Angiotensin II-Induced Apoptosis of Human Umbilical Vein Endothelial Cells was Inhibited by Blueberry Anthocyanin Through Bax- and Caspase 3-Dependent Pathways

Du, Jinyan; Leng, Jinhua; Zhang, Li; Bai, Guangxin; Yang, Di; Lin, Huan Xin; Qin, Junjie

doi:10.12659/msm.896916

Cited by 17 publications

(7 citation statements)

References 33 publications

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“…HUVEC viability was measured with alamarBlue ( Sarig et al, 2018 ; Krishnamoorthi et al, 2020 ) and the viability trend we observed in our work is comparable to the endothelial viability studied with the presence of TGF-β1, L-NAME, and Ang II as shown by others ( Hirai and Kaji, 1992 ; Mocellin et al, 2004 ; Du et al, 2016 ; Zhang et al, 2020 ). While reversibility of markers of EndoMT in endothelial cells has been reported previously, this reversibility has not been previously characterized as a functional reversal.…”

Section: Discussionsupporting

confidence: 89%

An In Vitro Platform to Study Reversible Endothelial-to-Mesenchymal Transition

et al. 2022

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Endothelial cells can acquire a mesenchymal phenotype in response to external stimuli through both mechanical and biological factors, using a process known as endothelial-to-mesenchymal (EndoMT) transition. EndoMT is characterized by the decrease in endothelial characteristics, increase in mesenchymal markers, and morphological changes. It has been recognized not only during development but also in different pathological conditions including organ/tissue fibrosis in adults. The ability to modulate the EndoMT process could have a therapeutic potential in many fibrotic diseases. An in vitro method is presented here to induce EndoMT with Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) and angiotensin II (Ang II) followed by a protocol to study the reversibility of EndoMT. Using this method, we furnish evidence that the combination of L-NAME and Ang II can stimulate EndoMT in Human umbilical vascular endothelial cells (HUVECs) and this process can be reversed as observed using endothelial functionality assays. This method may serve as a model to screen and identify potential pharmacological molecules to target and regulate the EndoMT process, with applications in drug discovery for human diseases.

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Section: Discussionsupporting

confidence: 89%

An In Vitro Platform to Study Reversible Endothelial-to-Mesenchymal Transition

et al. 2022

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“…activated Bax can induce the release of pro-apoptotic factors and cytochrome c (55). caspase-3 is a member of the cysteine-aspartic acid protease family and plays a central role in cell apoptosis (56,57). The results of the present study indicated that ccnd1 promoted the expression of Ki67 and Bcl-2, and inhibited Bax and cleaved caspase-3, while mir-628-5p partially reversed the effect of ccnd1 on these genes.…”

Section: Ccnd1 Is Required For the Proliferation And Apoptosis Of Ht-mentioning

confidence: 50%

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Guo

Xue

2020

Mol Med Report

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Microrna (mir)-628-5p serves as an antitumor gene in a variety of cancers; however, the role of mir-628-5p in colorectal cancer remains largely unclear. The purpose of this study was to investigate the role and mechanism of mir-628-5p in colorectal cancer. reverse transcription-quantitative Pcr (RT-qPCR), colony formation assays and flow cytometric analysis were used to determine the expression levels of mir-628-5p in colorectal cancer tissues and cell lines, and the proliferative ability of colorectal cancer cells. TargetScan version 7.2 and dual-luciferase reporter assay were performed to predict and confirm mir-628-5p target genes. The expression levels of cyclin d1 (ccnd1) and related genes were determined using rT-qPcr or/and western blotting analysis. mir-628-5p mimics and ccnd1 plasmids were used to overexpress mir-628-5p and ccnd1; it was demonstrated that the expression levels of miR-628-5p were significantly downregulated in colorectal cancer tissues and cell lines. mir-628-5p mimic-transfected cells inhibited the proliferation and induced apoptosis of HT-29 cells. ccnd1, a downstream effector of mir-628-5p, promoted the proliferation and suppressed apoptosis of HT-29 cells, and the effects were reversed by mir-628-5p mimics. in conclusion, the present study suggested that colorectal cancer progression may be regulated through the mir-628-5p/ccnd1 axis, and mir-628-5p could be used as a potential diagnostic and prognostic biomarker for colorectal cancer.

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“…The effect of Ang II on the function of vascular endothelial cells has attracted increasing attention from cardiologists. Previous studies have shown that Ang II can promote cellular functions by stimulating reactive oxygen species production, promoting thrombosis (14), inhibiting nitric oxide production, and promoting vascular endothelial cell apoptosis (15). Our previous studies also showed that Ang II can affect the normal function of endothelial cells by inhibiting nitric oxide synthase or inducing inflammatory reactions in cells (12,16).…”

Section: Discussionmentioning

confidence: 93%

Angiotensin II inhibits the protein expression of ZO‑1 in vascular endothelial cells by downregulating VE‑cadherin

et al. 2018

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Angiotensin II (Ang II) is reported to be involved in the development of various cardiovascular diseases by disrupting microvessel permeability, however, the underlying mechanism remains to be elucidated. The present study aimed to investigate the mechanism by which Ang II disrupts microvascular permeability. Rat endothelial cells were subjected to primary culture and identification. Cells in passages 4‑7 were then used for the following experiments. The cells were divided into control, Ang II, and Ang II + valsartan groups, and reverse transcription‑quantitative polymerase chain reaction and western blot analyses were perform to evaluate the expression of zonula occludens‑1 (ZO‑1) and vascular endothelial (VE)‑cadherin in the cells. The distribution of ZO‑1 protein was also detected using immunofluorescence assays. It was found that, compared with the control group, lower expression levels of ZO‑1 and VE‑cadherin were present in the Ang II group (P<0.01). ZO‑1 was also irregularly distributed at the periphery of the cells. In addition, the overexpression of VE‑cadherin reversed the effect of Ang II on the expression and distribution of ZO‑1 in endothelial cells. Together, these results suggested that Ang II inhibited the protein expression of ZO‑1 in vascular endothelial cells by downregulating VE‑cadherin, thus destroying the tight junctions between endothelial cells, which may also be the mechanism by which Ang II is involved in the development of cardiovascular diseases.

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Angiotensin II-Induced Apoptosis of Human Umbilical Vein Endothelial Cells was Inhibited by Blueberry Anthocyanin Through Bax- and Caspase 3-Dependent Pathways

Cited by 17 publications

References 33 publications

An In Vitro Platform to Study Reversible Endothelial-to-Mesenchymal Transition

An In Vitro Platform to Study Reversible Endothelial-to-Mesenchymal Transition

MicroRNA‑628‑5p inhibits cell proliferation and induces apoptosis in colorectal cancer through downregulating CCND1 expression levels

Angiotensin II inhibits the protein expression of ZO‑1 in vascular endothelial cells by downregulating VE‑cadherin

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