C5a promotes migration, proliferation, and vessel formation in endothelial cells

Ryuji Kurihara, Kunihiro Yamaoka, Norifumi Sawamukai, Shohei Shimajiri, Koichi Oshita, Sonosuke Yukawa, Mikiko Tokunaga, Shigeru Iwata, Kazuyoshi Saito, Kenji Chiba, Yoshiya Tanaka

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Objectives: The goal of this paper is to investigate the effects of activated complement C5a on vascular endothelium during vessel formation. Methods: A human microvascular endothelial cell line (HMEC-1) derived from post-capillary venules in skin was used to measure DNA synthesis, proliferation and cell-cycle progression. In vitro ring-shaped formation by the cells was assessed by using type I collagen gel matrix and a cell-migration assay using the Chemotaxicell chamber. A Matrigel plug assay was performed to confirm the effect of C5a in vivo. Results: C5a progressed the cell cycle of HMEC-1 into G2/M phases, and induced DNA synthesis and proliferation in a dose-dependent manner. C5a efficiently induced migration and ring-shaped structure formation both in vitro and in vivo. Furthermore, a C5a receptor antagonist (W-54011) suppressed all HMEC-1 activities including proliferation and migration. Conclusions: Proliferation, migration, and ring-shaped formation by HMEC-1 cells was induced by C5a. The actions were efficiently inhibited by a specific antagonist against C5a. Our results implicated C5a in vessel formation and as a potent target for management of inflammatory diseases.

Original languageEnglish
Pages (from-to)659-666
Number of pages8
JournalInflammation Research
Volume59
Issue number8
DOIs
Publication statusPublished - 2010 Aug 1

Keywords

  • Activated complement
  • Angiogenesis
  • C5a
  • Endothelial cell
  • Inflammatory diseases

ASJC Scopus subject areas

  • Immunology
  • Pharmacology

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    Kurihara, R., Yamaoka, K., Sawamukai, N., Shimajiri, S., Oshita, K., Yukawa, S., Tokunaga, M., Iwata, S., Saito, K., Chiba, K., & Tanaka, Y. (2010). C5a promotes migration, proliferation, and vessel formation in endothelial cells. Inflammation Research, 59(8), 659-666. https://doi.org/10.1007/s00011-010-0178-4