biostudies-literatureUnknown7(5)Yang XMicroRNAs 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.International journal of biological sciences685-90https://www.ebi.ac.uk/biostudies/studies/S-EPMC3107477biostudies-literaturemiR-21 promotes keratinocyte migration and re-epithelialization during wound healing.PMC3107477Yang XFan KJWang YLGuo SLLi JTeng YWang JfalsemiR-21 promotes keratinocyte migration and re-epithelialization during wound healing.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.2011-01-01T00:00:00Z20112021-02-21T08:23:07Z2019-03-27T00:42:15ZS-EPMC31074772164725110.7150/ijbs.7.685