{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(5)"],"submitter":["Yang X"],"pubmed_abstract":["MicroRNAs involved in keratinocyte migration and wound healing are largely unknown. Here, we revealed the indispensable role of miR-21 in keratinocyte migration and in re-epithelialization during wound healing in mice. In HaCaT cell, miR-21 could be upregulated by TGF-?1. Similar to the effect of TGF-?1, miR-21 overexpression promoted keratinocyte migration. Conversely, miR-21 knockdown attenuated TGF-?1-induced keratinocyte migration, suggesting that miR-21 was essential for TGF-?-driven keratinocyte migration. Furthermore, we found that miR-21 was upregulated during wound healing, coincident with the temporal expression pattern of TGF-?1. Consistently, knockdown of endogenous miR-21 using a specific antagomir dramatically delayed re-epithelialization possibly due to the reduced keratinocyte migration. TIMP3 and TIAM1, direct targets of miR-21, were verified to be regulated by miR-21 in vitro and in vivo, indicating that these two molecules might contribute to miR-21-induced keratinocyte migration. Taken together, our results demonstrate that miR-21 promotes keratinocyte migration and boosts re-epithelialization during skin wound healing."],"journal":["International journal of biological sciences"],"pagination":["685-90"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3107477"],"repository":["biostudies-literature"],"pubmed_title":["miR-21 promotes keratinocyte migration and re-epithelialization during wound healing."],"pmcid":["PMC3107477"],"pubmed_authors":["Yang X","Fan KJ","Wang YL","Guo SL","Li J","Teng Y","Wang J"],"additional_accession":[]},"is_claimable":false,"name":"miR-21 promotes keratinocyte migration and re-epithelialization during wound healing.","description":"MicroRNAs involved in keratinocyte migration and wound healing are largely unknown. Here, we revealed the indispensable role of miR-21 in keratinocyte migration and in re-epithelialization during wound healing in mice. In HaCaT cell, miR-21 could be upregulated by TGF-?1. Similar to the effect of TGF-?1, miR-21 overexpression promoted keratinocyte migration. Conversely, miR-21 knockdown attenuated TGF-?1-induced keratinocyte migration, suggesting that miR-21 was essential for TGF-?-driven keratinocyte migration. Furthermore, we found that miR-21 was upregulated during wound healing, coincident with the temporal expression pattern of TGF-?1. Consistently, knockdown of endogenous miR-21 using a specific antagomir dramatically delayed re-epithelialization possibly due to the reduced keratinocyte migration. TIMP3 and TIAM1, direct targets of miR-21, were verified to be regulated by miR-21 in vitro and in vivo, indicating that these two molecules might contribute to miR-21-induced keratinocyte migration. Taken together, our results demonstrate that miR-21 promotes keratinocyte migration and boosts re-epithelialization during skin wound healing.","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011","modification":"2021-02-21T08:23:07Z","creation":"2019-03-27T00:42:15Z"},"accession":"S-EPMC3107477","cross_references":{"pubmed":["21647251"],"doi":["10.7150/ijbs.7.685"]}}