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Integrin β3 overexpression contributes to podocyte injury through inhibiting RhoA/YAP signaling pathway

Zhuo Li1, Zhiwen Lian1, Jianchao Ma1

  • 1Department of Nephrology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.

Bioengineered
|April 5, 2021
PubMed

Insights

Integrin β3 (ITGβ3) promotes podocyte injury in high-glucose conditions by inhibiting the RhoA-YAP pathway. Targeting ITGβ3 may offer a new strategy for preventing podocyte damage.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pathology

Background:

  • The integrin β3 (ITGβ3)-Ras homolog gene family, member A (RhoA)-Yes-associated protein (YAP) axis is implicated in atherosclerosis.
  • ITGβ3 is overexpressed in podocytes exposed to high glucose (HG).

Purpose of the Study:

  • To investigate the role of ITGβ3 in regulating the RhoA-YAP axis in HG-induced podocyte injury.
  • To elucidate the mechanism by which ITGβ3 influences podocyte function under HG conditions.

Main Methods:

  • In vitro assays including wound-healing, flow cytometry, RT-qPCR, and western blot.
  • Manipulation of ITGβ3 and RhoA expression in podocytes.
  • Assessment of podocyte apoptosis and wound closure.
  • Analysis of RhoA and YAP protein levels.

Main Results:

  • HG treatment increased podocyte wound closure and apoptosis.
  • ITGβ3 inhibition mitigated HG-induced podocyte injury, while ITGβ3 overexpression exacerbated it.
  • ITGβ3 knockdown upregulated RhoA and YAP expression, whereas ITGβ3 overexpression had the opposite effect.
  • RhoA overexpression reversed the effects of ITGβ3 overexpression on podocyte injury and YAP expression.

Conclusions:

  • ITGβ3 overexpression promotes podocyte injury by inhibiting the RhoA-YAP axis.
  • Targeting the ITGβ3-RhoA-YAP pathway presents a potential therapeutic strategy for preventing podocyte damage.
Keywords:
ITGβ3RhoA/YAP pathwayhigh glucosepodocyte

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