloy, D. J. (2007) · New England Journal of Medicine · doi:10.1056/nejmra071667 · Cited by 3,797
The nitrate-nitrite-nitric oxide pathway in physiology and therapeutics
Lundberg, J. O., Weitzberg, E., & Gladwin, M. T. (2008) · Nature Reviews Drug Discovery · doi:10.1038/nrd2466 · Cited by 2,739
Srere, P. A. (1969) · Methods in Enzymology · doi:10.1016/0076-6879(69)13005-0 · Cited by 2,005
Wittig, I., Braun, H., & Schägger, H. (2006) · Nature Protocols · doi:10.1038/nprot.2006.62 · Cited by 1,741
Mechanisms Underlying Acute Protection From Cardiac Ischemia-Reperfusion Injury
Murphy, E., & Steenbergen, C. (2008) · Physiological Reviews · doi:10.1152/physrev.00024.2007 · Cited by 1,504
Clementi, E., Brown, G. C., Feelisch, M., & Moncada, S. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.13.7631 · Cited by 863
Crystal structure of the entire respiratory complex I
Baradaran, R., Berrisford, J. M., Minhas, G. S., & Sazanov, L. A. (2013) · Nature · doi:10.1038/nature11871 · Cited by 797
Structure of the Hydrophilic Domain of Respiratory Complex I from Thermus thermophilus
Sazanov, L. A., & Hinchliffe, P. (2006) · Science · doi:10.1126/science.1123809 · Cited by 763
Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver
Duranski, M. R., Greer, J. J. M., Dejam, A., Jaganmohan, S., Hogg, N., Langston, W., Patel, R. P., Yet, S.-F., Wang, X., Kevil, C. G., et al. (2005) · Journal of Clinical Investigation · doi:10.1172/jci22493 · Cited by 674
Cited by
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Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS
Chouchani, E. T., Pell, V. R., Gaude, E., Aksentijević, D., Sundier, S. Y., Robb, E. L., Logan, A., Nadtochiy, S. M., Ord, E. N. J., Smith, A. C., et al. (2014) · Nature · doi:10.1038/nature13909 · Cited by 2,907
Self-citationZielonka, J., Joseph, J., Sikora, A., Hardy, M., Ouari, O., Vasquez-Vivar, J., Cheng, G., Lopez, M., & Kalyanaraman, B. (2017) · Chemical Reviews · doi:10.1021/acs.chemrev.7b00042 · Cited by 1,683
An overview of nanoparticles commonly used in fluorescent bioimaging
Wolfbeis, O. S. (2015) · Chemical Society Reviews · doi:10.1039/c4cs00392f · Cited by 1,631
Reperfusion injury and reactive oxygen species: The evolution of a concept
Granger, D. N., & Kvietys, P. R. (2015) · Redox Biology · doi:10.1016/j.redox.2015.08.020 · Cited by 1,550
Redox metabolism: ROS as specific molecular regulators of cell signaling and function
Lennicke, C., & Cochemé, H. M. (2021) · Molecular Cell · doi:10.1016/j.molcel.2021.08.018 · Cited by 1,313
Self-citation
Metadata
- Authors
- Chouchani, E. T., Methner, C., Nadtochiy, S. M., Logan, A., Pell, V. R., Ding, S., James, A. M., Cochemé, H. M., Reinhold, J., Lilley, K. S., Partridge, L., Fearnley, I. M., Robinson, A. J., Hartley, R. C., Smith, R. A. J., Krieg, T., Brookes, P. S., & Murphy, M. P.
- Affiliations
- MRC Mitochondrial Biology Unit (GB)
- Max Planck Society (DE)
- Corresponding author
- Murphy, Michael P
- ORCID
- Venue
- Nature Medicine
- Published
- 2013-05-26
- Volume
- 19
- Issue
- 6
- Pages
- 753-759
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC4019998
- OpenAlex
- W1994270731
- Semantic Scholar
- 97e1eb3beeba3f16e5a83fa5a94d80446f1bb0b7
- Cited by
- 619
- References
- 46
- Citations by year
- 2026: 19 · 2025: 38 · 2024: 39 · 2023: 31 · 2022: 42 · 2021: 51 · 2020: 59 · 2019: 37 · 2018: 60 · 2017: 50 · 2016: 60 · 2015: 54 · 2014: 58 · 2013: 20
- FWCI
- 47.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- UEA Digital Repository (University of East Anglia) (submittedVersion)
- Funders
- Wellcome Trust (098565)
- British Heart Foundation (PG/12/42/29655)
- Canadian Institutes of Health Research
- Biotechnology and Biological Sciences Research Council (BB/I012923/1, BB/I012826/1, BB/I012923)
- National Heart, Lung, and Blood Institute (R01HL071158)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- S-nitrosylation, mitochondrial complex I, nitric oxide donors, myocardial ischemia-reperfusion injury, cardioprotection, reactive oxygen species, oxidative damage, mitochondrial respiratory chain, myocardial infarction, stroke
- MeSH terms
- Animals, Cysteine, Male, Mice, Inbred C57BL, Mitochondria, Heart, Myocardial Reperfusion Injury, Nitrosation, Reactive Oxygen Species, Protein Subunits, Mitochondrial Proteins, Electron Transport Complex I, Mice, Rats
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