miR-320/VEGFA axis affects high glucose-induced metabolic memory during human umbilical vein endothelial cell dysfunction in diabetes pathology

Gao, Jing; Maimaiti, Ailifeire; Wang, Chenfei; Lu, Luo; Zhang, Jie; Li, Yuan; Zhang, Li; Li, Xiaolan; Wang, Minzhe

doi:10.1016/j.mvr.2019.103913

Cited by 15 publications

(4 citation statements)

References 32 publications

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“…In addition to MMVECs, Feng et al showed that miR-320 could regulate glucose-induced gene expression in human umbilical vein endothelial cells (HUVECs), including Endothelin-1 (ET-1), Vascular Endothelial Growth Factor (VEGF) and Fibronectin (FN), which also participate in angiogenesis [107]. Furthermore, Gao et al found that the miR-320/ VEGFA axis was crucial to high-glucose-induced metabolic memory during HUVEC dysfunction and might be involved in the pathology of diabetes [108]. In the hyperlipidemic state, oxidative low-density lipoprotein (ox-LDL) induces endothelial dysfunction and apoptosis by increasing oxidative stress in endothelial cells [109].…”

Section: The Effects Of Mir-320 On Glucose and Lipid Metabolism In Enmentioning

confidence: 99%

The role of miR-320 in glucose and lipid metabolism disorder-associated diseases

Zhang

Yin

et al. 2021

Int. J. Biol. Sci.

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Section: The Effects Of Mir-320 On Glucose and Lipid Metabolism In Enmentioning

confidence: 99%

The role of miR-320 in glucose and lipid metabolism disorder-associated diseases

Zhang

Yin

et al. 2021

Int. J. Biol. Sci.

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“…Herein, VEGFA was confirmed as a downstream target of miR-324-3p. Additionally, previous researches reported that VEGFA was implicated in the pathogenesis of various diseases, including IS [51][52][53]. In terms of ceRNA regulatory mechanisms, we discovered that SNHG11 up-regulated VEGFA expression by targeting miR-324-3p.…”

Section: Discussionmentioning

confidence: 71%

Dexmedetomidine improves oxygen-glucose deprivation/reoxygenation (OGD/R) -induced neurological injury through regulating SNHG11/miR-324-3p/VEGFA axis

Chen

Fan

2021

Bioengineered

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Dexmedetomidine (Dex) has been reported to exhibit neuroprotective effects through various regulatory mechanisms. This study aims to investigate the role and molecular mechanism of SNHG11 in Dex-mediated neuroprotection. The ischemic stroke (IS) model was established in vivo by middle cerebral artery occlusion (MCAO) and in vitro by oxygen-glucose deprivation and reperfusion (OGD/R)-treated SH-SY5Y. SNHG11 was highly expressed after OGD/R, and Dex improved OGD/R-induced neurological injury. Additionally, Dex reversed the effects of SNHG11 on OGD/R-induced neurological injury. Furthermore, we found that SNHG11 upregulated vascular endothelial growth factor A (VEGFA) expression by targeting miR-324-3p. Through rescue assays, it was confirmed that SNHG11 regulated OGD/R-induced neurological injury through increasing VEGFA expression. At last, Dex was also discovered to improve neurological injury through regulating SNHG11 in the rat model. In conclusion, our work demonstrated that Dex improved OGD/R-induced neurological injury via SNHG11/miR-324-3p/VEGFA axis. These findings may offer a novel therapeutic strategy for IS treatment.

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“…Previous studies have shown that the miR‐320 family is involved in the regulation of the function of vascular endothelial cells and inhibits the expression of vascular endothelial factor, thereby inhibiting the proliferation and migration of vascular endothelial cells. [ 30–32 ] However, the regulation of target genes by miRNA is only at the transcriptional and posttranscriptional level, and the expression regulation mechanism for AREL1 remains to be explored.…”

Section: Discussionmentioning

confidence: 99%

AREL1 resists the apoptosis induced by TGF‐β by inhibiting SMAC in vascular endothelial cells

Liu

Song

Yuan

2023

J Biochem & Molecular Tox

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Abnormal apoptosis of vascular endothelial cells is an important feature of arteriosclerosis (AS). Here, we induced apoptosis in human umbilical vein endothelial cells (HUVECs) using transforming growth factor‐β (TGF‐β), and investigated the role of antiapoptotic E3 ubiquitin ligase (AREL1) in the apoptosis of vascular endothelial cells. We proved that AREL1 is downregulated in TGF‐β treated HUVECs. The overexpression of AREL1 inhibits the activation of Caspase‐3 and Caspase‐9 and attenuates cell apoptosis induced by TGF‐β. According to the result of coimmunoprecipitation, AREL1 interacts with the proapoptotic proteins the second mitochondria‐derived activator of caspases (SMAC) in TGF‐β treated HUVECs. In addition, miR‐320b inhibits the expression of AREL1, and the overexpression of AREL1 attenuates the apoptosis induced by miR‐320b mimics in HUVECs. In conclusion, AREL1 is downregulated by miR‐320b. AREL1 overexpression inhibits TGF‐β induced apoptosis through downregulating SMAC in vascular endothelial cells. Our study explores pathogenesis regulation mechanism and new biological therapeutic targets for vascular disease.

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miR-320/VEGFA axis affects high glucose-induced metabolic memory during human umbilical vein endothelial cell dysfunction in diabetes pathology

Cited by 15 publications

References 32 publications

The role of miR-320 in glucose and lipid metabolism disorder-associated diseases

The role of miR-320 in glucose and lipid metabolism disorder-associated diseases

Dexmedetomidine improves oxygen-glucose deprivation/reoxygenation (OGD/R) -induced neurological injury through regulating SNHG11/miR-324-3p/VEGFA axis

AREL1 resists the apoptosis induced by TGF‐β by inhibiting SMAC in vascular endothelial cells

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