Hepatocyte growth factor prevents advanced glycation end products-induced injury and oxidative stress through a PI3K/Akt-dependent pathway in human endothelial cells

Zhou, Yijun; Yang, Hongwu; Wang, Xiaoge; Zhang, Heng

doi:10.1016/j.lfs.2009.09.006

Cited by 38 publications

(19 citation statements)

References 25 publications

(24 reference statements)

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“…Cell activation, proinflammatory cytokine release and oxidative stress, induced by the interaction of AGEs with their receptors, may lead to endothelial injury and dysfunction [25,26]. Growing evidence suggests that EPCs, mobilized from bone marrow and other sites, contribute to the structural integrity of the vasculature, and also restore endothelial dysfunction [3].…”

Section: Discussionmentioning

confidence: 99%

Advanced glycation end products impair the migration, adhesion and secretion potentials of late endothelial progenitor cells

Zhang

Guan

et al. 2012

Cardiovasc Diabetol

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BackgroundEndothelial progenitor cells (EPCs), especially late EPCs, play a critical role in endothelial maintenance and repair, and postnatal vasculogenesis. Advanced glycation end products (AGEs) have been shown to impair EPC functions, such as proliferation, migration and adhesion. However, their role in the regulation of the production of vasoactive substances in late EPCs is less well defined.MethodsPassages of 3~5 EPCs, namely late EPCs, were cultured with different concentrations (0~500 μg/ml) of AGEs, and the apoptosis, adhesion and migration were subsequently determined. The release of vasoactive substances, such as stromal cell-derived factor-1 (SDF-1), nitric oxide (NO), prostaglandin I2 (PGI2), plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA), and in addition the activity of superoxide dismutase (SOD), were evaluated by ELISA. At the same time, the gene and protein expressions of CXCR4 were assayed by real-time RT-PCR and western-blot.ResultsAGEs promoted late EPC apoptosis. Moreover, AGEs impaired late EPC migration and adhesion in a concentration-dependent manner. Accordingly, the production of SDF-1 was decreased by AGEs. Although the CXCR4 expressions of late EPCs were up-regulated for AGE concentrations of 50, 100 or 200 μg/ml, a marked decrease was observed for the higher concentration of 500 μg/ml. Furthermore, co-culturing with AGEs decreased the levels of NO, t-PA, PGI2, and the activity of SOD but up-regulated the production of PAI-1.ConclusionOur data provide evidence that AGEs play an important role in impairing late EPC functions, which could contribute to the development of vascular diseases in diabetes.

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Section: Discussionmentioning

confidence: 99%

Advanced glycation end products impair the migration, adhesion and secretion potentials of late endothelial progenitor cells

Zhang

Guan

et al. 2012

Cardiovasc Diabetol

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“…Blockage of HGF by specific antibodies resulted in an increase of myocyte cell death. Additionally, HGF is thought to be involved in the recruitment of stem cells into ischaemic myocardium21 and to suppress oxidative stress 22. These cardioprotective effects were also associated with improvement of functional parameters such as perfusion and left ventricular function 4 6.…”

Section: Discussionmentioning

confidence: 99%

Hepatocyte growth factor is a strong predictor of mortality in patients with advanced heart failure

Rychli

Richter

Hohensinner

et al. 2011

Heart

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“…HGF activated NADPH oxidase and increased ROS generation (10,40,41); however, the role of HGF in lamellipodial ROS generation is unclear. Therefore, we hypothesized that HGF may stimulate ROS accumulation in lamellipodia.…”

Section: Hgf Stimulates Lamellipodia Formation In Lung Ecs-cellmentioning

confidence: 99%

Role of c-Met/Phosphatidylinositol 3-Kinase (PI3k)/Akt Signaling in Hepatocyte Growth Factor (HGF)-mediated Lamellipodia Formation, Reactive Oxygen Species (ROS) Generation, and Motility of Lung Endothelial Cells

Usatyuk

Mohan

et al. 2014

Journal of Biological Chemistry

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Background: Lamellipodia structures provide a platform for the spatio-temporal localization of key components necessary for cell migration. Results: HGF activates c-Met/PI3k/Akt signaling axis, which is essential for the recruitment of actin, cortactin, p47phox , and Rac1and ROS production in lamellipodia. Conclusion: HGF-induced spatio-temporal localization of cytoskeletal proteins and NADPH oxidase components regulate lamellipodial ROS and cell migration. Significance: This study identifies a novel role for lamellipodial ROS in cell motility.

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Hepatocyte growth factor prevents advanced glycation end products-induced injury and oxidative stress through a PI3K/Akt-dependent pathway in human endothelial cells

Cited by 38 publications

References 25 publications

Advanced glycation end products impair the migration, adhesion and secretion potentials of late endothelial progenitor cells

Advanced glycation end products impair the migration, adhesion and secretion potentials of late endothelial progenitor cells

Hepatocyte growth factor is a strong predictor of mortality in patients with advanced heart failure

Role of c-Met/Phosphatidylinositol 3-Kinase (PI3k)/Akt Signaling in Hepatocyte Growth Factor (HGF)-mediated Lamellipodia Formation, Reactive Oxygen Species (ROS) Generation, and Motility of Lung Endothelial Cells

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