TRAIL protects against endothelium injury in diabetes via Akt-eNOS signaling

Liu, Min; Gao, Xiang; Lu, Junyan; Xiang, Lin; Dong, Jing; Wen, Mei

doi:10.1016/j.atherosclerosis.2014.10.013

Cited by 40 publications

(36 citation statements)

References 30 publications

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“…Consistent with these functional data, we also identified increased Akt protein expression in the coronary arteries of rats with infarction as compared with the SO animals, whereas the AMPK protein expression was not different between the groups. The present findings appear to be consistent with the literature, which indicates that an activated PI3-kinase/Akt pathway increased eNOS/NO production and ameliorated the endothelial dysfunction in the peripheral arteries of diabetic and infarcted rats [39,40]. In addition, the PI3-kinase/Akt signalling pathway increases NO production in vascular smooth muscle cells and endothelial cells via nNOS/NO activation [35,36].…”

Section: Discussionsupporting

confidence: 92%

Enhanced nitric oxide bioavailability in coronary arteries prevents the onset of heart failure in rats with myocardial infarction

Couto¹,

Britto²,

Mill³

et al. 2015

Journal of Molecular and Cellular Cardiology

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Section: Discussionsupporting

confidence: 92%

Enhanced nitric oxide bioavailability in coronary arteries prevents the onset of heart failure in rats with myocardial infarction

Couto¹,

Britto²,

Mill³

et al. 2015

Journal of Molecular and Cellular Cardiology

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“…IL-1β is also implicated in cardiovascular and microvascular long-term complications (nephropathy, retinopathy, and polyneuropathy) of diabetes (Herder et al, 2013(Herder et al, , 2015Agrawal and Kant, 2014;Stahel et al, 2016;Donath et al, 2019). Endothelial cell damage is a crucial and an early manifestation of diabetic-associated vascular complications (van den Oever et al, 2010;Gilbert, 2013;Liu et al, 2014). Among the multiple and potential mechanisms that contribute to this phenomenon, a crucial role is played by chronic low-grade inflammation.…”

Section: Molecular Pathways Linking Obesity-induced Inflammation and Irmentioning

confidence: 99%

Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes

et al. 2020

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“…8 Increasing researches indicated that PI3K/Akt/eNOS signaling pathway possesses a crucial role in the repair of endothelial damage under HG condition. 50,51 Once activated, phosphorylated PI3K/Akt can directly phosphorylate eNOS followed by the generation of NO, which acts as an endothelial cell survival factor. 52 Yan et al found that the impaired vascular regeneration was partially ascribed to the deficiency of NO accounts in diabetic ischemic injury animal model.…”

Section: Dovepressmentioning

confidence: 99%

<p>Hydrogen Sulfide Protects Against High Glucose-Induced Human Umbilical Vein Endothelial Cell Injury Through Activating PI3K/Akt/eNOS Pathway</p>

Lin

Yang

Wei

et al. 2020

DDDT

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Dysfunction of endothelial cells plays a key role in the pathogenesis of diabetic atherosclerosis. High glucose (HG) has been found as a key factor in the progression of diabetic complications, including atherosclerosis. PI3K/Akt/eNOS signaling pathway has been shown to involve in HG-induced vascular injuries. Hydrogen sulfide (H 2 S) has been found to exhibit protective effects on HG-induced vascular injuries. Moreover, H 2 S activates PI3K/Akt/eNOS pathway in endothelial cells. Thus, the present study aimed to determine if H 2 S exerts protective effects against HG-induced injuries of human umbilical vein endothelial cells (HUVECs) via activating PI3K/Akt/eNOS signaling. Materials and Methods: The endothelial protective effects of H 2 S were evaluated and compared to the controlled groups. Cell viability, cell migration and tube formation were determined by in vitro functional assays; protein levels were evaluated by Western blot assay and ELISA; cell apoptosis was determined by Hoechst 33258 nuclear staining; Reactive oxygen species (ROS) production was evaluated by the ROS detection kit. Results: HG treatment significantly inhibited PI3K/Akt/eNOS signaling in HUVECs, which was partially reversed by the H2S treatment. HG treatment inhibited cell viability of HUVECs, which were markedly prevented by H 2 S or PI3K agonist Y-P 740. HG treatment also induced HUVEC cell apoptosis by increasing the protein levels of cleaved caspase 3, Bax and Bcl-2, which were significantly attenuated by H 2 S or 740 Y-P. ROS production and gp91 phox protein level were increased by HG treatment in HUVECs and this effect can be blocked by the treatment with H 2 S or Y-P 740. Moreover, HG treatment increased the protein levels of pro-inflammatory cytokines, caspase-1 and phosphorylated JNK, which was significantly attenuated by H 2 S or Y-P 740. Importantly, the cytoprotective effect of H 2 S against HG-induced injury was inhibited by LY294002 (an inhibitor of PI3K/Akt/eNOS signaling pathway). Conclusion: The present study demonstrated that exogenous H 2 S protects endothelial cells against HG-induced injuries by activating PI3K/Akt/eNOS pathway. Based on the above findings, we proposed that reduced endogenous H 2 S levels and the subsequent PI3K/Akt/ eNOS signaling impairment may be the important pathophysiological mechanism underlying hyperglycemia-induced vascular injuries.

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TRAIL protects against endothelium injury in diabetes via Akt-eNOS signaling

Cited by 40 publications

References 30 publications

Enhanced nitric oxide bioavailability in coronary arteries prevents the onset of heart failure in rats with myocardial infarction

Enhanced nitric oxide bioavailability in coronary arteries prevents the onset of heart failure in rats with myocardial infarction

Chronic Adipose Tissue Inflammation Linking Obesity to Insulin Resistance and Type 2 Diabetes

<p>Hydrogen Sulfide Protects Against High Glucose-Induced Human Umbilical Vein Endothelial Cell Injury Through Activating PI3K/Akt/eNOS Pathway</p>

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