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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
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Apelin-13 attenuates high glucose-induced calcification of MOVAS cells by regulating MAPKs and PI3K/AKT pathways and

Pu Zhang1, Ai-Ping Wang2, Hong-Peng Yang2

  • 1Department of Cardiovascular Medicine, Taian City Central Hospital, Taian, Shandong, 271000, China; College of Veterinary Medicine, Shandong Agricultural University, Taian, Shandong 271018, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|May 26, 2020
PubMed

Insights

Apelin-13 peptide effectively inhibits high glucose-induced vascular calcification in mouse cells. It works by reducing DNA damage and regulating key signaling pathways, offering a potential new treatment for diabetes-related cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Cellular and Molecular Medicine
  • Endocrinology

Background:

  • Vascular calcification (VC) is a significant risk factor for cardiovascular diseases, often exacerbated by diabetes.
  • The precise mechanisms underlying diabetes-induced VC remain incompletely understood.
  • Apelin, a peptide hormone in the cardiovascular system, shows promise in inhibiting VC, but its specific role in high glucose conditions requires investigation.

Purpose of the Study:

  • To investigate the inhibitory effect of apelin-13 on high glucose-induced vascular calcification (VC) in mouse aortic vascular smooth muscle cells (MOVAS).
  • To explore the underlying molecular mechanisms by which apelin-13 exerts its protective effects against high glucose-induced VC.

Main Methods:

  • MOVAS cells were treated with high glucose and apelin-13.
  • Cell proliferation, migration, invasion, and alkaline phosphatase (ALP) activity/expression were assessed.
  • Reactive oxygen species (ROS) generation, DNA damage, and the activation of MAPKs and PI3K/AKT pathways were analyzed.
  • The role of MAPKs was further confirmed using the ERK inhibitor U0126.

Main Results:

  • Apelin-13 significantly inhibited high glucose-induced proliferation, migration, and invasion of MOVAS cells.
  • Apelin-13 attenuated high glucose-induced calcification by reducing ALP activity and expression.
  • Apelin-13 suppressed high glucose-induced DNA damage by inhibiting ROS generation.
  • Apelin-13 improved high glucose-induced dysfunction in MAPKs and PI3K/AKT signaling pathways.
  • Inhibition of ERK signaling blocked high glucose-induced calcification, highlighting the role of MAPKs.

Conclusions:

  • Apelin-13 demonstrates significant potential in attenuating high glucose-induced vascular calcification in MOVAS cells.
  • The mechanism involves the inhibition of ROS-mediated DNA damage and the regulation of MAPKs and PI3K/AKT pathways.
  • Apelin-13 represents a promising therapeutic strategy for managing high glucose-mediated vascular calcification.
Keywords:
Alkaline phosphataseApelin-13ROSVascular calcification

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