SIRT1 mediates Sphk1/S1P-induced proliferation and migration of endothelial cells

Gao, Zhan; Wang, Hua; Xiao, Fengjun; Shi, Xuefeng; Zhang, Yikun; Xu, Qin Qin; Zhang, Xiaoyan; Ha, Xiaoqin; Wang, Lisheng

doi:10.1016/j.biocel.2016.02.018

Cited by 33 publications

(26 citation statements)

References 34 publications

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“…Gao et al [15]. have also found that overexpression of Sirt1 may regulate endothelial cell proliferation and migration and proposed that Sirt1 could play a role in angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…The transfection of PMVECs with the Sirt1 lentiviral vector was carried out as described previously [15]. PMVECs were plated in 6-well plates at a density of 2 x 10 5 per well and then were infected with lentiviral vectors at a multiplicity of infection (MOI) of 20.…”

Section: Methodsmentioning

confidence: 99%

“…Sirt1 is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase protease which is thought to be involved in many regulatory processes through deacylation and interaction with several transcription factors and signalling molecules including those involved in neovascularisation [15]. Upregulated Sirt1 expression was found to downregulate FOXO3 acetylation to confer a protective role in IIR acute lung injury by modulating the effects of downstream anti-oxidative and anti-apoptotic factors [1].…”

Section: Introductionmentioning

confidence: 99%

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Nrf2 Activation Induced by Sirt1 Ameliorates Acute Lung Injury After Intestinal Ischemia/Reperfusion Through NOX4-Mediated Gene Regulation

Chai

Zhang

Shen

et al. 2018

Cell Physiol Biochem

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Background/Aims: Nuclear erythroid 2-related factor-2 (Nrf2) is a major stress-response transcription factor that has been implicated in regulating ischemic angiogenesis. We investigated the effects of Nrf2 in regulating revascularization and modulating acute lung injury. Methods: The expression of Nrf2 and sirtuin1 (Sirt1) was assessed in lung tissue by western blotting and immunofluorescence staining after intestinal ischemia/reperfusion (IIR) in Nrf2–/– and wild-type (WT) mice. The involvement of Nrf2 in angiogenesis, cell viability, and migration was investigated in human pulmonary microvascular endothelial cells (PMVECs). Additionally, the influence of Nrf2 expression on NOX pathway activation was measured in PMVECs after oxygen–glucose deprivation/reoxygenation. Results: We found activation and nuclear accumulation of Nrf2 in lung tissue after IIR. Compared to IIR in WT mice, IIR in Nrf2–/– mice significantly enhanced leukocyte infiltration and collagen deposit, and inhibited endothelial cell marker CD31 expression. Nrf2 upregulation and translocation into the nucleus stimulated by Sirt1 overexpression exhibited remission of histopathologic changes and enhanced CD31 expression. Nrf2 knockdown repressed non-phagocytic cell oxidase 4 (NOX4), hypoxia-inducible factor (HIF-1α) and vascular endothelial growth factor (VEGF) expression after IIR. Nrf2 upregulation by Sirt1 enhances NOX4, HIF-1α and VEGF expression after IIR in WT mice. Furthermore, Nrf2 knockdown suppressed cell viability, capillary tube formation and cell migration in PMVECs after oxygen–glucose deprivation/reoxygenation and also inhibited NOX4, HIF-1 and VEGF expression. Moreover, NOX4 knockdown in PMVECs decreased the levels of VEGF, HIF-1α and angiogenesis. Conclusion: Nrf2 stimulation by Sirt1 plays an important role in sustaining angiogenic potential through NOX4-mediated gene regulation.

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“…Gao et al [15]. have also found that overexpression of Sirt1 may regulate endothelial cell proliferation and migration and proposed that Sirt1 could play a role in angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Nrf2 Activation Induced by Sirt1 Ameliorates Acute Lung Injury After Intestinal Ischemia/Reperfusion Through NOX4-Mediated Gene Regulation

Chai

Zhang

Shen

et al. 2018

Cell Physiol Biochem

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“…Regulation of angiogenesis by SIRT has been reported by our group as well as other groups. There are, however, contradicting reports on the role of SIRT‐1 in inducing or inhibition of angiogenesis where, Potente et al () and Gao et al () have shown that activation of SIRT 1 can induce angiogenic process, accompanied by proliferation and migration of endothelial cells. On the contrary, Zhang et al () described the role miR‐217 in development of angiogenesis by down regulating SIRT1 and FOXO3A.…”

Section: Discussionmentioning

confidence: 94%

Horizontal transfer of miR‐23a from hypoxic tumor cell colonies can induce angiogenesis

Sruthi

Edatt

Raji

et al. 2017

Journal Cellular Physiology

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Neo vessel formation by angiogenesis is an important event during many pathological conditions including cancer, where it is indispensable for tumor growth and survival. Although, various pro-angiogenic cytokines and soluble factors, secreted by tumor cells, have been reported to promote angiogenesis, recent studies have shown regulatory role of exosomes, secreted by tumor cells in the process of angiogenesis. These exosomes are capable of carrying nucleic acids, proteins, etc., as their cargo. Under the light of these facts and considering the presence of miRNAs, the non-coding RNAs capable of regulating target gene expression, as one of the major cargos in the exosomes, we investigated, whether exosomes derived from normoxic and hypoxic tumor cell colonies exhibit difference in levels of miR-23∼27∼24 cluster members and if so, to check the significance of their horizontal transfer on the process of angiogenesis. Results of our study showed that exosomes secreted by hypoxic tumor cell colonies possess significantly higher levels of miR23a and can induce angiogenesis. Further, we have shown that exosomes secreted by cells that ectopically over express miR23a is capable of inducing angiogenesis in different angiogenic model systems such as CAM, in ovo Xenograft and HUVEC models systems. Further, mechanistic analysis revealed that miR23a driven regulation of angiogenesis is brought about by down regulation of SIRT1 in the recipient cells. Collectively, the results presented here suggest that exosomal transfer of miR23a from tumor cell colonies can induce the process of angiogenesis by targeting SIRT1 in the recipient endothelial cells.

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“…In addition, AKT has been reported to be related to sirtuin 1. Gao et al reported that sirtuin 1 was upregulated through the AKT signaling pathway in the proliferation and migration of endothelial cells (50). It has also been found that the PI3K-AKT-GSK3β signaling pathway is required for sirtuin 1 induction by endoplasmic reticulum stress (51).…”

Section: Discussionmentioning

confidence: 99%

Simvastatin ameliorates ionizing radiation-induced apoptosis in the thymus by activating the AKT/sirtuin 1 pathway in mice

Yang

Huang

Tao

et al. 2017

International Journal of Molecular Medicine

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Simvastatin is a HMG-CoA reductase inhibitor widely used to lower plasma cholesterol and to protect against cardiovascular risk factors. The aim of this study was to investigate whether simvastatin attenuates ionizing radiation-induced damage in the mouse thymus and to elucidate the possible mechanisms invovled. For this purpose, male C57BL/6J mice aged 6 weeks were used and exposed to 4 Gy 60Co γ-radiation with or without simvastatin (20 mg/kg/day, for 14 days). Apoptosis was determined by terminal deoxynucle-otidyltransferase-mediated dUTP nick-end labeling (TUNEL) assay or transmission electron microscopy (TEM) examination. Thymocytes were also isolated and incubated in DMEM supplemented with 10% FBS at 37°C and exposed to 8 Gy 60Co γ-radiation with or without simvastatin (20 µM). The expression levels of Bcl-2, p53, p-p53, AKT, sirtuin 1 and poly(ADP-ribose) polymerase (PARP) were determined by western blot analysis. TUNEL and TEM examination revealed that simvastatin treatment significantly mitigated ionizing radiation-induced apoptosis in the mouse thymus. It was also found that simvastatin treatment increased AKT/sirtuin 1 expression following exposure to ionizing radiation in vivo and in vitro. In the in vivo model, but not in the in vitro model, Bcl-2 and PARP expression was augmented and that of p53/p-p53 decreased following treatment with simvastatin. On the whole, our findings indicate that simvastatin exerts a protective effect against ionizing radiation-induced damage in the mouse thymus, which may be partially attributed to the activation of the AKT/sirtuin 1 pathway.

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SIRT1 mediates Sphk1/S1P-induced proliferation and migration of endothelial cells

Cited by 33 publications

References 34 publications

Nrf2 Activation Induced by Sirt1 Ameliorates Acute Lung Injury After Intestinal Ischemia/Reperfusion Through NOX4-Mediated Gene Regulation

Nrf2 Activation Induced by Sirt1 Ameliorates Acute Lung Injury After Intestinal Ischemia/Reperfusion Through NOX4-Mediated Gene Regulation

Horizontal transfer of miR‐23a from hypoxic tumor cell colonies can induce angiogenesis

Simvastatin ameliorates ionizing radiation-induced apoptosis in the thymus by activating the AKT/sirtuin 1 pathway in mice

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