<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ghatak S</submitter><funding>NIDDK NIH HHS</funding><funding>NINR NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>454-470</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9931555</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(2)</volume><pubmed_abstract>Fetal cutaneous wound closure and repair differ from that in adulthood. In this work, we identify an oxidant stress sensor protein, nonselenocysteine-containing phospholipid hydroperoxide glutathione peroxidase (NPGPx), that is abundantly expressed in normal fetal epidermis (and required for fetal wound closure), though not in adult epidermis, but is variably re-induced upon adult tissue wounding. NPGPx is a direct target of the miR-29 family. Following injury, abundance of miR-29 is lowered, permitting a prompt increase in NPGPx transcripts and protein expression in adult wound-edge tissue. NPGPx expression was required to mediate increased keratinocyte migration induced by miR-29 inhibition in vitro and in vivo. Increased NPGPx expression induced increased SOX2 expression and β-catenin n</pubmed_abstract><journal>Molecular therapy : the journal of the American Society of Gene Therapy</journal><pubmed_title>Driving adult tissue repair via re-engagement of a pathway required for fetal healing.</pubmed_title><pmcid>PMC9931555</pmcid><funding_grant_id>R01 GM077185</funding_grant_id><funding_grant_id>R56 DK076566</funding_grant_id><funding_grant_id>R01 GM069589</funding_grant_id><funding_grant_id>R01 NR013898</funding_grant_id><funding_grant_id>K25 GM143572</funding_grant_id><funding_grant_id>R01 GM108014</funding_grant_id><funding_grant_id>R01 DK076566</funding_grant_id><funding_grant_id>R01 DK114718</funding_grant_id><pubmed_authors>Ghatak S</pubmed_authors><pubmed_authors>Wilgus TA</pubmed_authors><pubmed_authors>Wulff BC</pubmed_authors><pubmed_authors>Sen CK</pubmed_authors><pubmed_authors>Xuan Y</pubmed_authors><pubmed_authors>Sharma A</pubmed_authors><pubmed_authors>Palakurti R</pubmed_authors><pubmed_authors>Ghosh N</pubmed_authors><pubmed_authors>Khanna S</pubmed_authors><pubmed_authors>Roy S</pubmed_authors><pubmed_authors>El Masry MS</pubmed_authors><pubmed_authors>Maulik N</pubmed_authors><pubmed_authors>Thirunavukkarasu M</pubmed_authors><pubmed_authors>Pradeep SR</pubmed_authors><pubmed_authors>Yoder MC</pubmed_authors></additional><is_claimable>false</is_claimable><name>Driving adult tissue repair via re-engagement of a pathway required for fetal healing.</name><description>Fetal cutaneous wound closure and repair differ from that in adulthood. In this work, we identify an oxidant stress sensor protein, nonselenocysteine-containing phospholipid hydroperoxide glutathione peroxidase (NPGPx), that is abundantly expressed in normal fetal epidermis (and required for fetal wound closure), though not in adult epidermis, but is variably re-induced upon adult tissue wounding. NPGPx is a direct target of the miR-29 family. Following injury, abundance of miR-29 is lowered, permitting a prompt increase in NPGPx transcripts and protein expression in adult wound-edge tissue. NPGPx expression was required to mediate increased keratinocyte migration induced by miR-29 inhibition in vitro and in vivo. Increased NPGPx expression induced increased SOX2 expression and β-catenin n</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Feb</publication><modification>2025-05-29T21:29:39.935Z</modification><creation>2025-05-29T21:29:39.935Z</creation></dates><accession>S-EPMC9931555</accession><cross_references><pubmed>36114673</pubmed><doi>10.1016/j.ymthe.2022.09.002</doi></cross_references></HashMap>