Effect of HSP27 and Cofilin in the injury of hypoxia/reoxygenation on hepatocyte membrane F-actin microfilaments

Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.

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PARP Inhibitor Protects Against Chronic Hypoxia/Reoxygenation-Induced Retinal Injury by Regulation of MAPKs, HIF1α, Nrf2, and NFκB

Investigative Opthalmology & Visual Science ◽

10.1167/iovs.18-25936 ◽

2019 ◽

Vol 60 (5) ◽

pp. 1478 ◽

Cited By ~ 12

Author(s):

Krisztina Kovacs ◽

Alexandra Vaczy ◽

Katalin Fekete ◽

Petra Kovari ◽

Tamas Atlasz ◽

...

Keyword(s):

Chronic Hypoxia ◽

Parp Inhibitor ◽

Retinal Injury ◽

Hypoxia Reoxygenation

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FoxO4 negatively modulates USP10 transcription to aggravate the apoptosis and oxidative stress of hypoxia/reoxygenation-induced cardiomyocytes by regulating the Hippo/YAP pathway

Journal of Bioenergetics and Biomembranes ◽

10.1007/s10863-021-09910-7 ◽

2021 ◽

Author(s):

Jingwen Huang ◽

Yu Liu ◽

Mei Wang ◽

Rong Wang ◽

Huifen Ling ◽

...

Keyword(s):

Oxidative Stress ◽

And Oxidative Stress ◽

Hypoxia Reoxygenation

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Transcriptional response of key metabolic and stress response genes of a nuculanid bivalve, Lembulus bicuspidatus from an oxygen minimum zone exposed to hypoxia-reoxygenation

Comparative Biochemistry and Physiology Part B Biochemistry and Molecular Biology ◽

10.1016/j.cbpb.2021.110617 ◽

2021 ◽

pp. 110617

Author(s):

Katherine Amorim ◽

Helen Piontkivska ◽

Michael L. Zettler ◽

Eugene Sokolov ◽

Tjorven Hinzke ◽

...

Keyword(s):

Stress Response ◽

Transcriptional Response ◽

Oxygen Minimum Zone ◽

Stress Response Genes ◽

Minimum Zone ◽

Oxygen Minimum ◽

Hypoxia Reoxygenation

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

Cell Death Discovery ◽

10.1038/s41420-021-00514-z ◽

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.

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