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A role of MCP-1-CCR2 axis in migration and fusion of skeletal myoblasts.
Li-Z; Summan-M; Hulderman-T; Simeonova-P
FASEB J 2004 Mar; 18(5):A31
Recent studies highlighted the expression of C-C chemokines and their receptors in the injured skeletal muscle. We have demonstrated that absence or attenuation of the macrophage chemoattractant protein (MCP)-I-CCR2 pathway by genetic modulation or immune neutralization lead to impaired functional muscle recovery post-injury. In the present study, we hypothesized that the MCP-l-CCR2 axis orchestrates the migration and/or fusion of myoblasts. In transwell cell culture chambers, myoblasts from wild type (WT) C57BL/6 mice exposed to 10ng/ml MCP-l migrated to a significantly great extent when compared to untreated controls. In contrast, MCP-1 failed to induce migration of myoblasts from trangenic mice deficient of its major receptor (CCR2-/-). Furthermore, growth media- or TNFa-driven migration of WT myoblasts was blocked by anti-MCP-l neutralizing antibody. These data suggest that the MCP-l-CCR2 axis regulates the migratory activities of myoblasts in vitro. In the in vib"O fusion assay, myoblasts from CCR2-/- mice showed dramatically reduced fusion, compared to the WT myoblasts. However, anti-MCP-1 neutralizing antibody failed to inhibit the fusion of the WT myoblasts, indicating fusion activities might be regulated by CCR2-dependent but MCP-I- independent mechanisms. These data demonstrate that signaling through the CCR2 chemokine receptor might playa direct role in post- natal myogenesis by regulating myoblasts migration and fusion.
Skeletal-system; Skeletal-movement; Skeletal-system-disorders; Animal-studies; Animals; In-vitro-study
Issue of Publication
Research Tools and Approaches: Exposure Assessment Methods
The FASEB Journal, Experimental Biology 2004, Late Breaking Abstracts, Washington, DC April 17-21, 2004
Page last reviewed: May 24, 2019
Content source: National Institute for Occupational Safety and Health Education and Information Division