Galectin-3 Enhances Vascular Endothelial Growth Factor-A Receptor 2 Activity in the Presence of Vascular Endothelial Growth Factor.

angiogenesis endothelium glycocalyx migration ranibizumab

Journal

Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250

Informations de publication

Date de publication:
2021
Historique:
received: 01 07 2021
accepted: 30 08 2021
entrez: 7 10 2021
pubmed: 8 10 2021
medline: 8 10 2021
Statut: epublish

Résumé

Galectin-3 (Gal3) is a carbohydrate-binding protein reported to promote angiogenesis by influencing vascular endothelial growth factor-A receptor 2 (VEGFR2) signal transduction. Here we evaluated whether the ability of Gal3 to function as an angiogenic factor involved vascular endothelial growth factor (VEGF). To address this possibility we used human retinal microvascular endothelial cells (HRECs) to determine whether exogenous Gal3 requires VEGF to activate VEGFR2 signaling and if Gal3 is required for VEGF to activate VEGFR2. VEGFR2 phosphorylation and HREC migration assays, following either VEGF neutralization with ranibizumab or Gal3 silencing, revealed that VEGF endogenously produced by the HRECs was essential for the effect of exogenous Gal3 on VEGFR2 activation and cell migration, and that VEGF-induced VEGFR2 activation was not dependent on Gal3 in HRECs. Gal3 depletion led to no reduction in VEGF-induced cell function. Since Gal3 has been suggested to be a potential therapeutic target for VEGFR2-mediated angiogenesis, it is crucial to define the possible Gal3-mediated VEGFR2 signal transduction mechanism to aid the development of efficacious therapeutic strategies.

Identifiants

pubmed: 34616740
doi: 10.3389/fcell.2021.734346
pmc: PMC8488270
doi:

Types de publication

Journal Article

Langues

eng

Pagination

734346

Subventions

Organisme : NEI NIH HHS
ID : R01 EY026539
Pays : United States

Informations de copyright

Copyright © 2021 Cano, Hu, AbuSamra, Saint-Geniez, Ng, Argüeso and D’Amore.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Issahy Cano (I)

Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, MA, United States.
Department of Ophthalmology, Harvard Medical School, Boston, MA, United States.

Zhengping Hu (Z)

Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, MA, United States.
Department of Ophthalmology, Harvard Medical School, Boston, MA, United States.

Dina B AbuSamra (DB)

Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, MA, United States.
Department of Ophthalmology, Harvard Medical School, Boston, MA, United States.

Magali Saint-Geniez (M)

Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, MA, United States.
Department of Ophthalmology, Harvard Medical School, Boston, MA, United States.

Yin Shan Eric Ng (YSE)

Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, MA, United States.
Department of Ophthalmology, Harvard Medical School, Boston, MA, United States.

Pablo Argüeso (P)

Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, MA, United States.
Department of Ophthalmology, Harvard Medical School, Boston, MA, United States.

Patricia A D'Amore (PA)

Schepens Eye Research Institute of Massachusetts Eye and Ear, Boston, MA, United States.
Department of Ophthalmology, Harvard Medical School, Boston, MA, United States.
Department of Pathology, Harvard Medical School, Boston, MA, United States.

Classifications MeSH