Premium
Complement activation and regulator expression after anoxic injury of human endothelial cells
Author(s) -
VÄKEVÄ A.,
MERI S.
Publication year - 1998
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1998.tb00271.x
Subject(s) - complement system , cd46 , cd59 , decay accelerating factor , microbiology and biotechnology , complement membrane attack complex , biology , endothelial stem cell , classical complement pathway , alternative complement pathway , chemistry , immune system , immunology , biochemistry , in vitro
Complement activation is involved in the ischemia‐reperfusion injury of various organs, but the mechanisms leading to activation of the complement system are incompletely understood. In this study we show that EA. hy 926 human endothelial cells cultured under anoxic conditions (24 or 48 h) become activators of the homologous complement system. Flow cytometric analysis indicated that C1q, C3c, C3d, C4, C5, C9 components of complement are deposited on anoxic but not on normoxic cells after incubation with normal human serum. Cell membrane‐associated regulators of complement, membrane cofactor protein (CD46), decay‐accelerating factor (CD55) and protectin (CD59) were expressed on EA. hy 926 cells grown under normal oxygen tension. Under anoxic conditions the expression of protectin was clearly decreased, whereas the expression of CD46 and CD55 diminished only slightly. Our results suggest that anoxia can convert human endothelial cells to activators of the complement system. The diminished expression of protectin, CD46 and CD55 can sensitize the cells to complement‐mediated damage. Activation of the complement system due to the anoxic injury of human endothelial cells might be an important triggering mechanism in the pathogenesis of ischemia‐reperfusion injury of human heart.