2007Unpublished venueRequires access

Study on angiotensinII inducing endothelial cell aging in vitro

Xiangmei Chen

Open publisher page 0 citations

Abstract

[Objective] To study if angiotensin Ⅱ (AngⅡ) could induce human umbilical endothelial cells (HUVECs) aging, and to determine the possible mechanism. [Methods] The cultured HUVECs in vitro were divided into 3 groups, the control group, AngⅡgroup(stimulated with 10-6 mol/L AngⅡ for 48 h), AngⅡ plus valsartan group(valsartan was added to cells 1h before 10-6 mol/L AngⅡ ). Superoxide() level in cells and medium were examined. RT-PCR and Western blot were used to analyse mRNA and protein expression of NADPH oxidase p22phox, angiotensin type 1 and 2 receptor(AT1R,AT2R). [Results] AngⅡ stimulation enhanced the positive cell number of β-gal stained HUVEC, depressed cell proliferation, and increased the protein expression of P16, at the same time, stimulated cells produced less NO and more. The mRNA and protein expression of p22phox and AT2R in cells stimulated with AngⅡ increased, the expression of AT1R decreased; valsartan treatment alleviated aging associated changes, decreased production and increased NO production, and downregulated the mRNA and protein expression of p22phox. [Conclusion] The study indicated AngⅡ upregulates the expression of NAD(P)H oxidase subunit-p22phox at the transcriptional degree, hence increases production and ultimately induces HUVECs in vitro senescent; valsartan treatment protects endothelial cells from aging at a certain extent.

About this research paper

What this paper is about

[Objective] To study if angiotensin Ⅱ (AngⅡ) could induce human umbilical endothelial cells (HUVECs) aging, and to determine the possible mechanism. [Methods] The cultured HUVECs in vitro were divided into 3 groups, the control group, AngⅡgroup(stimulated with 10-6 mol/L AngⅡ for 48 h), AngⅡ plus valsartan group(valsartan was added to cells 1h before 10-6 mol/L AngⅡ ). Superoxide() level in cells and medium were examined. RT-PCR and Western blot were used to analyse mRNA and protein expression of NADPH oxidase p22phox, angiotensin type 1 and 2 receptor(AT1R,AT2R). [Results] AngⅡ stimulation enhanced the positive cell number of β-gal stained HUVEC, depressed cell proliferation, and increased the protein expression of P16, at the same time, stimulated cells produced less NO and more. The mRNA and protein expression of p22phox and AT2R in cells stimulated with AngⅡ increased, the expression of AT1R decreased; valsartan treatment alleviated aging associated changes, decreased production and increased NO production, and downregulated the mRNA and protein expression of p22phox. [Conclusion] The study indicated AngⅡ upregulates the expression of NAD(P)H oxidase subunit-p22phox at the transcriptional degree, hence increases production and ultimately induces HUVECs in vitro senescent; valsartan treatment protects endothelial cells from aging at a certain extent.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

[Objective] To study if angiotensin Ⅱ (AngⅡ) could induce human umbilical endothelial cells (HUVECs) aging, and to determine the possible mechanism. [Methods] The cultured HUVECs in vitro were divided into 3 groups, the control group, AngⅡgroup(stimulated with 10-6 mol/L AngⅡ for 48 h), AngⅡ plus valsartan group(valsartan was added to cells 1h before 10-6 mol/L AngⅡ ). Superoxide() level in cells and medium were examined. RT-PCR and Western blot were used to analyse mRNA and protein expression of NADPH oxidase p22phox, angiotensin type 1 and 2 receptor(AT1R,AT2R). [Results] AngⅡ stimulation enhanced the positive cell number of β-gal stained HUVEC, depressed cell proliferation, and increased the protein expression of P16, at the same time, stimulated cells produced less NO and more. The mRNA and protein expression of p22phox and AT2R in cells stimulated with AngⅡ increased, the expression of AT1R decreased; valsartan treatment alleviated aging associated changes, decreased production and increased NO production, and downregulated the mRNA and protein expression of p22phox. [Conclusion] The study indicated AngⅡ upregulates the expression of NAD(P)H oxidase subunit-p22phox at the transcriptional degree, hence increases production and ultimately induces HUVECs in vitro senescent; valsartan treatment protects endothelial cells from aging at a certain extent.

Key concepts: P22phox, Angiotensin II, Valsartan, NADPH oxidase, In vitro, Western blot, Endothelial stem cell, Chemistry

Related papers

Back to paper searchBrowse research topicsOriginal source
Study on angiotensinII inducing endothelial cell aging in vitro — Research Paper | ScholarLens