Imperial College London
Alternate

DrWeiCui

Faculty of Medicine, Department of Metabolism, Digestion and Reproduction

Senior Lecturer
 
 
 
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Contact

 

+44 (0)20 7594 2124wei.cui Website

 
 
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Location

 

1010Institute of Reproductive and Developmental BiologyHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Shi:2018:10.1016/j.jid.2018.03.1521,
author = {Shi, J and Ma, X and Su, Y and Song, Y and Tian, Y and Yuan, S and Zhang, X and Yang, D and Zhang, H and Shuai, J and Cui, W and Ren, F and Plikus, MV and Chen, Y and Luo, J and Yu, Z},
doi = {10.1016/j.jid.2018.03.1521},
journal = {Journal of Investigative Dermatology},
pages = {2253--2263},
title = {MiR-31 mediates inflammatory signaling to promote re-epithelialization during skin wound healing},
url = {http://dx.doi.org/10.1016/j.jid.2018.03.1521},
volume = {138},
year = {2018}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Wound healing is essential for skin repair after injury, and consists of hemostasis, inflammation, re-epithelialization and remodeling phases. Successful re-epithelialization, which relies on proliferation and migration of epidermal keratinocytes, requires 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-κB and STAT3 signaling pathways during inflammation phase. We utilized miR-31 loss-of-function mouse models to demonstrate that miR-31 promotes keratinocyte proliferation and migration. Mechanistically, miR-31 activates the RAS/MAPK signaling by directly targeting Rasa1, Spred1, Spred2 and Spry4, which are negative regulators of the RAS/MAPK 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.
AU  - Shi,J
AU  - Ma,X
AU  - Su,Y
AU  - Song,Y
AU  - Tian,Y
AU  - Yuan,S
AU  - Zhang,X
AU  - Yang,D
AU  - Zhang,H
AU  - Shuai,J
AU  - Cui,W
AU  - Ren,F
AU  - Plikus,MV
AU  - Chen,Y
AU  - Luo,J
AU  - Yu,Z
DO  - 10.1016/j.jid.2018.03.1521
EP  - 2263
PY  - 2018///
SN  - 0022-202X
SP  - 2253
TI  - MiR-31 mediates inflammatory signaling to promote re-epithelialization during skin wound healing
T2  - Journal of Investigative Dermatology
UR  - http://dx.doi.org/10.1016/j.jid.2018.03.1521
UR  - https://www.ncbi.nlm.nih.gov/pubmed/29605672
UR  - http://hdl.handle.net/10044/1/59735
VL  - 138
ER  -
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