Protective effect of sphingosine-1-phosphate for chronic intermittent hypoxia-induced endothelial cell injury

2018 ◽  
Vol 498 (4) ◽  
pp. 1016-1021 ◽  
Author(s):  
Fu-chao Yu ◽  
Chu-xiao Yuan ◽  
Jia-yi Tong ◽  
Guang-hao Zhang ◽  
Fang-ping Zhou ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Protective Effect ◽  
Intermittent Hypoxia ◽  
Cell Injury ◽  
Chronic Intermittent Hypoxia ◽  
Endothelial Cell Injury ◽  
Sphingosine 1 Phosphate

scholarly journals MicroRNA-421 protects against chronic intermittent hypoxia-induced vascular endothelial cell injury by targeting TLR4

2020 ◽  
Vol 19 (3) ◽  
pp. 525-532
Author(s):  
Jie Yuan ◽  
Jiankuan Shi ◽  
Shuqi Yu ◽  
Hong Zhang
Keyword(s):  
Endothelial Cell ◽  
Intermittent Hypoxia ◽  
Cell Injury ◽  
Vascular Endothelial Cells ◽  
Chronic Intermittent Hypoxia ◽  
Vascular Endothelial ◽  
Oxygen Species ◽  
Endothelial Cell Injury ◽  
Protein Levels ◽  
Cellular Reactive Oxygen Species

Purpose: To investigate the role of miR-421 in endothelial cell injury caused by chronic intermittent hypoxia (CIH), and to unravel the mechanism of action. Methods: A rat aortic endothelial cell model of CIH was established by 18-h exposure to hypoxic treatment. Cell viability was evaluated by MTT while cell apoptosis was determined by flow cytometry. Cellular reactive oxygen species (ROS) levels were assessed by cellular reactive oxygen species (ROS) assay kit. The mRNA and protein levels were also determined. Sprague Dawley rats were used to establish a rat CIH model over a 6-week hypoxic exposure. The degree of lung and renal injuries in the rats were observed by HE staining. Results: MiR-421 was downregulated and toll-like receptor 4 (TLR4) upregulated in CIH cells compared to control cells. Treatment of CIH cells decreased their viability, increased cellular ROS levels, promoted cell apoptosis, and caused changes in protein levels of apoptosis- and inflammation-related genes. However, miR-421 mimics reversed these results caused by CIH treatment. Dual luciferase reporter assay verified that TLR4 was targeted by miR-421. Moreover, TLR4 overexpression suppressed the protective effect of miR-421 on CIH cells. Finally, miR-421 agomiR inhibited CIH-induced TLR4 upregulation in rats. Histopathological examinations confirmed that miR-421 agomiR inhibited CIHinduced injury and collagen deposition in rat lungs and kidneys. Conclusion: MiR-421 protects vascular endothelial cells against CIH-induced injury in rats by targeting TLR4, which may provide a biomarker for the diagnosis and treatment of CIH-induced injury. Keywords: Obstructive sleep apnea syndrome, MiR-421, TLR4, Chronic intermittent hypoxia, Vascular endothelial cells

scholarly journals Protective Effect of Atorvastatin on Radiation-induced Vascular Endothelial Cell Injury In Vitro

2010 ◽  
Vol 51 (5) ◽  
pp. 527-533 ◽  
Author(s):  
Xin-Ze RAN ◽  
Xi RAN ◽  
Zhao-Wen ZONG ◽  
Deng-Qun LIU ◽  
Gui-Ming XIANG ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Protective Effect ◽  
Cell Injury ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Injury ◽  
Radiation Induced

scholarly journals Protective effect of tetrahydrobiopterin against SIN-1-induced endothelial cell injury

1998 ◽  
Vol 76 ◽  
pp. 146
Author(s):  
Masakazu Ishii ◽  
Shunichi Shimizu ◽  
Yutaka Kawakami ◽  
Kazutaka Momose ◽  
Toshinori Yamamoto
Keyword(s):  
Endothelial Cell ◽  
Protective Effect ◽  
Cell Injury ◽  
Endothelial Cell Injury

Characterization of the Protective Effect of Tetrahydrobiopterin Against S-Nitroso-N -Acetyl-D ,L-Penicillamine Induced Endothelial Cell Injury

Pteridines ◽  
1999 ◽  
Vol 10 (1) ◽  
pp. 14-19 ◽  
Author(s):  
Masakazu Ishii ◽  
Shunichi Shimizu ◽  
Kazutaka Momose ◽  
Yuji Kiuchi ◽  
Toshinori Yamamoto
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Protective Effect ◽  
Cell Injury ◽  
Oxygen Species ◽  
No Donor ◽  
Endothelial Cell Injury ◽  
Ros Scavenger ◽  
Intracellular Oxidative Stress

The purpose of this study was to characterize the protective effect of tetrahydrobiopterin (BH4), one of the cofactors of nitric oxide (NO) synthase, against NO-induced endothelial cell injury. The addition of S-nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor, to endothelial cells induced the release of lactate dehydrogenase (LDH), a marker for cell injury. The SNAP-induced endothelial cell injury was markedly reduced by pretreatment with sepiapterin, a precursor of BH4 synthesis. On the other hand, exogenous BH4 had little effect on the SNAP-induced endothelial cell injury. We recently found that NO-induced endothelial cell injury involves a part of H202 production, since the injury was blocked by the treatment with catalase. Although BH4 released reactive oxygen species (ROS) in cell-free conditions, the increase in intracellular BH4 by pretreatment with sepiapterin strongly reduced H202-induced intracellular oxidative stress. These findings suggest that the increase in intracellular BH4 content but not extracellular BH4, strongly attenuates NO-induced endothelial cell injury by at least one of the mechanisms by which BH4 reduces H202-induced oxidative stress. Intracellular BH4 seems mainly to play a role as an antioxidant or as a ROS-scavenger.

scholarly journals Protective effect of berberine against LPS-induced endothelial cell injury via the JNK signaling pathway and autophagic mechanisms

Bioengineered ◽  
2021 ◽  
Vol 12 (1) ◽  
pp. 1324-1337
Author(s):  
Junping Guo ◽  
Wei Chen ◽  
Beibei Bao ◽  
Dayong Zhang ◽  
Jianping Pan ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Cell Injury ◽  
Endothelial Cell Injury ◽  
Jnk Signaling ◽  
Jnk Signaling Pathway
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