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Abstract

Synaptic Adhesion Like Molecules (SALMs) is the adhesion molecules, highly enriched in nervous system, include five members (SALM 1-5). All SALMs promote neurite outgrowth, while SALM4 uniquely increases the number of primary processes extending from the cell body. However, the property of SALM4 in Endothelial Cell (EC) is still unknown. Here, we discovered that SALM4 mRNA expression was increased during differentiation from Endothelial Progenitor Cell (EPC) to EC. Unlike other SALMs, SALM4 was expressed specifically in EC. To find functions of SALM4, we performed in vitro assays. Wound and chemotactic migration assays showed that knock down of SALM4 attenuates EC migration. Next, we found tube formation was decreased tube length in SALM4 deletion EC. EC Survival was reduced in SALM4 depletion. In mouse organs, SALM4 shows organ specificity, it was mainly expressed brain and kidney. Consistent with this observation, EC recruitment impaired in SALM4 KO mice injected matrigel with VEGF. Aortic sprouting reduced in SALM4 KO mice aorta implanted matrigel. To elucidate the mechanism of SALM4 under VEGF treatment, we analyzed VEGFR2 activation. Silencing SALM4 in EC suppressed phosphorylation of VEGFR2. Moreover, downstream of VEGFR2 signaling was also reduced. These results suggest that SALM4 has a potential role in regulating EC migration via activation of VEGFR2.

Biography

Dong Young Kim is currently pursuing his Doctor’s course in Vascular Biology at Yonsei University, Republic of Korea. He has completed his Bachelor’s degree in Biochemistry at Yonsei University. His research fields are tumor angiogenesis and identifying angiogenic functions of endothelial cell enriched genes in endothelial cells.