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Shingo Yasuda, Takayoshi Sumioka, Yuka Okada, Masayasu Miyajima, Kana Ichikawa, Shizuya Saika; Signals from sphingosine-1-phosphate receptor type 3 involvement in vascular formation by endothelium and in VEGF expression in macrophages in vitro.. Invest. Ophthalmol. Vis. Sci. 2019;60(9):948. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
We here examined here roles of signals derived from sphingosine-1-phosphate (S1P) or its receptor type 3 (S1PR3) on neovascularization activity of human retinal microvascular endothelial cells (HRMECs) and on angiogenic growth factor expression in macrophages. Purpose was to clear the mechanism of suppression of corneal neovascularization in a mouse that lacks sphingosine-1-phosphate receptor type 3 (S1PR3) (reported by us in ARVO 2018) by using cell culture.
(1) HRMECs were cultured on matrigel and allowed to form vessel-like structures in three dimension culture. The degree of the formation of the structure was compared in the three groups (S1P+ group, S1P+ and S1PR3 inhibitor+ group, and control group) (2) Peritoneal macrophages were harvested 4 days after i. p. oyster glycogen (5 %, sterilized) in wild-type or S1PR3-null mice. mRNA expression levels of VEGF-A in macrophages were compared and examined using real-time RT-PCR.
(1) Formation of vessel-like structute by HRMECs was promoted by S1P addition, and inhibited by further addition of S1PR3 inhibitor concentration-dependently. (2) The expression level of VEGF-A in macrophages was significantly suppressed by the loss of S1PR3.
The mechanisms of inhibition of neovascularization in the absence of S1PR3, reported in ARVO 2018, include both impairment of vascular structure formation by endothelial cells and reduction of VEGF-A in macrophages.
This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.
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