Identification of RUNX1 as a Mediator of Aberrant Retinal Angiogenesis | Zendy

Jonathan D. Lam | Zendy; Daniel J. Oh | Zendy; Lindsay L. Wong | Zendy; Dhanesh Amarnani | Zendy; Cindy ParkWindhol | Zendy; Angie V. Sanchez | Zendy; Jonathan Cardona-Vélez | Zendy; Declan McGuone | Zendy; Anat StemmerRachamimov | Zendy; Dean Eliott | Zendy; Diane R. Bielenberg | Zendy; Tavé van Zyl | Zendy; Li Shen | Zendy; Xiaowu Gai | Zendy; Patricia A. D’Amore | Zendy; Leo A. Kim | Zendy; Joseph F. ArboledaVelásquez | Zendy

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Identification of RUNX1 as a Mediator of Aberrant Retinal Angiogenesis

Author(s) -

Jonathan D. Lam,

Daniel J. Oh,

Lindsay L. Wong,

Dhanesh Amarnani,

Cindy ParkWindhol,

Angie V. Sanchez,

Jonathan Cardona-Vélez,

Declan McGuone,

Anat StemmerRachamimov,

Dean Eliott,

Diane R. Bielenberg,

Tavé van Zyl,

Li Shen,

Xiaowu Gai,

Patricia A. D’Amore,

Leo A. Kim,

Joseph F. ArboledaVelásquez

Publication year - 2017

Publication title -

diabetes

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.219

H-Index - 330

eISSN - 1939-327X

pISSN - 0012-1797

DOI - 10.2337/db16-1035

Subject(s) - angiogenesis , retina , cd31 , retinal , biology , downregulation and upregulation , diabetic retinopathy , runx1 , cancer research , pathology , endocrinology , microbiology and biotechnology , medicine , stem cell , diabetes mellitus , neuroscience , genetics , biochemistry , gene , haematopoiesis

Proliferative diabetic retinopathy (PDR) is a common cause of blindness in the developed world’s working adult population and affects those with type 1 and type 2 diabetes. We identified Runt-related transcription factor 1 (RUNX1) as a gene upregulated in CD31+ vascular endothelial cells obtained from human PDR fibrovascular membranes (FVMs) via transcriptomic analysis. In vitro studies using human retinal microvascular endothelial cells (HRMECs) showed increased RUNX1 RNA and protein expression in response to high glucose, whereas RUNX1 inhibition reduced HRMEC migration, proliferation, and tube formation. Immunohistochemical staining for RUNX1 showed reactivity in vessels of patient-derived FVMs and angiogenic tufts in the retina of mice with oxygen-induced retinopathy, suggesting that RUNX1 upregulation is a hallmark of aberrant retinal angiogenesis. Inhibition of RUNX1 activity with the Ro5–3335 small molecule resulted in a significant reduction of neovascular tufts in oxygen-induced retinopathy, supporting the feasibility of targeting RUNX1 in aberrant retinal angiogenesis.

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