title: Skeletal muscle cells express ICAM-1 after muscle overload and ICAM-1 contributes to the ensuing hypertrophic response.
abstract: We previously reported that leukocyte specific β2 integrins contribute to hypertrophy after muscle overload in mice. Because intercellular adhesion molecule-1 (ICAM-1) is an important ligand for β2 integrins, we examined ICAM-1 expression by murine skeletal muscle cells after muscle overload and its contribution to the ensuing hypertrophic response. Myofibers in control muscles of wild type mice and cultures of skeletal muscle cells (primary and C2C12) did not express ICAM-1. Overload of wild type plantaris muscles caused myofibers and satellite cells/myoblasts to express ICAM-1. Increased expression of ICAM-1 after muscle overload occurred via a β2 integrin independent mechanism as indicated by similar gene and protein expression of ICAM-1 between wild type and β2 integrin deficient (CD18-/-) mice. ICAM-1 contributed to muscle hypertrophy as demonstrated by greater (p<0.05) overload-induced elevations in muscle protein synthesis, mass, total protein, and myofiber size in wild type compared to ICAM-1-/- mice. Furthermore, expression of ICAM-1 altered (p<0.05) the temporal pattern of Pax7 expression, a marker of satellite cells/myoblasts, and regenerating myofiber formation in overloaded muscles. In conclusion, ICAM-1 expression by myofibers and satellite cells/myoblasts after muscle overload could serve as a mechanism by which ICAM-1 promotes hypertrophy by providing a means for cell-to-cell communication with β2 integrin expressing myeloid cells.
authors.affiliation: Department of Kinesiology, The University of Toledo, Toledo, Ohio, United States of America.
authors.forename: Christopher L
authors.initials: CL
authors.lastname: Dearth
authors.forename: Qingnian
authors.initials: Q
authors.lastname: Goh
authors.forename: Joseph S
authors.initials: JS
authors.lastname: Marino
authors.forename: Peter A
authors.initials: PA
authors.lastname: Cicinelli
authors.forename: Maria J
authors.initials: MJ
authors.lastname: Torres-Palsa
authors.forename: Philippe
authors.initials: P
authors.lastname: Pierre
authors.forename: Randall G
authors.initials: RG
authors.lastname: Worth
authors.forename: Francis X
authors.initials: FX
authors.lastname: Pizza
mesh_terms: D000818:Animals; D039481:CD11b Antigen / Q000378:metabolism; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000378:metabolism; D015870:Gene Expression; D006984:Hypertrophy; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism*; D017493:Leukocyte Common Antigens / Q000378:metabolism; D007962:Leukocytes / Q000378:metabolism; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D018485:Muscle Fibers, Skeletal / Q000378:metabolism* / Q000473:pathology*; D022423:Myeloid Cells / Q000378:metabolism; D051763:PAX7 Transcription Factor / Q000235:genetics / Q000378:metabolism; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D021381:Protein Transport; D032496:Satellite Cells, Skeletal Muscle / Q000378:metabolism
chemical_list: D039481:CD11b Antigen; D051763:PAX7 Transcription Factor; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D017493:Leukocyte Common Antigens