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 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.

An in vitro model of warm hypoxia–reoxygenation injury in human liver endothelial cells

2012 ◽  
Vol 178 (1) ◽  
pp. e35-e41 ◽  
Author(s):  
Neal R. Banga ◽  
K. Raj Prasad ◽  
J. Lance Burn ◽  
Shervanthi Homer-Vanniasinkam ◽  
Anne Graham
Keyword(s):  
Endothelial Cells ◽  
Human Liver ◽  
In Vitro Model ◽  
Reoxygenation Injury ◽  
Liver Endothelial Cells ◽  
Vitro Model ◽  
Hypoxia Reoxygenation

scholarly journals miR-19a protects cardiomyocytes from hypoxia/reoxygenation-induced apoptosis via PTEN/PI3K/p-Akt pathway

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Guochao Sun ◽  
Ying Lu ◽  
Yingxia Li ◽  
Jun Mao ◽  
Jun Zhang ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Ischemic Injury ◽  
Cardiomyocyte Apoptosis ◽  
Luciferase Reporter ◽  
H9c2 Cells ◽  
Rat Cardiomyocytes ◽  
Protein Levels ◽  
Myocardial Ischemic Injury ◽  
Hypoxia Reoxygenation

miRNAs have been implicated in processing of cardiac hypoxia/reoxygenation (H/R)-induced injury. Recent studies demonstrated that miR-19a might provide a potential cardioprotective effect on myocardial disease. However, the effect of miR-19a in regulating myocardial ischemic injury has not been previously addressed. The present study was to investigate the effect of miR-19a on myocardial ischemic injury and identified the potential molecular mechanisms involved. Using the H/R model of rat cardiomyocytes H9C2 in vitro, we found that miR-19a was in low expression in H9C2 cells after H/R treatment and H/R dramatically decreased cardiomyocyte viability, and increased lactate dehydrogenase (LDH) release and cardiomyocyte apoptosis, which were attenuated by co-transfection with miR-19a mimic. Dual-luciferase reporter assay and Western blotting assay revealed that PTEN was a direct target gene of miR-19a, and miR-19a suppressed the expression of PTEN via binding to its 3′-UTR. We further identified that overexpression of miR-19a inhibited the expression of PTEN at the mRNA and protein levels. Moreover, PTEN was highly expressed in H/R H9C2 cells and the apoptosis induced by H/R was associated with the increase in PTEN expression. Importantly, miR-19a mimic significantly increased p-Akt levels under H/R. In conclusion, our findings indicate that miR-19a could protect against H/R-induced cardiomyocyte apoptosis by inhibiting PTEN /PI3K/p-Akt signaling pathway.

β2-adrenergic agonist protects human endothelial cells from hypoxia/reoxygenation injury in vitro

2006 ◽  
Vol 34 (1) ◽  
pp. 165-172 ◽  
Author(s):  
Julien Pottecher ◽  
Gaëlle Cheisson ◽  
Olivier Huet ◽  
Christian Laplace ◽  
Eric Vicaut ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Human Endothelial Cells ◽  
Adrenergic Agonist ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

scholarly journals Naringin Effectively Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury

2021 ◽  
Vol 37 (3) ◽  
Author(s):  
Vu Thi Thu ◽  
Ngo Thi Hai Yen
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Cell Group ◽  
H9c2 Cell ◽  
H9c2 Cells ◽  
H9c2 Cardiomyocytes ◽  
Reoxygenation Injury ◽  
Hypoxia Reoxygenation

This study was conducted to evaluate the protective effect of Naringin (NAR) on H9C2 cardiomyocytes in hypoxia/reoxygenation (HR) injury in vitro induced by the hypoxia chamber. Methods: H9C2 cells were grown under normal (control) and HR conditions. The viability, cardiolipin content and mitochondrial membrane potential of H9C2 cells in experimental groups were analyzed by using suitable kits. Results: The obtained results showed that the addition of Naringin (16÷160 µM) significantly increased the survival rate of H9C2 cells under HR conditions. In particular, NAR had the highest efficiency in preserving mitochondrial function at concentrations of 80 µM and 160 µM. In HR-exposed H9C2 cell group, the cardiolipin content and mitochondrial membrane potential values of H9C2 cells were decreased sharply with that of control (71,64±1,37% and 68,12±2,78%, p<0,05). Interestingly, mitochondrial cardiolipin contents were signigicantly increased in H9C2 cells post-hypoxic treated wtih NAR at dose of 80 µM 160 µM to 87,76±1,89% and 81,09±1,21%. Additionally, post-hypoxic supplementation of NAR at concentration of 80 µM and 160 µM effectively increased mitochondrial membrane potential values. Conclusion: The obtained results are preliminary data on the effects of NAR in protecting mitochondrial-targeted cardiomyocytes against HR injury.

scholarly journals Glutamate as a potential “survival factor” in an in vitro model of neuronal hypoxia/reoxygenation injury: leading role of the Na+/Ca2+ exchanger

2018 ◽  
Vol 9 (7) ◽  
Author(s):  
Silvia Piccirillo ◽  
Pasqualina Castaldo ◽  
Maria Loredana Macrì ◽  
Salvatore Amoroso ◽  
Simona Magi
Keyword(s):  
In Vitro Model ◽  
Survival Factor ◽  
Leading Role ◽  
Reoxygenation Injury ◽  
Vitro Model ◽  
Hypoxia Reoxygenation
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