Premium
Expression of CD59, a regulator of the membrane attack complex of complement, on human skeletal muscle fibers
Author(s) -
Navenot JeanMarc,
Villanova Marcello,
LucasHéron Brigitte,
Malandrini Alessandro,
Blanchard Dominique,
Louboutin JeanPierre
Publication year - 1997
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199701)20:1<92::aid-mus12>3.0.co;2-3
Subject(s) - cd59 , complement membrane attack complex , complement system , skeletal muscle , decay accelerating factor , microbiology and biotechnology , cd46 , immunostaining , monoclonal antibody , biology , immunocytochemistry , complement component 5 , chemistry , antibody , immunology , immunohistochemistry , anatomy , endocrinology
Control of complement deposition on autologous cells is mediated by a group of complement regulatory membrane proteins acting at different levels of the complement cascade. Decay accelerating factor (CD55) prevents the assembly of C3 convertases and CD59 membrane inhibitor of reactive lysis (MIRL) restricts homologous complement lysis by the membrane attack complex of complement (MAC) by inhibition of C5b‐8 catalyzed insertion of C9. The aim of this work was to study the eventual expression of CD55 and CD59 on human skeletal muscle fibers. Highly sensitive immunoblotting using murine monoclonal antibodies showed that CD59, but not CD55, was present in skeletal muscle fibers. Immunocytochemistry with a monoclonal antibody against CD59 demonstrated a dense granular immunostaining mainly localized at the level of the sarcolemma. Thus, CD59, but not CD55, is expressed on normal skeletal muscle fibers. CD59 may play a prominent role in preventing MAC deposition and subsequent complement‐mediated damage in myopathies where the complement system activation is involved. © 1997 John Wiley & Sons, Inc.