Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 43, Issue 5, Pages 1742-1754Publisher
KARGER
DOI: 10.1159/000484061
Keywords
Nogo-B; Angiogenesis; Proliferative diabetic retinopathy
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Funding
- General Program of Shanghai Municipal Health and Family Planning Commission [201440522]
- National Natural Science Foundation [81300777]
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Background/Aims: Nogo-B, a conservative protein of endoplasmic reticulum, is a member of the reticulon family of proteins. Proliferative diabetic retinopathy (PDR) is the major concerning problem of diabetic retinopathy. This study explored the role of Nogo-B in the regulation of angiogenesis in PDR patients and primary human retinal endothelial cells (HRMECs). Methods: Nogo-B was down-regulated through the use of Lentivirus-NogoBRNAi, the effects of Nogo-B on angiogenesis under high glucose stimulation were evaluated via CCK-8 assay, wound closure assay, transwell assay, and tube formation assay. Expression of Nogo-B, VEGF, PI3K and Akt were determined by western blotting, immunofluorescence, enzyme-linked immunosorbent assay (ELISA). Co-culture systerm was used to explore cell communication. Results: Nogo-B was highly enriched in ocular tissues of PDR patients and in HRMECs exposed to high glucose. Down-regulation of Nogo-B attenuated high glucose induced cell migration and tube formation in HRMECs. Mechanistically, in comparison with the negative control group, Lentivirus-NogoB-RNAi group had exhibited reduced VEGF secretion, weakened PI3K and Akt activation. Besides, high glucose treatment promoted the secretion of Nogo-B and presented as a long-term memory. Conclusions: These data collectively indicated that Nogo-B promoted angiogenesis in HRMECs via VEGF/PI3K/Akt pathway in an autocrine manner. (C) 2017 The Author(s) Published by S. Karger AG, Basel
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