Apelin attenuates UVB-induced edema and inflammation by promoting vessel function.

Mika Sawane, Hiroyasu Kidoya, Fumitaka Muramatsu, Nobuyuki Takakura, Kentaro Kajiya

Shiseido Innovative Science Research Center, Yokohama, Japan.

The American journal of pathology 2011 Dec

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Apelin, the ligand of the G protein-coupled receptor APJ, is involved in the regulation of cardiovascular functions, fluid homeostasis, and vessel formation. Recent reports indicate that apelin secreted from endothelial cells mediates APJ regulation of blood vessel caliber size; however, the function of apelin in lymphatic vessels is unclear. Here we report that APJ was expressed by human lymphatic endothelial cells and that apelin induced migration and cord formation of lymphatic endothelial cells dose-dependently in vitro. Furthermore, permeability assays demonstrated that apelin stabilizes lymphatic endothelial cells. In vivo, transgenic mice harboring apelin under the control of keratin 14 (K14-apelin) exhibited attenuated UVB-induced edema and a decreased number of CD11b-positive macrophages. Moreover, activation of apelin/APJ signaling inhibited UVB-induced enlargement of lymphatic and blood vessels. Finally, K14-apelin mice blocked the hyperpermeability of lymphatic vessels in inflamed skin. These results indicate that apelin plays a functional role in the stabilization of lymphatic vessels in inflamed tissues and that apelin might be a suitable target for prevention of UVB-induced inflammation. Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.

Citation

Mika Sawane, Hiroyasu Kidoya, Fumitaka Muramatsu, Nobuyuki Takakura, Kentaro Kajiya. Apelin attenuates UVB-induced edema and inflammation by promoting vessel function. The American journal of pathology. 2011 Dec;179(6):2691-7