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Updated: May 26, 2025

Author Spotlight: Investigating Angiogenesis and Vessel Permeability Through a Modified Matrix Gel Plug Assay
09:03

Author Spotlight: Investigating Angiogenesis and Vessel Permeability Through a Modified Matrix Gel Plug Assay

Published on: June 30, 2023

840

Mitsugumin 53 Inhibits Angiogenesis Through Regulating Focal Adhesion Turnover and Tip Cell Formation

Shuangshuang Yuan1,2, Qin Yu1, Tangting Chen3

  • 1Basic Medicine Research Innovation Center for Cardiometabolic Diseases, Ministry of Education, Luzhou Municipal Key Laboratory of Thrombosis and Vascular Biology, Laboratory for Cardiovascular Pharmacology, Department of Pharmacology, School of Pharmacy, Southwest Medical University, Luzhou, China.

Journal of Cellular and Molecular Medicine
|February 24, 2025
PubMed

Insights

Recombinant human mitsugumin 53 (rhMG53) enters endothelial cells via caveolae- and clathrin-dependent pathways, inhibiting angiogenesis by reducing focal adhesion turnover and tip cell formation.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Mitsugumin 53 (MG53) is a novel regulator of angiogenesis.
  • The cellular uptake mechanisms and cell movement mediation by MG53 remain largely unknown.

Purpose of the Study:

  • To elucidate the cellular uptake mechanisms of recombinant human MG53 (rhMG53) in endothelial cells.
  • To investigate how rhMG53 modulates endothelial cell function and migration.
  • To evaluate the therapeutic potential of rhMG53 in inhibiting excessive angiogenesis.

Main Methods:

  • Investigated rhMG53 uptake using caveolin-1 knockdown and pitstop-2 (clathrin inhibitor).
  • Assessed the effects of rhMG53 on focal adhesion kinase (FAK) and paxillin phosphorylation.
  • Utilized a 3D collagen culture model to analyze tip cell formation and tubulogenesis.
  • Evaluated rhMG53's efficacy in preventing corneal neovascularization in vivo.

Main Results:

  • rhMG53 uptake is dependent on both caveolae- and clathrin-mediated endocytosis.
  • Internalized rhMG53 inhibits FAK and paxillin phosphorylation, reducing focal adhesion turnover.
  • rhMG53 significantly suppresses tip cell formation and tubulogenesis in vitro.
  • rhMG53 effectively prevents corneal neovascularization following alkaline injury in vivo.

Conclusions:

  • rhMG53 inhibits angiogenesis by regulating focal adhesion turnover and tip cell formation.
  • This study reveals novel mechanisms of rhMG53 cellular uptake and function.
  • rhMG53 shows potential as a therapeutic agent for diseases characterized by excessive angiogenesis.
Keywords:
angiogenesisendocytosisfocal adhesionmitsugumin 53tip cell

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