CoChat
Sign Up
Cited by 163

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

miR-212-5p attenuates ferroptotic neuronal death after traumatic brain injury by targeting Ptgs2

Xiao, Xiao, Jiang, Youjing, Liang, Weibo, Wang, Yanyun, Cao, Shuqiang, Yan, He, Gao, Linbo, Zhang, Lin·2019·Molecular Brain
DOI 10.1186/s13041-019-0501-0PMC PMC6749650
Open this paper in CoChat — free account

Abstract

Ferroptosis, a newly discovered form of iron-dependent regulated cell death, has been implicated in traumatic brain injury (TBI). MiR-212-5p has previously been reported to be downregulated in extracellular vesicles following TBI. To investigate whether miR-212-5p is involved in the ferroptotic neuronal death in TBI mice, we first examined the accumulation of malondialdehyde (MDA) and ferrous ion, and the expression of ferroptosis-related molecules at 6 h, 12 h, 24 h, 48 h and 72 h following controlled cortical impact (CCI) in mice. There was a significant upregulation in the expression of Gpx4 and Acsl4 at 6 h, Slc7a11 from 12 h to 72 h, and Nox2 and Sat1 from 6 h to 72 h post injury. Similarly, an upregulation in the expression of Gpx4 at 6 h, Nox2 from 6 h to 72 h, xCT from 12 h to 72 h, and Sat1 at 72 h after CCI was observed at the protein level. Interestingly, MDA and ferrous ion were increased whereas miR-212-5p was decreased in the CCI group compared to the sham group. Furthermore, we found that overexpression of miR-212-5p attenuated ferroptosis while downregulation of miR-212-5p promoted ferroptotic cell death partially by targeting prostaglandin-endoperoxide synthase-2 (Ptgs2) in HT-22 and Neuro-2a cell lines. In addition, administration of miR-212-5p in CCI mice significantly improved learning and spatial memory. Collectively, these findings indicate that miR-212-5p may protect against ferroptotic neuronal death in CCI mice partially by targeting Ptgs2.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1186/s13041-019-0501-0

Cites

6 of 6 references verified0 citation errors · 0 not checkable

Statistics

Figures

Fig. 1 The concentration of MDA and Fe2+ and the mRNA levels of ferroptosis-related molecules following CCI. MDA (a) and Fe2+ (b) levels in the ipsilateral cortex at 6 h, 12 h, 24 h, 48 h, and 72 h after CCI (n = 6 for each group). Quantitative RT-PCR showing the relative expression levels of Gpx4 (c), Acsl4 (d), Slc7a11 (e), Nox2 (f), Sat1 (g) in the cortex at the indicated times after injury (n = 9 for each group). Data are expressed as mean ± SEM. Data were analyzed using the student’s t-test. *p < 0.05, **p < 0.01, ***p < 0.001. MDA, malondialdehyde; CCI, controlled cortical impact; Fe2+, ferrous ion
Fig. 1 The concentration of MDA and Fe2+ and the mRNA levels of ferroptosis-related molecules following CCI. MDA (a) and Fe2+ (b) levels in the ipsilateral cortex at 6 h, 12 h, 24 h, 48 h, and 72 h after CCI (n = 6 for each group). Quantitative RT-PCR showing the relative expression levels of Gpx4 (c), Acsl4 (d), Slc7a11 (e), Nox2 (f), Sat1 (g) in the cortex at the indicated times after injury (n = 9 for each group). Data are expressed as mean ± SEM. Data were analyzed using the student’s t-test. *p < 0.05, **p < 0.01, ***p < 0.001. MDA, malondialdehyde; CCI, controlled cortical impact; Fe2+, ferrous ionCC BY · PubMed Central
Fig. 2 The protein levels of ferroptosis-related molecules at the indicated times after CCI. Cortical expression of Gpx4, Acsl4, Nox2, xCT and Sat1 were measured in CCI and sham groups at 6 h (a), 12 h (b), 24 h (c), 48 h (d), 72 h (e). Data are expressed as mean ± SEM and analyzed with the student’s t-test, n = 5 per group, *p < 0.05, **p < 0.01, ***p < 0.001. CCI, controlled cortical impact
Fig. 2 The protein levels of ferroptosis-related molecules at the indicated times after CCI. Cortical expression of Gpx4, Acsl4, Nox2, xCT and Sat1 were measured in CCI and sham groups at 6 h (a), 12 h (b), 24 h (c), 48 h (d), 72 h (e). Data are expressed as mean ± SEM and analyzed with the student’s t-test, n = 5 per group, *p < 0.05, **p < 0.01, ***p < 0.001. CCI, controlled cortical impactCC BY · PubMed Central
Fig. 3 miR-212-5p was constantly downregulated after CCI and negatively regulated ferroptosis in neuronal cell lines. a Quantitative RT-PCR showing the relative expression levels of miR-212-5p in the cortex at 6 h, 12 h, 1d, 2d, 3d after injury (n = 9 for each group). b The HT-22 and Neuro-2a cells were treated with Rsl3 (3 μM) with or without a cell death inhibitor (ferrostatin-1, 1 μM; zVAD-fmk, 10 μM; necrosulfonamide, 0.5 μM) for 24 h. Data were analyzed using analysis of variance (ANOVA) with Tukey’s post hoc test. c Overexpression of miR-212-5p suppressed Rsl3-induced cell death in HT-22 and Neuro-2a cells. d Inhibition of endogenous miR-212-5p enhanced Rsl3-induced cell death in HT-22 and Neuro-2a cells. Indicated cells were treated with Rsl3 (3 μM) for 24 h. The transfection efficacy of overexpression (e) or inhibition (f) was confirmed by qRT-PCR analysis. Cell death was assayed using the Cytotoxicity Detection kit. Data shown represent mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001. CCI, controlled cortical impact
Fig. 3 miR-212-5p was constantly downregulated after CCI and negatively regulated ferroptosis in neuronal cell lines. a Quantitative RT-PCR showing the relative expression levels of miR-212-5p in the cortex at 6 h, 12 h, 1d, 2d, 3d after injury (n = 9 for each group). b The HT-22 and Neuro-2a cells were treated with Rsl3 (3 μM) with or without a cell death inhibitor (ferrostatin-1, 1 μM; zVAD-fmk, 10 μM; necrosulfonamide, 0.5 μM) for 24 h. Data were analyzed using analysis of variance (ANOVA) with Tukey’s post hoc test. c Overexpression of miR-212-5p suppressed Rsl3-induced cell death in HT-22 and Neuro-2a cells. d Inhibition of endogenous miR-212-5p enhanced Rsl3-induced cell death in HT-22 and Neuro-2a cells. Indicated cells were treated with Rsl3 (3 μM) for 24 h. The transfection efficacy of overexpression (e) or inhibition (f) was confirmed by qRT-PCR analysis. Cell death was assayed using the Cytotoxicity Detection kit. Data shown represent mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001. CCI, controlled cortical impactCC BY · PubMed Central
Fig. 4 miR-212-5p directly targets Ptgs2 in HT22 and Neuro-2a cell lines. Schematic diagram of strategy to discover the target gene of miR-212-5p is shown in (a). b The expression of Ptgs2 was significantly increased at all indicated time points after CCI. c Sequence alignment of miR-212-5p and the 3′-UTR of Ptgs2. The seed sequence of miR-212-5p and the binding sites in 3′-UTR are marked with underscores. d miR-212-5p overexpression inhibited the expression of 3′-UTR-luciferase reporter of Ptgs2 in HT-22 and Neuro-2a cells, but the mutant construct was immune to miR-212-5p. The 3′-UTR mutants containing mismatched nucleotides are shown at the bottom. In HT-22 (e) or Neuro-2a (f) cells, miR-212-5p overexpression inhibited the expression of Ptgs2, while inhibition of miR-212-5p caused the downregulation of Ptgs2. Data are presented as mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001
Fig. 4 miR-212-5p directly targets Ptgs2 in HT22 and Neuro-2a cell lines. Schematic diagram of strategy to discover the target gene of miR-212-5p is shown in (a). b The expression of Ptgs2 was significantly increased at all indicated time points after CCI. c Sequence alignment of miR-212-5p and the 3′-UTR of Ptgs2. The seed sequence of miR-212-5p and the binding sites in 3′-UTR are marked with underscores. d miR-212-5p overexpression inhibited the expression of 3′-UTR-luciferase reporter of Ptgs2 in HT-22 and Neuro-2a cells, but the mutant construct was immune to miR-212-5p. The 3′-UTR mutants containing mismatched nucleotides are shown at the bottom. In HT-22 (e) or Neuro-2a (f) cells, miR-212-5p overexpression inhibited the expression of Ptgs2, while inhibition of miR-212-5p caused the downregulation of Ptgs2. Data are presented as mean ± SEM from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001CC BY · PubMed Central
Fig. 5 miR-212-5p improved water maze performance after CCI in mice. a Intracerebroventricular (i.c.v.) injection site brain schematic diagram. b time course of the experiments. c in MWM test, mean escape latency for each group was plotted during the 7th to 13th day. Data of escape latency are performed using two-way analysis of variance (ANOVA) for repeated measures. d The frequency of crossing the platform was recorded on the 15th day. The speed of each mouse in the spatial probe test was recorded and shown in (e). These Data are presented as mean ± SEM (n = 13 for each group) and analyzed with the student’s t-test. *p < 0.05, **p < 0.01. CCI, controlled cortical impact; MWM, Morris Water Maze
Fig. 5 miR-212-5p improved water maze performance after CCI in mice. a Intracerebroventricular (i.c.v.) injection site brain schematic diagram. b time course of the experiments. c in MWM test, mean escape latency for each group was plotted during the 7th to 13th day. Data of escape latency are performed using two-way analysis of variance (ANOVA) for repeated measures. d The frequency of crossing the platform was recorded on the 15th day. The speed of each mouse in the spatial probe test was recorded and shown in (e). These Data are presented as mean ± SEM (n = 13 for each group) and analyzed with the student’s t-test. *p < 0.05, **p < 0.01. CCI, controlled cortical impact; MWM, Morris Water MazeCC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 6 references

Research works printed but not linked: 67

  1. Rubiano AM, Carney N, Chesnut R, Puyana JC. Global neurotrauma research challenges and opportunities. Nature. 2015;527(7578):S193–7. · DOI
  2. Iaccarino C, Carretta A, Nicolosi F, Morselli C. Epidemiology of severe traumatic brain injury. J Neurosurg Sci. 2018;62:535–41. · DOI
  3. Majdan M, Plancikova D, Maas A, Polinder S, Feigin V, Theadom A, et al. Years of life lost due to traumatic brain injury in Europe: a cross-sectional analysis of 16 countries. PLoS Med. 2017;14(7):e1002331. · DOI
  4. Cheng P, Yin P, Ning P, Wang L, Cheng X, Liu Y, et al. Trends in traumatic brain injury mortality in China, 2006–2013: a population-based longitudinal study. PLoS Med. 2017;14(7):e1002332. · DOI
  5. Ved R, Zaben M. Biomarkers for traumatic brain injury. J Neurol. 2018;265(5):1241–3. · DOI
  6. Stockwell BR, Friedmann Angeli JP, Bayir H, Bush AI, Conrad M, Dixon SJ, et al. Ferroptosis: a regulated cell death Nexus linking metabolism, redox biology, and disease. Cell. 2017;171:273–85. · DOI · Paper page
  7. Fricker M, Tolkovsky AM, Borutaite V, Coleman M, Brown GC. Neuronal cell death. Physiol Rev. 2018;98(2):813–80. https://doi.org/10.1152/physrev.00011.2017 . · DOI
  8. Gaschler MM, Hu F, Feng H, Linkermann A, Min W, Stockwell BR. Determination of the subcellular localization and mechanism of action of Ferrostatins in suppressing Ferroptosis. ACS Chem Biol. 2018;13(4):1013–20. · DOI
  9. Wenzel SE, Tyurina YY, Zhao J, St Croix CM, Dar HH, Mao G, et al. PEBP1 Wardens Ferroptosis by Enabling Lipoxygenase Generation of Lipid Death Signals. Cell. 2017;171(3):628–641.e26. · DOI
  10. Cao JY, Dixon SJ. Mechanisms of ferroptosis. Cell Mol Life Sci. 2016;73:2195–209. · DOI · Paper page
  11. Lane DJR, Ayton S, Bush AI. Iron and Alzheimer’s disease: an update on emerging mechanisms. J Alzheimers Dis. 2018;64(s1):S379–95. Available from: http://www.medra.org/servlet/aliasResolver?alias=iospress&doi=10.3233/JAD-179944 . · DOI
  12. Becker RE, Kapogiannis D, Greig NH. Does traumatic brain injury hold the key to the Alzheimer’s disease puzzle? Alzheimers Dement. 2018;14(4):431–43. https://doi.org/10.1016/j.jalz.2017.11.007 . · DOI
  13. Rosenfeld JV, McFarlane AC, Bragge P, Armonda RA, Grimes JB, Ling GS. Blast-related traumatic brain injury. Lancet Neurol. 2013;12(9):882–93. · DOI
  14. Pan YB, Sun ZL, Feng DF. The role of MicroRNA in traumatic brain injury. Neuroscience. 2017;367:189–99. · DOI
  15. Wanet A, Tacheny A, Arnould T, Renard P. MiR-212/132 expression and functions: within and beyond the neuronal compartment. Nucleic Acids Res. 2012;40(11):4742–53. · DOI
  16. Aten S, Hansen KF, Hoyt KR, Obrietan K. The miR-132/212 locus: a complex regulator of neuronal plasticity, gene expression and cognition. RNA Dis. 2016;3:e1375.
  17. Hansen KF, Sakamoto K, Aten S, Snider KH, Loeser J, Hesse AM, et al. Targeted deletion of miR-132/−212 impairs memory and alters the hippocampal transcriptome. Learn Mem. 2016;23(2):61–71. · DOI · Paper page
  18. Hernandez-Rapp J, Smith PY, Filali M, Goupil C, Planel E, Magill ST, et al. Memory formation and retention are affected in adult miR-132/212 knockout mice. Behav Brain Res. 2015;287:15–26. · DOI · Paper page
  19. Burek M, König A, Lang M, Fiedler J, Oerter S, Roewer N, et al. Hypoxia-induced MicroRNA-212/132 Alter blood-brain barrier integrity through inhibition of tight junction-associated proteins in human and mouse brain microvascular endothelial cells. Transl Stroke Res. 2019. https://doi.org/10.1007/s12975-018-0683-2 . · DOI
  20. Smith PY, Hernandez-Rapp J, Jolivette F, Lecours C, Bisht K, Goupil C, et al. MiR-132/212 deficiency impairs tau metabolism and promotes pathological aggregation in vivo. Hum Mol Genet. 2015;24(23):6721–35. · DOI · Paper page
  21. Hernandez-Rapp J, Rainone S, Goupil C, Dorval V, Smith PY, Saint-Pierre M, et al. MicroRNA-132/212 deficiency enhances Aβ production and senile plaque deposition in Alzheimer’s disease triple transgenic mice. Sci Rep. 2016;6:30953. · DOI
  22. Lighthall JW. Controlled cortical impact: a New experimental brain injury model. J Neurotrauma. 2009;5(1):1–15. · DOI
  23. Dean DD, Frank JA, Turtzo LC. Controlled cortical impact in the rat. Curr Protoc Neurosci. 2017;81:9.62.1–9.62.12. · DOI
  24. Romine J, Gao X, Chen J. Controlled cortical impact model for traumatic brain injury. J Vis Exp. 2014;(90):e51781. https://doi.org/10.3791/51781 . · DOI
  25. Lyeth BG, Ray M, Hamm RJ, Schnabel J, Saady JJ, Poklis A, et al. Postinjury scopolamine administration in experimental traumatic brain injury. Brain Res. 1992;569(2):281–6. · DOI
  26. Bermpohl D, You Z, Korsmeyer SJ, Moskowitz MA, Whalen MJ. Traumatic brain injury in mice deficient in bid: effects on histopathology and functional outcome. J Cereb Blood Flow Metab. 2006;26(5):625–33. · DOI
  27. He J, Yang X, Men B, Wang D. Interfacial mechanisms of heterogeneous Fenton reactions catalyzed by iron-based materials: a review. J Environ Sci (China). 2016;39:97–109. · DOI
  28. Sticht C, De La Torre C, Parveen A, Gretz N. Mirwalk: an online resource for prediction of microrna binding sites. PLoS One. 2018;13(10):e0206239. · DOI · Paper page
  29. Jiang YN, Yang SW, Zhang X, Luo LM, Zhang Z, Chen NH. Mechanism of ferroptosis and its role in neurological diseases. Chinese Pharmacol Bull. 2018;34(2):166–9.
  30. Xie BS, Wang YQ, Lin Y, Mao Q, Feng JF, Gao GY, et al. Inhibition of ferroptosis attenuates tissue damage and improves long-term outcomes after traumatic brain injury in mice. CNS Neurosci Ther. 2018;25:465–75. · DOI
  31. Kenny EM, Fidan E, Yang Q, Anthonymuthu TS, New LA, Meyer EA, et al. Ferroptosis contributes to neuronal death and functional outcome after traumatic brain injury. Crit Care Med. 2019;47(3):410–8. · DOI
  32. Devos D, Moreau C, Kyheng M, Garçon G, Rolland AS, Blasco H, et al. A ferroptosis–based panel of prognostic biomarkers for amyotrophic lateral sclerosis. Sci Rep. 2019;9(1):2198. · DOI
  33. Wu Y, Song J, Wang Y, Wang X, Culmsee C, Zhu C. The potential role of Ferroptosis in neonatal brain injury. Front Neurosci. 2019;13:115. · DOI
  34. Magtanong L, Dixon SJ. Ferroptosis and brain injury. Dev Neurosci. 2019;40:382–95. · DOI
  35. Hu C, Dong ZL. MicroRNA-212 promotes the recovery function and vascular regeneration of endothelial progenitor cells in mice with ischemic stroke through inactivation of the notch signaling pathway via downregulating MMP9 expression. J Cell Physiol. 2019;234(5):7090–103. · DOI
  36. Mendoza-Viveros L, Chiang CK, Ong JLK, Hegazi S, Cheng AH, Bouchard-Cannon P, et al. miR-132/212 modulates seasonal adaptation and dendritic morphology of the central circadian clock. Cell Rep. 2017;19(3):505–20. · DOI
  37. Wang CY, Deneen B, Tzeng SF. MicroRNA-212 inhibits oligodendrocytes during maturation by down-regulation of differentiation-associated gene expression. J Neurochem. 2017;143(1):112–25. · DOI
  38. Garcia-Concejo A, Jimenez-Gonzalez A, Rodriguez RE. Opioid and notch signaling pathways are reciprocally regulated through miR- 29a and miR-212 expression. Biochim Biophys Acta Gen Subj. 2018;1862(12):2605–12. · DOI
  39. Weigelt K, Bergink V, Burgerhout KM, Pescatori M, Wijkhuijs A, Drexhage HA. Down-regulation of inflammation-protective microRNAs 146a and 212 in monocytes of patients with postpartum psychosis. Brain Behav Immun. 2013;29:147–55. · DOI
  40. Keller RF, Kanlikilicer P, Dragomir A, Fan Y, Akay YM, Akay M. Investigating the effect of perinatal nicotine exposure on dopaminergic neurons in the VTA using miRNA expression profiles. IEEE Trans Nanobiosci. 2017;16(8):843–9. · DOI
  41. Wang Y, Veremeyko T, Wong AHK, El Fatimy R, Wei Z, Cai W, et al. Downregulation of miR-132/212 impairs S-nitrosylation balance and induces tau phosphorylation in Alzheimer’s disease. Neurobiol Aging. 2017;51:156–66. · DOI · Paper page
  42. Pichler S, Gu W, Hartl D, Gasparoni G, Leidinger P, Keller A, et al. The miRNome of Alzheimer’s disease: consistent downregulation of the miR-132/212 cluster. Neurobiol Aging. 2017;50:167.e1–167.e10. · DOI · Paper page
  43. Amadio P, Tarantino E, Sandrini L, Tremoli E, Barbieri SS. Prostaglandin-Endoperoxide Synthase-2 deletion affects the natural trafficking of annexin A2 in monocytes and favours venous thrombosis in mice. Thromb Haemost. 2017;117(8):1486–97. · DOI
  44. Hua X, Chi W, Su L, Li J, Zhang Z, Yuan X. ROS-induced oxidative injury involved in pathogenesis of fungal keratitis via p38 MAPK activation. Sci Rep. 2017;7(1):10421. · DOI
  45. Kong Z, Liu R, Cheng Y. Artesunate alleviates liver fibrosis by regulating ferroptosis signaling pathway. Biomed Pharmacother. 2019;109:2043–53. · DOI
  46. Zhang Z, Yao Z, Wang L, Ding H, Shao J, Chen A, et al. Activation of ferritinophagy is required for the RNA-binding protein ELAVL1/HuR to regulate ferroptosis in hepatic stellate cells. Autophagy. 2018;14(12):2083–103. · DOI
  47. Li Q, Han X, Lan X, Gao Y, Wan J, Durham F, et al. Inhibition of neuronal ferroptosis protects hemorrhagic brain. JCI Insight. 2017;2(7):e90777. · DOI
  48. Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE, et al. Ferroptosis: an iron-dependent form of nonapoptotic cell death. Cell. 2012;149(5):1060–72. · DOI · Paper page
  49. Sui X, Zhang R, Liu S, Duan T, Zhai L, Zhang M, et al. RSL3 drives ferroptosis through GPX4 inactivation and ros production in colorectal cancer. Front Pharmacol. 2018;9:1371. · DOI · Paper page
  50. Hirschhorn T, Stockwell BR. The development of the concept of ferroptosis. Free Radic Biol Med. 2019;133:130–43. · DOI · Paper page
  51. Liu X, Moon SH, Jenkins CM, Sims HF, Gross RW. Cyclooxygenase-2 mediated oxidation of 2-Arachidonoyl-Lysophospholipids identifies unknown lipid signaling pathways. Cell Chem Biol. 2016;23(10):1217–27. · DOI
  52. Bretscher P, Egger J, Shamshiev A, Trotzmuller M, Kofeler H, Carreira EM, et al. Phospholipid oxidation generates potent anti-inflammatory lipid mediators that mimic structurally related pro-resolving eicosanoids by activating Nrf2. EMBO Mol Med. 2015;7(5):593–607. · DOI
  53. Hambright WS, Fonseca RS, Chen L, Na R, Ran Q. Ablation of ferroptosis regulator glutathione peroxidase 4 in forebrain neurons promotes cognitive impairment and neurodegeneration. Redox Biol. 2017;12:8–17. · DOI · Paper page
  54. Guiney SJ, Adlard PA, Bush AI, Finkelstein DI, Ayton S. Ferroptosis and cell death mechanisms in Parkinson’s disease. Neurochem Int. 2017;104:34–48. · DOI
  55. Ilmaniemi S, Taipale H, Tanskanen A, Tiihonen J, Hartikainen S, Tolppanen AM. Incidence of head injury and traumatic brain injury among people with Alzheimer’s disease. J Epidemiol Community Health. 2019;73:451–4. · DOI
  56. Mohamed AZ, Cumming P, Götz J, Nasrallah F. Tauopathy in veterans with long-term posttraumatic stress disorder and traumatic brain injury. Eur J Nucl Med Mol Imaging. 2019;46:1139–51. · DOI
  57. Lee Y-S, Lee D-H, Choudry HA, Bartlett DL, Lee YJ. Ferroptosis-induced endoplasmic reticulum stress: crosstalk between Ferroptosis and apoptosis. Mol Cancer Res. 2018;16:1073–6. https://doi.org/10.1158/1541-7786.MCR-18-0055 . · DOI
  58. Sun D, Chen X, Gu G, Wang J, Zhang J. Potential roles of mitochondria-associated ER membranes (MAMs) in traumatic brain injury. Cell Mol Neurobiol. 2017;37:1349–57. · DOI
  59. Gao M, Monian P, Pan Q, Zhang W, Xiang J, Jiang X. Ferroptosis is an autophagic cell death process. Cell Res. 2016;26(9):1021–32. · DOI · Paper page
  60. Kang R, Tang D. Autophagy and Ferroptosis - What’s the connection? Curr Pathobiol Rep. 2017;5(2):153–9 Available from: http://www.ncbi.nlm.nih.gov/pubmed/29038744 . · DOI
  61. Sun S, Han X, Li X, Song Q, Lu M, Jia M, et al. MicroRNA-212-5p prevents dopaminergic neuron death by inhibiting SIRT2 in MPTP-induced mouse model of Parkinson’s disease. Front Mol Neurosci. 2018;11:381. · DOI · Paper page
  62. Chen W, Zhou Y, Zhi X, Ma T, Liu H, Chen BW, et al. Delivery of miR-212 by chimeric peptide-condensed supramolecular nanoparticles enhances the sensitivity of pancreatic ductal adenocarcinoma to doxorubicin. Biomaterials. 2019;192:590–600. · DOI
  63. Zhang X, Lu L, Zhang X, Zhang B, Wu J. Synaptic acetylcholinesterase targeted by microRNA-212 functions as a tumor suppressor in non-small cell lung cancer. Int J Biochem Cell Biol. 2013;45:2530–40. · DOI
  64. Guo Y, Yu J, Wang C, Li K, Liu B, Du Y, et al. MiR-212-5p suppresses lipid accumulation by targeting FAS and SCD1. J Mol Endocrinol. 2017;59:205–17. · DOI
  65. Xiao J, Bei Y, Liu J, Dimitrova-Shumkovska J, Kuang D, Zhou Q, et al. miR-212 downregulation contributes to the protective effect of exercise against non-alcoholic fatty liver via targeting FGF-21. J Cell Mol Med. 2016;20:204–16. · DOI
  66. Fiedler SD, Carletti MZ, Hong X, Christenson LK. Hormonal regulation of MicroRNA expression in Periovulatory mouse mural granulosa Cells1. Biol Reprod. 2008;79:1030–7. · DOI
  67. Shang J, Li J, Keller MP, Hohmeier HE, Wang Y, Feng Y, et al. Induction of miR-132 and miR-212 expression by glucagon-like peptide 1 (GLP-1) in rodent and human pancreatic β-cells. Mol Endocrinol. 2015;29:1243–53. · DOI

Cited by

Sorted by citations

See all 163

Metadata

Authors
Xiao, X., Jiang, Y., Liang, W., Wang, Y., Cao, S., Yan, H., Gao, L., & Zhang, L.
Venue
Molecular Brain
Publisher
Springer Science and Business Media LLC
Published
2019-09-18
Volume
12
Issue
1
ISSN
1756-6606
DOI
10.1186/s13041-019-0501-0
PMC
PMC6749650
Cited by
163
References
6
Language
en
Licence
Funders
  • Fundamental Research Funds for the Central Universities (No. 2018SCUH0053)
  • Science and Technology Major Projects of Sichuan Province of China (No.2017SZDZX0013)
  • Science and Technology Support Program of Sichuan Province of China (No.2016SZ0013)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: miR-212-5p attenuates ferroptotic neuronal death after traumatic brain injury by targeting Ptgs2. https://app.cochat.ai/papers/10.1186/s13041-019-0501-0
The paper
Xiao, X., Jiang, Y., Liang, W., Wang, Y., Cao, S., Yan, H., Gao, L., & Zhang, L. (2019). miR-212-5p attenuates ferroptotic neuronal death after traumatic brain injury by targeting Ptgs2. Molecular Brain. https://doi.org/10.1186/s13041-019-0501-0