MicroRNA-22 Induces Endothelial Progenitor Cell Senescence by Targeting AKT3

Zheng, Yue; Xu, Zhiwei

doi:10.1159/000366358

Cited by 45 publications

(40 citation statements)

References 35 publications

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“…EPCs have strong proliferative and migratory capacity, indicating that they may be regarded as a potential therapeutic target for vascular disease. Many studies have demonstrated that abnormal EPC migration and tube formation induce angiogenesis injury [29]. Our results are in agreement with previous studies showing that AngII reduced EPC viability and migration.…”

Section: Discussionsupporting

confidence: 93%

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

et al. 2019

J Vasc Res

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Vitamin D has an important protective effect on chronic inflammatory disease. Angiotensin II (AngII) triggers vascular damage and plays a key role in vascular diseases via several mechanisms, including inflammation. Conversely, vitamin D has been shown to have an important protective effect on chronic inflammation. There is evidence showing that vitamin D can reverse the effects of AngII, but the molecular mechanisms by which this occurs are not known. Our results demonstrate that vitamin D improved the viability, migration ability, and tube formation of AngII-pretreated endothelial progenitor cells (EPCs) and inhibited the apoptosis of EPCs induced by AngII. Vitamin D also reversed reactive oxygen species production, vascular inflammatory cytokine generation, and nuclear factor kappa-B activation in EPCs induced by AngII. Furthermore, EPC pretreatment with GW9662 (the antagonist for PPAR-γ) or siHO-1 decreased the protective effect of vitamin D on AngII-induced EPC injury. Overall, our data indicate that vitamin D ameliorated AngII-induced abnormal EPC injury by decreasing oxidative stress and inflammatory cytokine levels. These findings also suggest that vitamin D protected EPCs from AngII-induced vascular injury via the activation of the PPAR-γ/HO-1 signaling pathway.

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Section: Discussionsupporting

confidence: 93%

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

et al. 2019

J Vasc Res

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“…Like in obesity [57], it is caused by elevated miRNA-34a [106,184], a proposed brain ageing marker [108] which is capable of modulating cellular senescence [9,83]. A similar effect on senescence has been noted for other microRNAs that target Sirt1: miRNA-22 [81,241] and miRNA-217 [129]. Sirt-1 reduction by up-regulated miRNA (miR-181) also occurs in the hippocampus of a mouse AD model (3×Tg) [170].…”

Section: A B Cmentioning

confidence: 76%

Sirtuins and their interactions with transcription factors and poly(ADP-ribose) polymerases

Jęśko¹,

Strosznajder²

2016

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A b s t r a c tSirtuins vast number of targets in many cellular compartments, and some display additional enzymatic activities including mono(ADP-ribosyl)ation. SIRTs interact with multiple signalling proteins, transcription factors and enzymes including p53, FOXOs (forkhead box subgroup O), PPARs (peroxisome proliferator-activated receptors), NF-κB, and DNA-PK (DNA-dependent protein kinase). Sirtuins also interact extensively with the family of poly(ADPribose) polymerases (PARPs), a crucial and widespread class of NAD

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“…One study showed that AKT3 is involved in the regulation of RCAS1 and VEGF secretion in ovarian cancer cells [32]. Another study also demonstrated that restoration of AKT3 expression could prevent the impaired angiogenesis induced by miR-22 in endothelial progenitor cells [33], which suggested that AKT3 played a functional role in promoting angiogenesis. In the present study, we found that HG-induced up-regulation of AKT3 in HRECs and knockdown of AKT3 by siRNA in HRECs decreased the level of VEGF with an associated decrease in vascular permeability and angiogenesis.…”

Section: Discussionmentioning

confidence: 98%

MiR-20b targets AKT3 and modulates vascular endothelial growth factor-mediated changes in diabetic retinopathy

Qin

Liu

et al. 2016

ABBS

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Diabetic retinopathy (DR) is the leading cause of new-onset blindness. The roles of microRNAs in diabetic retinopathy are largely unknown. The aim of this study is to investigate the role of miR20b in DR. Transfection of miR-20b mimic in high glucose (HG)-treated human retinal endothelial cells (HRECs) increased miR-20b expression and decreased the expression level of VEGF mRNA, while transfection of miR-20b inhibitor in control HRECs reduced the miR-20b expression with a corresponding increase of VEGF mRNA. In vitro functional assay showed that transfection of miR-20b mimic prevented HG-induced increase in transendothelial permeability and tube formation in HRECs. Transfection of miR-20b inhibitor or treatment of VEGF increased transendothelial permeability and tube formation in control HRECs. Luciferase reported assay showed that AKT3 is a target of miR-20b. Transfection of miR-20b mimic prevented the up-regulation of AKT3 induced by HG without changing the protein levels of other isoforms of AKT, and silencing of AKT3 caused decrease of VEGF mRNA and protein levels as well as prevented HG-induced increase in transendothelial permeability and tube formation. Finally, we showed that miR-20b was down-regulated in the retina and retinal endothelial cells in diabetic rats, with a correlated up-regulation of VEGF and AKT3. Intravitreal injection of miR-20b mimic in the diabetic rat significantly increased the miR-20b expression and decreased the expression levels of AKT3 and VEGF in the retina tissues, and intravitreal delivery of AKT3 siRNA in the diabetic rat significantly decreased the expressions of AKT3 and VEGF. Collectively, miR-20b is important for the regulation of VEGF-mediated changes in HRECs and rat retinal tissues under hyperglycemic conditions possibly via targeting AKT3.

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MicroRNA-22 Induces Endothelial Progenitor Cell Senescence by Targeting AKT3

Cited by 45 publications

References 35 publications

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

Vitamin D Ameliorates Angiotensin II-Induced Human Endothelial Progenitor Cell Injury via the PPAR-γ/HO-1 Pathway

Sirtuins and their interactions with transcription factors and poly(ADP-ribose) polymerases

MiR-20b targets AKT3 and modulates vascular endothelial growth factor-mediated changes in diabetic retinopathy

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