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Endothelial ELABELA improves post-ischemic angiogenesis by upregulating VEGFR2 expression.

Jia-Yu Peng1, Xiao Fu2, Xue-Yang Luo2

  • 1Institute for Developmental and Regenerative Cardiovascular Medicine, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China; Department of Pediatric Cardiology, Xin Hua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China; Department of Child Healthcare, The International Peace Maternity & Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

Translational Research : the Journal of Laboratory and Clinical Medicine
|March 28, 2024
PubMed
Summary

Endothelial ELABELA (ELA) promotes blood vessel growth after ischemia by increasing VEGFR2. Lower ELA levels in diabetic foot ulcer patients suggest ELA as a therapeutic target for peripheral arterial diseases.

Keywords:
AngiogenesisELABELAEndothelial cellHind limb ischemiaVEGFR2

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Angiogenesis Research

Background:

  • Post-ischemic angiogenesis is crucial for tissue repair and blood flow restoration.
  • ELABELA (ELA) is known for its role in embryonic development but its function in post-ischemic angiogenesis is unclear.
  • Understanding ELA's mechanism in angiogenesis can reveal new therapeutic strategies.

Purpose of the Study:

  • To investigate the role and mechanism of ELABELA (ELA) in post-ischemic angiogenesis.
  • To determine if endothelial ELA influences perfusion recovery and capillary formation after hind limb ischemia (HLI).
  • To explore the potential of ELA as a therapeutic target for peripheral arterial diseases.

Main Methods:

  • Assessed ELA expression in a murine hind limb ischemia (HLI) model.
  • Utilized tamoxifen-inducible endothelial-specific ELA knockout mice (ELAECKO) to evaluate perfusion recovery and angiogenesis.
  • Performed in vitro experiments using lentivirus/siRNA for ELA knockdown and ELA peptides to assess endothelial cell function and VEGFR2 pathway activation.
  • Measured serum ELA levels in healthy individuals, T2DM patients, and DFU patients via ELISA.

Main Results:

  • ELA expression was significantly upregulated in ischemic hindlimbs of mice.
  • Endothelial-specific ELA deletion impaired perfusion recovery and angiogenesis, reducing VEGFR2, p-VEGFR2, and p-AKT expression post-ischemia.
  • In vitro, ELA knockdown inhibited endothelial cell proliferation and tube formation, while ELA peptides promoted these processes by upregulating VEGFR2 and downstream signaling.
  • DFU patients exhibited significantly lower serum ELA levels compared to T2DM patients.

Conclusions:

  • Endothelial ELA acts as a positive regulator of post-ischemic angiogenesis by enhancing VEGFR2 expression.
  • Targeting ELA presents a promising therapeutic avenue for treating peripheral arterial diseases.
  • Reduced serum ELA levels in DFU patients highlight its clinical relevance in diabetic complications.