<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Short WD</submitter><funding>National Institute of General Medical Sciences</funding><funding>NIGMS NIH HHS</funding><pagination>e22298</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9796147</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>36(7)</volume><pubmed_abstract>Endothelial progenitor cells (EPCs) contribute to de novo angiogenesis, tissue regeneration, and remodeling. Interleukin 10 (IL-10), an anti-inflammatory cytokine that primarily signals via STAT3, has been shown to drive EPC recruitment to injured tissues. Our previous work demonstrated that overexpression of IL-10 in dermal wounds promotes regenerative tissue repair via STAT3-dependent regulation of fibroblast-specific hyaluronan synthesis. However, IL-10's role and specific mode of action on EPC recruitment, particularly in dermal wound healing and neovascularization in both normal and diabetic wounds, remain to be defined. Therefore, inducible skin-specific STAT3 knockdown mice were studied to determine IL-10's impact on EPCs, dermal wound neovascularization and healing, and whether it </pubmed_abstract><journal>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</journal><pubmed_title>IL-10 promotes endothelial progenitor cell infiltration and wound healing via STAT3.</pubmed_title><pmcid>PMC9796147</pmcid><funding_grant_id>1R01GM111808NIH</funding_grant_id><funding_grant_id>R01 GM111808</funding_grant_id><pubmed_authors>Vangapandu HV</pubmed_authors><pubmed_authors>Butte MJ</pubmed_authors><pubmed_authors>Keswani SG</pubmed_authors><pubmed_authors>Steen E</pubmed_authors><pubmed_authors>Kaul A</pubmed_authors><pubmed_authors>Olutoye OO</pubmed_authors><pubmed_authors>Templeman N</pubmed_authors><pubmed_authors>Blum AJ</pubmed_authors><pubmed_authors>Narmoneva DA</pubmed_authors><pubmed_authors>Moles CM</pubmed_authors><pubmed_authors>Bollyky PL</pubmed_authors><pubmed_authors>Balaji S</pubmed_authors><pubmed_authors>Crombleholme TM</pubmed_authors><pubmed_authors>Wang X</pubmed_authors><pubmed_authors>Short WD</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-10 promotes endothelial progenitor cell infiltration and wound healing via STAT3.</name><description>Endothelial progenitor cells (EPCs) contribute to de novo angiogenesis, tissue regeneration, and remodeling. Interleukin 10 (IL-10), an anti-inflammatory cytokine that primarily signals via STAT3, has been shown to drive EPC recruitment to injured tissues. Our previous work demonstrated that overexpression of IL-10 in dermal wounds promotes regenerative tissue repair via STAT3-dependent regulation of fibroblast-specific hyaluronan synthesis. However, IL-10's role and specific mode of action on EPC recruitment, particularly in dermal wound healing and neovascularization in both normal and diabetic wounds, remain to be defined. Therefore, inducible skin-specific STAT3 knockdown mice were studied to determine IL-10's impact on EPCs, dermal wound neovascularization and healing, and whether it </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jul</publication><modification>2025-04-21T15:19:33.425Z</modification><creation>2025-04-21T15:19:33.425Z</creation></dates><accession>S-EPMC9796147</accession><cross_references><pubmed>35670763</pubmed><doi>10.1096/fj.201901024RR</doi></cross_references></HashMap>