[Angiotensin Ⅱ induces apoptosis of HEK293T cells by up-regulating Cyr61 expression]

Junjie Wang1, Yan Jiang2, Senouthai Soulixay1

  • 1Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, China.

Abstract

Insights

Down-regulating Cyr61 expression protects HEK293T cells from angiotensin II (Ang II)-induced injury. Cyr61 upregulation is linked to Ang II-induced cell damage, with knockdown reducing apoptosis.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Angiotensin II (Ang II) is a key hormone in regulating blood pressure and fluid balance.
  • HEK293 cells are commonly used in research to study cellular responses to various stimuli.
  • Cyr61, a member of the CCN family, plays roles in cell proliferation, migration, and survival.

Purpose of the Study:

  • To investigate the role of Cyr61 in Ang II-induced functional changes in HEK293 cells.
  • To explore the underlying mechanism of Cyr61's involvement in Ang II-induced cellular responses.
  • To assess the protective effect of Cyr61 knockdown against Ang II-induced cell injury.

Main Methods:

  • Cyr61 knockdown was performed in HEK293T cells using CRISPR/Cas9 technology.
  • Cells were treated with Ang II (10⁻⁷ mol/L) for 48 hours.
  • Apoptosis rates and expression levels of Cyr61 and Bcl-2 were analyzed via flow cytometry, qRT-PCR, and Western blotting.

Main Results:

  • Cyr61 knockdown significantly reduced Cyr61 protein expression.
  • Ang II treatment increased Cyr61 expression and decreased Bcl-2 expression in HEK293T cells.
  • Ang II treatment significantly increased the apoptotic rate in control HEK293T cells, while Cyr61 knockdown notably reduced Ang II-induced apoptosis.

Conclusions:

  • Cyr61 upregulation is associated with Ang II-induced injury in HEK293T cells.
  • Down-regulating Cyr61 expression effectively protects HEK293T cells against Ang II-induced damage.
  • Targeting Cyr61 may offer a therapeutic strategy for conditions involving Ang II-mediated cellular injury.

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