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Updated: Dec 30, 2025

Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
Published on: July 28, 2023
A novel regulatory function for miR-217 targetedly suppressing fibronectin expression in keloid fibrogenesis
1Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Abstract:
Fibronectin (FN) plays a critical role in the development and progression of keloid scarring (KS). In the present study, we hypothesized that a post-translational mechanism of microRNAs regulated the expression of FN in keloid scarring fibroblasts (KSFBs). Here, we collected 20 KS tissues and paired corresponding adjacent normal tissues from clinical patients and measured the expression of miRNA-217. First, by using PicTar, TargetScan and miRBase database, we found that miRNA-217 might be a regulator of FN in human species. Based on these hypotheses, the expression of miRNA-217 and FN in KS tissues was investigated. The results demonstrated that the expression of miRNA-217 was greatly suppressed, and FN was increased in KS tissues. Intriguingly, the expression levels of endogenous miRNA-217 negatively correlated with the FN mRNA levels (Pearson's correlation coefficient = -0.683, P < 0.001). In vitro, miRNA-217 could regulate FN through the predicted binding sites in its 3'-UTR. miRNA-217 played an impact on cell proliferation and apoptosis, thereby regulating KSFBs growth. Moreover, miRNA-217 gain-of function decreased FN, Col-1 and Col-3 protein expression, and miRNA-217 loss-of function increased FN, Col-1 and Col-3 protein expression in KSFBs. In conclusion, overexpressed miRNA-217 could inhibit KSFBs growth, and the underlying mechanism was mediated, at least partially, through the suppression of FN expression. But above all, miRNA-217 might play a potential therapeutic avenue for the treatment of keloid fibrogenesis.
Insights
MicroRNA-217 (miRNA-217) suppresses fibronectin (FN) expression, inhibiting keloid scarring fibroblast growth. This finding suggests miRNA-217 as a potential therapeutic target for keloid fibrogenesis.
Area of Science:
- Molecular Biology
- Dermatology
- Biochemistry
Background:
- Fibronectin (FN) is crucial in keloid scarring (KS) development.
- MicroRNAs (miRNAs) are implicated in post-translational gene regulation.
- The role of specific miRNAs in FN regulation within keloid fibroblasts (KSFBs) requires elucidation.
Purpose of the Study:
- To investigate the regulatory role of miRNA-217 on fibronectin (FN) expression in keloid scarring fibroblasts (KSFBs).
- To explore the potential of miRNA-217 as a therapeutic target for keloid fibrogenesis.
Main Methods:
- Analysis of miRNA-217 and FN expression in clinical KS tissues and adjacent normal tissues.
- Bioinformatic prediction of miRNA-217 targets using PicTar, TargetScan, and miRBase.
- In vitro experiments involving miRNA-217 gain-of-function and loss-of-function in KSFBs.
- Assessment of FN, Collagen-1 (Col-1), and Collagen-3 (Col-3) protein levels.
Main Results:
- miRNA-217 expression was significantly suppressed in KS tissues, inversely correlating with elevated FN mRNA levels.
- miRNA-217 directly targeted FN, impacting KSFB proliferation and apoptosis.
- Overexpression of miRNA-217 reduced FN, Col-1, and Col-3 protein levels, while its inhibition increased them.
Conclusions:
- miRNA-217 suppresses KSFB growth, primarily by inhibiting FN expression.
- miRNA-217 demonstrates potential as a therapeutic strategy for mitigating keloid fibrogenesis.
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