Universidad Peruana Cayetano Heredia

Endogenous erythropoietin signaling facilitates skeletal muscle repair and recovery following pharmacologically induced damage

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dc.contributor.author Jia, Y.
dc.contributor.author Suzuki, N.
dc.contributor.author Yamamoto, M.
dc.contributor.author Gassmann, M.
dc.contributor.author Noguchi, C.T.
dc.date.accessioned 2022-01-18T19:26:51Z
dc.date.available 2022-01-18T19:26:51Z
dc.date.issued 2012
dc.identifier.uri https://hdl.handle.net/20.500.12866/10956
dc.description.abstract Erythropoietin acts by binding to its cell surface receptor on erythroid progenitor cells to stimulate erythrocyte production. Erythropoietin receptor expression in nonhematopoietic tissue, including skeletal muscle progenitor cells, raises the possibility of a role for erythropoietin beyond erythropoiesis. Mice with erythropoietin receptor restricted to hematopoietic tissue were used to assess contributions of endogenous erythropoietin to promote skeletal myoblast proliferation and survival and wound healing in a mouse model of cardiotoxin induced muscle injury. Compared with wild-type controls, these mice had fewer skeletal muscle Pax-7+ satellite cells and myoblasts that do not proliferate in culture, were more susceptible to skeletal muscle injury and reduced maximum load tolerated by isolated muscle. In contrast, mice with chronic elevated circulating erythropoietin had more Pax-7+ satellite cells and myoblasts with increased proliferation and survival in culture, decreased muscle injury, and accelerated recovery of maximum load tolerated by isolated muscle. Skeletal muscle myoblasts also produced endogenous erythropoietin that increased at low O2. Erythropoietin promoted proliferation, survival, and wound recovery in myoblasts via the phosphoinositide 3-kinase/AKT pathway. Therefore, endogenous and exogenous erythropoietin contribute to increasing satellite cell number following muscle injury, improve myoblast proliferation and survival, and promote repair and regeneration in this mouse induced muscle injury model independent of its effect on erythrocyte production. en_US
dc.language.iso eng
dc.publisher Wiley
dc.relation.ispartofseries FASEB Journal
dc.rights info:eu-repo/semantics/restrictedAccess
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
dc.subject Humans en_US
dc.subject Controlled Study en_US
dc.subject Animal Cell en_US
dc.subject Mice Knockout en_US
dc.subject Skeletal Muscle en_US
dc.subject Cell Hypoxia en_US
dc.subject Oxygen en_US
dc.subject Signal Transduction en_US
dc.subject Cell Culture en_US
dc.subject Cell Proliferation en_US
dc.subject Recombinant Proteins en_US
dc.subject Mus en_US
dc.subject Erythropoietin|Mice Transgenic en_US
dc.subject Mus Musculus en_US
dc.subject Apoptosis en_US
dc.subject Cell Survival en_US
dc.subject Erythropoietin Receptor en_US
dc.subject GATA3 Transcription Factor en_US
dc.subject Mice Inbred C57BL en_US
dc.subject Muscle Injury en_US
dc.subject Myoblast en_US
dc.subject Myoblasts Skeletal en_US
dc.subject PAX7 Transcription Factor en_US
dc.subject Phosphatidylinositol 3 Kinase en_US
dc.subject PI3K en_US
dc.title Endogenous erythropoietin signaling facilitates skeletal muscle repair and recovery following pharmacologically induced damage en_US
dc.type info:eu-repo/semantics/article
dc.identifier.doi https://doi.org/10.1096/fj.11-196618
dc.subject.ocde https://purl.org/pe-repo/ocde/ford#1.06.01
dc.relation.issn 1530-6860


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