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CLEC3B protects H9c2 cardiomyocytes from apoptosis caused by hypoxia via the PI3K/Akt pathway

Fenghua Lv1, Zhuo Wang1, Yanli Huang1

  • 1Department of Cardiology, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, Henan, China.

Brazilian Journal of Medical and Biological Research = Revista Brasileira De Pesquisas Medicas E Biologicas
|July 23, 2020
PubMed

Insights

C-type lectin domain family 3 member B (CLEC3B) protects against ischemic heart disease (IHD) injury by activating the PI3K/Akt pathway. This study reveals CLEC3B

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Physiology

Background:

  • Ischemic heart disease (IHD) is a major global health concern.
  • C-type lectin domain family 3 member B (CLEC3B) is implicated in tissue remodeling, with lower serum levels in cardiovascular disease patients.
  • The precise role and molecular mechanisms of CLEC3B in IHD remain unclear.

Purpose of the Study:

  • To investigate the protective role and molecular mechanisms of CLEC3B in an in vitro model of IHD.
  • To elucidate the involvement of the PI3K/Akt signaling pathway in CLEC3B-mediated protection.

Main Methods:

  • Overexpression and silencing of CLEC3B in H9c2 rat cardiomyocytes.
  • Establishment of an in vitro IHD model using hypoxic conditions.
  • Assessment of cell viability, apoptosis, and protein expression via CCK-8, flow cytometry, qRT-PCR, and Western blot.

Main Results:

  • CLEC3B expression was reduced under hypoxic conditions.
  • CLEC3B overexpression enhanced cell viability, reduced apoptosis, and upregulated p-PI3K/PI3K and p-Akt/Akt levels.
  • CLEC3B overexpression downregulated cleaved-caspase 3 expression, while CLEC3B silencing had opposite effects.
  • Inhibition of the PI3K/Akt pathway abrogated the protective effects of CLEC3B.

Conclusions:

  • CLEC3B exerts a protective effect against hypoxic injury in cardiomyocytes.
  • CLEC3B alleviates IHD-induced cardiomyocyte injury by activating the PI3K/Akt signaling pathway.
  • CLEC3B represents a potential therapeutic target for managing ischemic heart disease.

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