scholarly journals Effects of Cornus Officinal Is Total Glycoside on Cardiomyocyte Apoptosis and Calcium Overload after Hypoxia/Reoxygenation Injury in Rats

2019 ◽  
Vol 10 (01) ◽  
pp. 1-10
Author(s):  
Ke Chen ◽  
Liudan Chen ◽  
Qihui Huang ◽  
Aizhen Pan ◽  
Kefang Chen ◽  
...  
Keyword(s):  
Calcium Overload ◽  
Cardiomyocyte Apoptosis ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

scholarly journals Antiphospholipid antibodies enhance rat neonatal cardiomyocyte apoptosis in an in vitro hypoxia/reoxygenation injury model via p38 MAPK

2017 ◽  
Vol 8 (1) ◽  
pp. e2549-e2549 ◽  
Author(s):  
Lauren T Bourke ◽  
Thomas McDonnell ◽  
James McCormick ◽  
Charis Pericleous ◽  
Vera M Ripoll ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Antiphospholipid Antibodies ◽  
Cardiomyocyte Apoptosis ◽  
Injury Model ◽  
Reoxygenation Injury ◽  
Neonatal Cardiomyocyte ◽  
Hypoxia Reoxygenation

scholarly journals Inhibition of miR-302 Suppresses Hypoxia-Reoxygenation-Induced H9c2 Cardiomyocyte Death by Regulating Mcl-1 Expression

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Yao-Ching Fang ◽  
Chi-Hsiao Yeh
Keyword(s):  
Leukemia Cell ◽  
Cardiomyocyte Apoptosis ◽  
Luciferase Reporter ◽  
Protein Levels ◽  
Reporter Assays ◽  
Reoxygenation Injury ◽  
Polymerase Chain ◽  
Apoptosis Related Protein ◽  
Hypoxia Reoxygenation

MicroRNAs play important roles in cell proliferation, differentiation, and apoptosis, and their expression influences cardiomyocyte apoptosis resulting from ischemia-induced myocardial infarction. Here, we determined the role of miR expression in cardiomyocyte apoptosis during hypoxia and reoxygenation. The rat cardiomyocyte cell line H9c2 was incubated for 3 h in normal or hypoxia medium, followed by reoxygenation for 24 h and transfection with a miR-302 mimic or antagomir. The effect of miR-302 on myeloid leukemia cell-differentiation protein-1 (Mcl-1) expression was determined by western blot, real-time polymerase chain reaction, and luciferase reporter assays, with cell viability assays. We observed that miR-302 expression was elevated by hypoxia/reoxygenation injury and increased further or decreased by transfection of the miR-302 mimic or miR-302 antagomir, respectively. Additionally, elevated miR-302 levels increased apoptosis-related protein levels and cardiomyocyte apoptosis, and luciferase reporter assays revealed miR-302 binding to the Mcl-1 mRNA 3′ untranslated region. Our findings suggested that miR-302 overexpression aggravated hypoxia/reoxygenation-mediated cardiomyocyte apoptosis by inhibiting antiapoptotic Mcl-1 expression, thereby activating proapoptotic molecules. Furthermore, results indicating cardiomyocyte rescue from hypoxia/reoxygenation injury following treatment with miR-302 antagomir suggested that miR-302 inhibition might constitute a therapeutic strategy for protection against cardiomyocyte apoptosis during hypoxia/reoxygenation injury.

scholarly journals H2S protects hippocampal neurons against hypoxia-reoxygenation injury by promoting RhoA phosphorylation at Ser188

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ye Chen ◽  
Jiyue Wen ◽  
Zhiwu Chen
Keyword(s):  
Endothelial Cells ◽  
Hippocampal Neurons ◽  
Glucose Deprivation ◽  
Rhoa Activity ◽  
Mercaptopyruvate Sulfurtransferase ◽  
Dependent Protein ◽  
Cerebral Vasodilatation ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

AbstractInhibition of RhoA-ROCK pathway is involved in the H2S-induced cerebral vasodilatation and H2S-mediated protection on endothelial cells against oxygen-glucose deprivation/reoxygenation injury. However, the inhibitory mechanism of H2S on RhoA-ROCK pathway is still unclear. The aim of this study was to investigate the target and mechanism of H2S in inhibition of RhoA/ROCK. GST-RhoAwild and GST-RhoAS188A proteins were constructed and expressed, and were used for phosphorylation assay in vitro. Recombinant RhoAwild-pEGFP-N1 and RhoAS188A-pEGFP-N1 plasmids were constructed and transfected into primary hippocampal nerve cells (HNCs) to evaluate the neuroprotective mechanism of endothelial H2S by using transwell co-culture system with endothelial cells from cystathionine-γ-lyase knockout (CSE−/−) mice and 3-mercaptopyruvate sulfurtransferase knockout (3-MST−/−) rats, respectively. We found that NaHS, exogenous H2S donor, promoted RhoA phosphorylation at Ser188 in the presence of cGMP-dependent protein kinase 1 (PKG1) in vitro. Besides, both exogenous and endothelial H2S facilitated the RhoA phosphorylation at Ser188 in HNCs, which induced the reduction of RhoA activity and membrane transposition, as well as ROCK2 activity and expression. To further investigate the role of endothelial H2S on RhoA phosphorylation, we detected H2S release from ECs of CSE+/+ and CSE−/− mice, and 3-MST+/+ and 3-MST−/− rats, respectively, and found that H2S produced by ECs in the culture medium is mainly catalyzed by CSE synthase. Moreover, we revealed that both endothelial H2S, mainly catalyzed by CSE, and exogenous H2S protected the HNCs against hypoxia-reoxygenation injury via phosphorylating RhoA at Ser188.

ELABELA alleviates syncytiotrophoblast hypoxia/reoxygenation injury and preeclampsia-like symptoms in mice by reducing apoptosis

Placenta ◽  
2021 ◽  
Vol 106 ◽  
pp. 30-39
Author(s):  
Jing Ma ◽  
Haoyue Hu ◽  
Miaoling Lin ◽  
Lu Chen ◽  
Mian Liu ◽  
...  
Keyword(s):  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation
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