Journal
EXPERIMENTAL AND THERAPEUTIC MEDICINE
Volume 16, Issue 2, Pages 1311-1317Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2018.6350
Keywords
hypertrophic scar; microRNA-663; transforming growth factor-beta 1
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Funding
- Science and Technology Development Project of Suzhou City [SYSD2015094]
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The present study determined the expression of microRNA (miR)-663 in hypertrophic scar (HS) tissues and investigate the regulatory mechanisms of miR-663 in HS. A total of 51 patients diagnosed with HS between December 2013 and February 2016 were included in the present study. HS tissues (experimental group) and HS-adjacent tissues (control group) were collected. Primary fibroblasts were obtained from HS tissue and transfected with small-interfering RNA against transforming growth factor (TGF)-beta 1 or miR-60 mimics. Reverse-transcription quantitative PCR was used to determine the levels of TGF-beta 1 mRNA and miR-663. Western blot analysis was performed to determine TGF-beta 1 protein expression. An MTT assay was employed to detect the proliferation of fibroblasts, and a dual luciferase reporter assay was performed to identify the binding of miR-663 with TGF-beta 1 mRNA. TGF-beta 1 was found to have a regulatory role in HS at the transcriptional level. The expression of TGF-beta 1 was upregulated in HS tissues, and knockdown of TGF-beta 1 in cultured fibroblasts led to inhibition of proliferation. The expression of miR-663 was downregulated in HS. miR-663 was revealed to regulate the expression of TGF-beta 1 by binding with the 3'-untranslated region of TGF-beta 1 mRNA. Elevated expression of miR-663 inhibited the proliferation of fibroblasts by regulating TGF-beta 1 expression. The present study demonstrated that upregulation of TGF-beta 1 in HS tissues is associated with the downregulation of miR-663 expression. miR-663 may regulate the proliferation of fibroblasts in HS and the expression of associated proteins.
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