scholarly journals Participation of Caspase-3-Like Protease in Necrotic Cell Death of Myocardium During Ischemia -Reperfusion Injury in Rat Hearts

2003 ◽  
Vol 67 (3) ◽  
pp. 248-252 ◽  
Author(s):  
Yoshihisa Naka ◽  
Yoshiki Sawa ◽  
Motonobu Nishimura ◽  
Nobuaki Hirata ◽  
Hideki Ueda ◽  
...  
Keyword(s):  
Cell Death ◽  
Reperfusion Injury ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Rat Hearts

scholarly journals Biomarkers distinguish apoptotic and necrotic cell death during hepatic ischemia/reperfusion injury in mice

2014 ◽  
Vol 20 (11) ◽  
pp. 1372-1382 ◽  
Author(s):  
Min Yang ◽  
Daniel J. Antoine ◽  
James L. Weemhoff ◽  
Rosalind E. Jenkins ◽  
Anwar Farhood ◽  
...  
Keyword(s):  
Cell Death ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Necrotic Cell Death ◽  
Necrotic Cell ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

scholarly journals Biomarkers of Cellular Apoptosis and Necrosis in Donor Myocardium Are Not Predictive of Primary Graft Dysfunction

2016 ◽  
pp. 251-257 ◽  
Author(s):  
O. SZARSZOI ◽  
J. BESIK ◽  
M. SMETANA ◽  
J. MALY ◽  
M. URBAN ◽  
...  
Keyword(s):  
Cell Death ◽  
Prospective Study ◽  
Reperfusion Injury ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Transplant Recipients ◽  
Primary Graft Dysfunction ◽  
Graft Dysfunction ◽  
Apoptosis Markers

Primary graft dysfunction (PGD) is a life-threatening complication among heart transplant recipients and a major cause of early mortality. Although the pathogenesis of PGD is still unclear, ischemia/reperfusion injury has been identified as a predominant factor. Both necrosis and apoptosis contribute to the loss of cardiomyocytes during ischemia/reperfusion injury, and this loss of cells can ultimately lead to PGD. The aim of our prospective study was to find out whether cell death, necrosis and apoptosis markers present in the donor myocardium can predict PGD. The prospective study involved 64 consecutive patients who underwent orthotopic heart transplantation at our institute between September 2010 and January 2013. High-sensitive cardiac troponin T (hs-cTnT) as a marker of minor myocardial necrosis was detected from arterial blood samples before the donor’s pericardium was opened. Apoptosis (caspase-3, active + pro-caspase-3, bcl-2, TUNEL) was assessed from bioptic samples taken from the right ventricle prior graft harvesting. In our study, 14 % of transplant recipients developed PGD classified according to the standardized definition proposed by the ISHLT Working Group. We did not find differences between the groups in regard to hs-cTnT serum levels. The mean hs-cTnT value for the PGD group was 57.4±22.9 ng/l, compared to 68.4±10.8 ng/l in the group without PGD. The presence and severity of apoptosis in grafted hearts did not differ between grafts without PGD and hearts that subsequently developed PGD. In conclusion, our findings did not demonstrate any association between measured myocardial cell death, necrosis or apoptosis markers in donor myocardium and PGD in allograft recipients. More detailed investigations of cell death signaling pathways in transplanted hearts are required.

Prevention of apoptotic and necrotic cell death, caspase‐3 activation, and renal dysfunction by melatonin after ischemia/reperfusion

2003 ◽  
Vol 17 (8) ◽  
pp. 1-17 ◽  
Author(s):  
Oxana R. Kunduzova ◽  
Ghislaine Escourrou ◽  
Marie-Helene Seguelas ◽  
Philippe Delagrange ◽  
France De La Farge ◽  
...  
Keyword(s):  
Cell Death ◽  
Renal Dysfunction ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Necrotic Cell Death ◽  
Necrotic Cell

scholarly journals miR-380-5p facilitates NRF2 and attenuates cerebral ischemia/reperfusion injury-induced neuronal cell death by directly targeting BACH1

2021 ◽  
Vol 12 (1) ◽  
pp. 210-217
Author(s):  
Yibiao Wang ◽  
Min Xu
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Luciferase Assay ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia Reperfusion

Abstract Background This study aimed to explore the role of miR-380-5p in cerebral ischemia/reperfusion (CIR) injury-induced neuronal cell death and the potential signaling pathway involved. Methodology Human neuroblastoma cell line SH-SY5Y cells were used in this study. Oxygen and glucose deprivation/reperfusion (OGD/R) model was used to mimic ischemia/reperfusion injury. CCK-8 assay and flow cytometry were used to examine cell survival. Quantitative real time PCR (RT-qPCR) assay and Western blotting were used to measure the change of RNA and protein expression, respectively. TargetScan and Luciferase assay was used to confirm the target of miR-380-5p. Malondialdehyde (MDA) superoxide dismutase (SOD) and glutathione peroxidase (GSHPx) were measured using commercial kits. Results miR-380-5p was downregulated in SH-SY5Y cells after OGD/R. Cell viability was increased by miR-380-5p, while cell apoptosis was reduced by miR-380-5p mimics. MDA was reduced by miR-380-5p mimics, while SOD and GSHPx were increased by miR-380-5p. Results of TargetScan and luciferase assay have showed that BACH1 is the direct target of miR-380-5p. Expression of NRF2 was upregulated after OGD/R, but was not affected by miR-380-5p. mRNA expression of HO-1 and NQO1 and ARE activity were increased by miR-380-5p. Overexpression of BACH1 reversed the antioxidant and neuroprotective effects of miR-380-5p. Conclusion miR-380-5p inhibited cell death induced by CIR injury through target BACH1 which also facilitated the activation of NRF2, indicating the antioxidant and neuroprotective effects of miR-380-5p.

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