The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Depressing Mitochondria-Reticulum Interactions Protects Cardiomyocytes From Lethal Hypoxia-Reoxygenation Injury
Abstract
Background—: Under physiological conditions, Ca 2+ transfer from the endoplasmic reticulum (ER) to mitochondria might occur at least in part at contact points between the 2 organelles and involves the VDAC1/Grp75/IP3R1 complex. Accumulation of Ca 2+ into the mitochondrial matrix may activate the mitochondrial chaperone cyclophilin D (CypD) and trigger permeability transition pore opening, whose role in ischemia/reperfusion injury is well recognized. We questioned here whether the transfer of Ca 2+ from ER to mitochondria might play a role in cardiomyocyte death after hypoxia-reoxygenation. Methods and Results—: We report that CypD interacts with the VDAC1/Grp75/IP3R1 complex in cardiomyocytes. Genetic or pharmacological inhibition of CypD in both H9c2 cardiomyoblasts and adult cardiomyocytes decreased the Ca 2+ transfer from ER to mitochondria through IP3R under normoxic conditions. During hypoxia-reoxygenation, the interaction between CypD and the IP3R1 Ca 2+ channeling complex increased concomitantly with mitochondrial Ca 2+ content. Inhibition of either CypD, IP3R1, or Grp75 decreased protein interaction within the complex, attenuated mitochondrial Ca 2+ overload, and protected cells from hypoxia-reoxygenation. Genetic or pharmacological inhibition of CypD provided a similar effect in adult mice cardiomyocytes. Disruption of ER-mitochondria interaction via the downregulation of Mfn2 similarly reduced the interaction between CypD and the IP3R1 complex and protected against hypoxia-reoxygenation injury. Conclusions—: Our data (1) point to a new role of CypD at the ER-mitochondria interface and (2) suggest that decreasing ER-mitochondria interaction at reperfusion can protect cardiomyocytes against lethal reperfusion injury through the reduction of mitochondrial Ca 2+ overload via the CypD/VDAC1/Grp75/IP3R1 complex.
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Citations
Cites
Mitofusin 2 tethers endoplasmic reticulum to mitochondria
de Brito, O. M., & Scorrano, L. (2008) · Nature · doi:10.1038/nature07534 · Cited by 2,442
Hayashi, T., & Su, T.-P. (2007) · Cell · doi:10.1016/j.cell.2007.08.036 · Cited by 1,826
Chaperone-mediated coupling of endoplasmic reticulum and mitochondrial Ca2+ channels
Szabadkai, G., Bianchi, K., Várnai, P., De Stefani, D., Wieckowski, M. R., Cavagna, D., Nagy, A. I., Balla, T., & Rizzuto, R. (2006) · The Journal of Cell Biology · doi:10.1083/jcb.200608073 · Cited by 1,413
Isolation of mitochondria-associated membranes and mitochondria from animal tissues and cells
Wieckowski, M. R., Giorgi, C., Lebiedzinska, M., Duszynski, J., & Pinton, P. (2009) · Nature Protocols · doi:10.1038/nprot.2009.151 · Cited by 979
Schinzel, A. C., Takeuchi, O., Huang, Z., Fisher, J. K., Zhou, Z., Rubens, J., Hetz, C., Danial, N. N., Moskowitz, M. A., & Korsmeyer, S. J. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0505294102 · Cited by 820
MAM: more than just a housekeeper
Hayashi, T., Rizzuto, R., Hajnoczky, G., & Su, T.-P. (2009) · Trends in Cell Biology · doi:10.1016/j.tcb.2008.12.002 · Cited by 787
Pinton, P. (2001) · The EMBO Journal · doi:10.1093/emboj/20.11.2690 · Cited by 599
PACS‐2 controls endoplasmic reticulum–mitochondria communication and Bid‐mediated apoptosis
Simmen, T., Aslan, J. E., Blagoveshchenskaya, A. D., Thomas, L., Wan, L., Xiang, Y., Feliciangeli, S. F., Hung, C., Crump, C. M., & Thomas, G. (2005) · The EMBO Journal · doi:10.1038/sj.emboj.7600559 · Cited by 592
Crompton, M., Virji, S., & Ward, J. M. (1998) · European Journal of Biochemistry · doi:10.1046/j.1432-1327.1998.2580729.x · Cited by 489
Ca2+ transfer from the ER to mitochondria: When, how and why
Rizzuto, R., Marchi, S., Bonora, M., Aguiari, P., Bononi, A., De Stefani, D., Giorgi, C., Leo, S., Rimessi, A., Siviero, R., et al. (2009) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/j.bbabio.2009.03.015 · Cited by 476
Cited by
Bøtker, H. E., Hausenloy, D., Andreadou, I., Antonucci, S., Boengler, K., Davidson, S. M., Deshwal, S., Devaux, Y., Di Lisa, F., Di Sante, M., et al. (2018) · Basic Research in Cardiology · doi:10.1007/s00395-018-0696-8 · Cited by 423
Self-citationTubbs, E., Theurey, P., Vial, G., Bendridi, N., Bravard, A., Chauvin, M.-A., Ji-Cao, J., Zoulim, F., Bartosch, B., Ovize, M., et al. (2014) · Diabetes · doi:10.2337/db13-1751 · Cited by 411
Self-citationOng, S.-B., Samangouei, P., Kalkhoran, S. B., & Hausenloy, D. J. (2015) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2014.11.005 · Cited by 323
Wu, S., Lu, Q., Ding, Y., Wu, Y., Qiu, Y., Wang, P., Mao, X., Huang, K., Xie, Z., & Zou, M.-H. (2019) · Circulation · doi:10.1161/circulationaha.118.033552 · Cited by 298
Theurey, P., Tubbs, E., Vial, G., Jacquemetton, J., Bendridi, N., Chauvin, M.-A., Alam, M. R., Le Romancer, M., Vidal, H., & Rieusset, J. (2016) · Journal of Molecular Cell Biology · doi:10.1093/jmcb/mjw004 · Cited by 175
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Metadata
- Authors
- Paillard, M., Tubbs, E., Thiebaut, P.-A., Gomez, L., Fauconnier, J., Crola Da Silva, C., Teixeira, G., Mewton, N., Belaidi, E., Durand, A., Abrial, M., Lacampagne, A., Rieusset, J., & Ovize, M.
- Venue
- Circulation
- Published
- 2013-10
- Volume
- 128
- Issue
- 14
- Pages
- 1555-1565
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W1996146434
- Cited by
- 279
- References
- 32
- FWCI
- 11.56
- Type
- journal article
- Language
- en
- Open access
- closed
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- Paillard, M., Tubbs, E., Thiebaut, P.-A., Gomez, L., Fauconnier, J., Crola Da Silva, C., Teixeira, G., Mewton, N., Belaidi, E., Durand, A., Abrial, M., Lacampagne, A., Rieusset, J., & Ovize, M. (2013). Depressing Mitochondria-Reticulum Interactions Protects Cardiomyocytes From Lethal Hypoxia-Reoxygenation Injury. Circulation. https://doi.org/10.1161/circulationaha.113.001225
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