| First Author | Shi J | Year | 2018 |
| Journal | J Invest Dermatol | Volume | 138 |
| Issue | 10 | Pages | 2253-2263 |
| PubMed ID | 29605672 | Mgi Jnum | J:283572 |
| Mgi Id | MGI:6355697 | Doi | 10.1016/j.jid.2018.03.1521 |
| Citation | Shi J, et al. (2018) MiR-31 Mediates Inflammatory Signaling to Promote Re-Epithelialization during Skin Wound Healing. J Invest Dermatol 138(10):2253-2263 |
| abstractText | Wound healing is essential for skin repair after injury, and it consists of hemostasis, inflammation, re-epithelialization, and remodeling phases. Successful re-epithelialization, which relies on proliferation and migration of epidermal keratinocytes, requires a reduction in tissue inflammation. Therefore, understanding the molecular mechanism underlying the transition from inflammation to re-epithelialization will help to better understand the principles of wound healing. Currently, the in vivo functions of specific microRNAs in wound healing are not fully understood. We observed that miR-31 expression is strongly induced in wound edge keratinocytes, and is directly regulated by the activity of NF-kappaB and signal transducer and activator of transcription 3 signaling pathways during the inflammation phase. We used miR-31 loss-of-function mouse models to demonstrate that miR-31 promotes keratinocyte proliferation and migration. Mechanistically, miR-31 activates the Ras/mitogen-activated protein kinase signaling by directly targeting Rasa1, Spred1, Spred2, and Spry4, which are negative regulators of the Ras/mitogen-activated protein kinase pathway. Knockdown of these miR-31 targets at least partially rescues the delayed scratch wound re-epithelialization phenotype observed in vitro in miR-31 knockdown keratinocytes. Taken together, these findings identify miR-31 as an important cell-autonomous mediator during the transition from inflammation to re-epithelialization phases of wound healing, suggesting a therapeutic potential for miR-31 in skin injury repair. |
