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

Kurihara R, Yamaoka K, Sawamukai N, Shimajiri S, Oshita K, Yukawa S, Tokunaga M, Iwata S, Saito K, Chiba K, Tanaka Y - Inflamm. Res. (2010)

Bottom Line: The goal of this paper is to investigate the effects of activated complement C5a on vascular endothelium during vessel formation.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.

View Article: PubMed Central - PubMed

Affiliation: The First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan.

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.

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Analysis of HMEC-1 migration. HMEC-1 cells migrated to the reverse side of the filters were removed with trypsin and counted. a FGF-2 (5 ng/ml) was used as a positive control for inducing HMEC-1 migration (open column). C5a increased the migration of HMEC-1 cells in a dose-dependent manner (closed column), while this induced migration was inhibited by W-54011. b In a dose-dependent manner. Bars represent mean ± SEM (n = 3). a **P < 0.01 by Bonferroni’s multiple comparison test, b **P < 0.01 by Dunnett’s multiple comparison test
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Fig6: Analysis of HMEC-1 migration. HMEC-1 cells migrated to the reverse side of the filters were removed with trypsin and counted. a FGF-2 (5 ng/ml) was used as a positive control for inducing HMEC-1 migration (open column). C5a increased the migration of HMEC-1 cells in a dose-dependent manner (closed column), while this induced migration was inhibited by W-54011. b In a dose-dependent manner. Bars represent mean ± SEM (n = 3). a **P < 0.01 by Bonferroni’s multiple comparison test, b **P < 0.01 by Dunnett’s multiple comparison test

Mentions: FGF-2 is a known inducer of endothelial cell migration [32]. The migration by FGF-2 was confirmed in this study with the HMEC-1 line using the Chemotaxicell chamber (Fig. 6a). C5a promoted HMEC-1 migration in a dose-dependent manner, an effect that was inhibited in the presence of W-54011 (Fig. 6a, b).Fig. 6


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

Kurihara R, Yamaoka K, Sawamukai N, Shimajiri S, Oshita K, Yukawa S, Tokunaga M, Iwata S, Saito K, Chiba K, Tanaka Y - Inflamm. Res. (2010)

Analysis of HMEC-1 migration. HMEC-1 cells migrated to the reverse side of the filters were removed with trypsin and counted. a FGF-2 (5 ng/ml) was used as a positive control for inducing HMEC-1 migration (open column). C5a increased the migration of HMEC-1 cells in a dose-dependent manner (closed column), while this induced migration was inhibited by W-54011. b In a dose-dependent manner. Bars represent mean ± SEM (n = 3). a **P < 0.01 by Bonferroni’s multiple comparison test, b **P < 0.01 by Dunnett’s multiple comparison test
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Related In: Results  -  Collection

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Fig6: Analysis of HMEC-1 migration. HMEC-1 cells migrated to the reverse side of the filters were removed with trypsin and counted. a FGF-2 (5 ng/ml) was used as a positive control for inducing HMEC-1 migration (open column). C5a increased the migration of HMEC-1 cells in a dose-dependent manner (closed column), while this induced migration was inhibited by W-54011. b In a dose-dependent manner. Bars represent mean ± SEM (n = 3). a **P < 0.01 by Bonferroni’s multiple comparison test, b **P < 0.01 by Dunnett’s multiple comparison test
Mentions: FGF-2 is a known inducer of endothelial cell migration [32]. The migration by FGF-2 was confirmed in this study with the HMEC-1 line using the Chemotaxicell chamber (Fig. 6a). C5a promoted HMEC-1 migration in a dose-dependent manner, an effect that was inhibited in the presence of W-54011 (Fig. 6a, b).Fig. 6

Bottom Line: The goal of this paper is to investigate the effects of activated complement C5a on vascular endothelium during vessel formation.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.

View Article: PubMed Central - PubMed

Affiliation: The First Department of Internal Medicine, University of Occupational and Environmental Health, Japan, Kitakyushu, Japan.

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.

Show MeSH
Related in: MedlinePlus