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MicroRNA-222 regulates the viability of fibroblasts in hypertrophic scars via matrix metalloproteinase 1
The present study aimed to determine the expression of microRNA (miR)-222 in hypertrophic scar (HS) tissues, and investigate the regulatory mechanism of miR-222 in HS. A total of 36 patients diagnosed with HS between August 2013 and May 2016 were included in the present study. HS tissues and HS-adja...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5776557/ https://www.ncbi.nlm.nih.gov/pubmed/29434768 http://dx.doi.org/10.3892/etm.2017.5634 |
Sumario: | The present study aimed to determine the expression of microRNA (miR)-222 in hypertrophic scar (HS) tissues, and investigate the regulatory mechanism of miR-222 in HS. A total of 36 patients diagnosed with HS between August 2013 and May 2016 were included in the present study. HS tissues and HS-adjacent tissues were collected from patients. Primary fibroblasts were obtained from HS tissue. Reverse transcription-quantitative polymerase chain reaction was used to measure mRNA levels of matrix metalloproteinase 1 (MMP1) and miR-222. Western blotting was conducted to determine MMP1 expression and an MTT assay was performed to measure the viability of fibroblasts. A dual luciferase reporter assay was used to identify the binding of miR-222 to MMP1 mRNA. It was demonstrated that MMP1 serves a role in HS at the transcription level and that increased MMP1 expression inhibited the viability of fibroblasts. miR-222 serves a regulatory role in HS by targeting its target gene MMP1 and regulates the expression of MMP1 by binding to its 3′-untranslated region. The decreased expression of miR-222 suppresses the viability of fibroblasts by regulating MMP1 expression. The present study demonstrated that the downregulation of MMP1 in HS tissues is associated with the upregulation of miR-222 expression. miR-222 may therefore regulate the viability of fibroblasts in HS and the expression of related proteins via MMP1. |
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