2026-04-13T03:07:04Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1264832025-12-05T12:02:16Zcom_2072_1057col_2072_478916col_2072_478917

00925njm 22002777a 4500 dc Díaz Ramos, M. Àngels author Roig Borrellas, Anna author García Melero, Ana author Llorens, Ana author López Alemany, Roser author 2018-11-27T10:51:48Z 2018-11-27T10:51:48Z 2012-12-11 2018-07-24T12:51:37Z Adult regenerative myogenesis is central for restoring normal tissue structure and function after muscle damage. In muscle repair after injury, as in severe myopathies, damaged and necrotic fibers are removed by infiltrating inflammatory cells and then replaced by muscle stem cells or satellite cells, which will fuse to form new myofibers. Extracellular proteolysis mediated by uPA-generated plasmin plays a critical role in controlling inflammation and satellite-cell-dependent myogenesis. alpha-enolase has been described as plasminogen receptor in several cell types, where it acts concentrating plasmin proteolytic activity on the cell surface. In this study, we investigated whether alpha-enolase plasminogen receptor plays a regulatory role during the muscular repair process. Inhibitors of alpha-enolase/plasminogen binding: MAb11G1 (a monoclonal antibody against alpha-enolase) and e-aminocaproic acid, EACA (a lysine analogue) inhibited the myogenic abilities of satellite cells-derived myoblasts. Furthermore, knockdown of alpha-enolase decreased myogenic fusion of myoblasts. Injured wild-type mice and dystrophic mdx mice were also treated with MAb11G1 and EACA. These treatments had negative impacts on muscle repair impairing satellite cell functions in vitro in agreement with blunted growth of new myofibers in vivo. Furthermore, both MAb11G1 and EACA treatments impaired adequate inflammatory cell infiltration and promoted extracellular matrix deposition in vivo, which resulted in persistent degeneration. These results demonstrate the novel requirement of alpha-enolase for restoring homeostasis of injured muscle tissue, by controlling the pericellular localization of plasmin activity. Miogènesi Múscul estriat Myogenesis Striated muscle Requirement of Plasminogen Binding to Its Cell-Surface Receptor α-Enolase for Efficient Regeneration of Normal and Dystrophic Skeletal Muscle