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Disease severity is reduced by NF-\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B inhibition in the\n                    <jats:italic>mdx<\/jats:italic>\n                    mouse, a murine DMD model; however, therapeutic targeting of NF-\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B remains problematic for patients because of its fundamental role in immunity. In this investigation, we found that the therapeutic effect of NF-\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B blockade requires hepatocyte growth factor (HGF) production by myogenic cells. We found that deleting one allele of the NF-\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B subunit p65 (\n                    <jats:italic>p65<\/jats:italic>\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    ) improved the survival and enhanced the anti-inflammatory capacity of muscle-derived stem cells (MDSCs) following intramuscular transplantation. Factors secreted from\n                    <jats:italic>p65<\/jats:italic>\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    MDSCs in cell cultures modulated macrophage cytokine expression in an HGF-receptor-dependent manner. Indeed, we found that following genetic or pharmacologic inhibition of basal NF-\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B\/p65 activity, HGF gene transcription was induced in MDSCs. We investigated the role of HGF in anti-NF-\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B therapy\n                    <jats:italic>in vivo<\/jats:italic>\n                    using\n                    <jats:italic>mdx<\/jats:italic>\n                    ;\n                    <jats:italic>p65<\/jats:italic>\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice, and found that accelerated regeneration coincided with HGF upregulation in the skeletal muscle. This anti-NF-\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B-mediated dystrophic phenotype was reversed by blocking\n                    <jats:italic>de novo<\/jats:italic>\n                    HGF production by myogenic cells following disease onset. HGF silencing resulted in increased inflammation and extensive necrosis of the diaphragm muscle. Proteolytic processing of matrix-associated HGF is known to activate muscle stem cells at the earliest stages of repair, but our results indicate that the production of a second pool of HGF by myogenic cells, negatively regulated by NF-\n                    <jats:italic>\u03ba<\/jats:italic>\n                    B\/p65, is crucial for inflammation resolution and the completion of repair in dystrophic skeletal muscle. Our findings warrant further investigation into the potential of HGF mimetics for the treatment of DMD.\n                  <\/jats:p>","DOI":"10.1038\/cddis.2015.66","type":"journal-article","created":{"date-parts":[[2015,4,23]],"date-time":"2015-04-23T08:48:05Z","timestamp":1429778885000},"page":"e1730-e1730","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["NF-\u03baB inhibition reveals a novel role for HGF during skeletal muscle repair"],"prefix":"10.1038","volume":"6","author":[{"given":"J D","family":"Proto","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Y","family":"Tang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"Lu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W C W","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E","family":"Stahl","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Poddar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S A","family":"Beckman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P D","family":"Robbins","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"L J","family":"Nidernhofer","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K","family":"Imbrogno","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T","family":"Hannigan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W M","family":"Mars","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"Huard","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2015,4,23]]},"reference":[{"key":"BFcddis201566_CR1","doi-asserted-by":"publisher","first-page":"889","DOI":"10.1172\/JCI30556","volume":"117","author":"S Archaryya","year":"2007","unstructured":"Archaryya S, Villalta SA, Bakkar N, Bupha-Intr T, Janssen PM, Carathers M et al. 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