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Experimental cell research v.361 no.2, 2017년, pp.201 - 209   SCI SCIE
본 등재정보는 저널의 등재정보를 참고하여 보여주는 베타서비스로 정확한 논문의 등재여부는 등재기관에 확인하시기 바랍니다.

Study on the role of Hsa-miR-31-5p in hypertrophic scar formation and the mechanism

Wang, X. (Department of Dermatology and Dermatologic Surgery, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, Shanghai 200011, PR China ) ; Zhang, Y. (Department of Orthopedics, Shanghai Tongji Hospital, Tongji University School of Medicine, 389 Xincun Road, Shanghai 200065, PR China ) ; Jiang, B.H. (Department of Plastic and Reconstructive Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu Medical College, Bengbu, An'hui, PR China ) ; Zhang, Q. (People's Hospital of Dancheng County, Dancheng City, Henan Province, PR China ) ; Zhou, R.P. (Department of Plastic and Reconstructive Surgery, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, Shanghai 200011, PR China ) ; Zhang, L. (Department of Plastic and Reconstructive Surgery, The First Affiliated Hospital of Bengbu Medical College, Bengbu Medical College, Bengbu, An'hui, PR China ) ; Wang, Chen (Department of Plastic and Reconstructive Surgery, Shanghai 9th People's Hospital, Shanghai Jiao Tong ) ;
  • 초록  

    Abstract Hypertrophic scar (HS) formation is associated with the fibrosis of fibrocytes caused by excessive extracellular matrix (ECM) synthesis and deposition, the initial event of HS formation. Our high throughput screen of miRNA expression profiles identified hsa-miR31-5p, whose transcription level was most differentially in normal skin fibroblasts (NS) and HS among other miRNAs. The level of hsa-miR31-5p in HS was significantly higher than in NS. In-vitro functional experiments showed hsa-miR31-5p knockdown remarkably suppressed the proliferation of hypertrophic scar fibroblasts (HSFBs) under hypoxia, promoted cell invasion, and inhibited the expression of Collagen I and III and Fibronectin (FN), suggesting that hsa-miR31-5p knockdown effectively reduces HS formation caused by excessive ECM synthesis and deposition in HSFBs under hypoxia. Mechanism study showed that the regulation of HS formation by hsa-miR31-5p was mediated by its target gene, factor-inhibiting HIF-1 (FIH): under hypoxia, hsa-miR31-5p down-regulated FIH and thus increased the level of hypoxia inducible factor-1α (HIF-1α), which subsequently activated the HIF-1α fibrosis regulation pathway in HSFBs, and stimulated the proliferation and ECM synthesis in HSFBs, eventually resulting in fibrosis and scar formation. The data also show that knockdown of hsa-miR31-5p in HSFBs impaired the trend of increased proliferation, reduced invasion and excessive ECM synthesis and deposition caused by HIF-1a activation under hypoxia through upregulating FIH, indicating that knockdown of hsa-miR31-5p effectively inhibits the formation of HS. In conclusion, hsa-miR31 -5p plays an important role in HS formation by inhibiting FIH and regulating the HIF-1α pathway. Therefore, hsa-miR31 -5p may be a novel therapeutic target for HS. Highlights The level of miR31-5p in HS was higher than in NS. MiR31-5p plays a central role for hypoxia induced ECM synthesis and contraction. Blocking miR31-5p inhibits HIF-1a activation in hypoxic via upregulating FIH.


  • 주제어

    Hypertrophic scar .   hsa-miR31-5p .   FIH .   HIF-1α .   Fibrosis.  

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