Chapter title |
VEGF as a Trophic Factor for Müller Glia in Hypoxic Retinal Diseases
|
---|---|
Chapter number | 58 |
Book title |
Retinal Degenerative Diseases
|
Published in |
Advances in experimental medicine and biology, January 2018
|
DOI | 10.1007/978-3-319-75402-4_58 |
Pubmed ID | |
Book ISBNs |
978-3-31-975401-7, 978-3-31-975402-4
|
Authors |
Shuhua Fu, Shuqian Dong, Meili Zhu, Yun-Zheng Le, Fu, Shuhua, Dong, Shuqian, Zhu, Meili, Le, Yun-Zheng |
Abstract |
Age-related macular degeneration (AMD) and diabetic retinopathy (DR), leading causes of blindness, share a common retinal environment: hypoxia which is a major stimulator for the upregulation of vascular endothelial growth factor (VEGF), a cardinal pathogenic factor for the breakdown of blood-retina barrier (BRB). As a result of intensive studies on VEGF pathobiology, anti-VEGF strategy has become a major therapeutics for wet AMD and DR. To investigate the potential impact of anti-VEGF strategy on major retinal supporting cells, Müller glia (MG), we disrupted VEGF receptor-2 (VEGFR2) in MG with conditional knockout (CKO) and examined the effect of VEGFR2-null on MG viability and neuronal integrity in mice. VEGFR2 CKO mice demonstrated a significant loss of MG density in diabetes/hypoxia, which in turn resulted in accelerated retinal degeneration. These defects appear similar to the clinical characteristics in a significant portion of wet-AMD patients with long-term anti-VEGF therapies. In this article, we will discuss the potential relevance of these clinical characteristics to the critical role of VEGF signaling in MG viability and neuronal integrity in hypoxia. |
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