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  MicroRNA-132 enhances transition from inflammation to proliferation during wound healing.

Li, D., Wang, A., Liu, X., Meisgen, F., Grünler, J., Botusan, I. R., et al. (2015). MicroRNA-132 enhances transition from inflammation to proliferation during wound healing. Journal of Clinical Investigation, 125(8), 3008-3026. doi:10.1172/JCI79052.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-334A-D Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-3403-7
Genre: Journal Article

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 Creators:
Li, D., Author
Wang, A., Author
Liu, X., Author
Meisgen, F., Author
Grünler, J., Author
Botusan, I. R., Author
Narayanan, S., Author
Erikci, E.1, Author              
Li, X., Author
Blomqvist, L., Author
Du, L., Author
Pivarcsi, A., Author
Sonkoly, E., Author
Chowdhury, K.1, Author              
Catrina, S. B., Author
Stahle, M., Author
Landen, N. X., Author
Affiliations:
1Facility of Microarray Analyses, MPI for biophysical chemistry, Max Planck Society, ou_578589              

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 Abstract: Wound healing is a complex process that is characterized by an initial inflammatory phase followed by a proliferative phase. This transition is a critical regulatory point; however, the factors that mediate this process are not fully understood. Here, we evaluated microRNAs (miRs) in skin wound healing and characterized the dynamic change of the miRNome in human skin wounds. miR-132 was highly upregulated during the inflammatory phase of wound repair, predominantly expressed in epidermal keratinocytes, and peaked in the subsequent proliferative phase. TGF-β1 and TGF-β2 induced miR-132 expression in keratinocytes, and transcriptome analysis of these cells revealed that miR-132 regulates a large number of immune response- and cell cycle-related genes. In keratinocytes, miR-132 decreased the production of chemokines and the capability to attract leukocytes by suppressing the NF-κB pathway. Conversely, miR-132 increased activity of the STAT3 and ERK pathways, thereby promoting keratinocyte growth. Silencing of the miR-132 target heparin-binding EGF-like growth factor (HB-EGF) phenocopied miR-132 overexpression in keratinocytes. Using mouse and human ex vivo wound models, we found that miR-132 blockade delayed healing, which was accompanied by severe inflammation and deficient keratinocyte proliferation. Together, our results indicate that miR-132 is a critical regulator of skin wound healing that facilitates the transition from the inflammatory to the proliferative phase.

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Language(s): eng - English
 Dates: 2015-06-292015-08-03
 Publication Status: Published in print
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 Rev. Method: Peer
 Identifiers: DOI: 10.1172/JCI79052
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Title: Journal of Clinical Investigation
Source Genre: Journal
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Pages: - Volume / Issue: 125 (8) Sequence Number: - Start / End Page: 3008 - 3026 Identifier: -