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Critical Role of caveolin-1 in Ocular Neovascularization and Multitargeted Antiangiogenic Effects of Cavtratin via JNK

Critical Role of caveolin-1 in Ocular Neovascularization and Multitargeted Antiangiogenic Effects of Cavtratin via JNK

Yida Jiang, Xianchai Lin, Zhongshu Tang, Chunsik Lee, Geng Tian, Yuxiang Du, Xiangke Yin, Xiangrong Ren, Lijuan Huang, Zhimin Ye, Wei Chen, Fan Zhang, Jia Mi, Zhiqin Gao, Shasha Wang, Qishan Chen, Liying Xing, etc.

Proc Natl Acad Sci U S A. 2017 Oct 3;114(40):10737-10742.

PMID: 28923916

Abstract:

Ocular neovascularization is a devastating pathology of numerous ocular diseases and is a major cause of blindness. Caveolin-1 (Cav-1) plays important roles in the vascular system. However, little is known regarding its function and mechanisms in ocular neovascularization. Here, using comprehensive model systems and a cell permeable peptide of Cav-1, cavtratin, we show that Cav-1 is a critical player in ocular neovascularization. The genetic deletion of Cav-1 exacerbated and cavtratin administration inhibited choroidal and retinal neovascularization. Importantly, combined administration of cavtratin and anti-VEGF-A inhibited neovascularization more effectively than monotherapy, suggesting the existence of other pathways inhibited by cavtratin in addition to VEGF-A. Indeed, we found that cavtratin suppressed multiple critical components of pathological angiogenesis, including inflammation, permeability, PDGF-B and endothelial nitric oxide synthase expression (eNOS). Mechanistically, we show that cavtratin inhibits CNV and the survival and migration of microglia and macrophages via JNK. Together, our data demonstrate the unique advantages of cavtratin in antiangiogenic therapy to treat neovascular diseases.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR4241337	Caveolin-1 Scaffolding Domain Peptide, Cell-permeable			Price

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