LncRNA MIR503HG promotes hypertrophic scar progression via miR-143-3p-mediated Smad3 expression.
Wound Repair Regen
; 29(5): 792-800, 2021 09.
Article
in En
| MEDLINE
| ID: mdl-33819360
ABSTRACT
Hypertrophic scars (HSs) form due to unchecked proliferation of fibrous tissue after an injury to the skin. Recently, lncRNA MIR503HG was shown to be involved in HS. However, the mechanism by which MIR503HG affects the formation and progression of HS still needs further study. qRT-PCR was applied to examine the levels of MIR503HG and miR-143-3p in HS tissues and human hypertrophic scar fibroblasts (hHSFs). The relationships of MIR503HG, miR-143-3p and Smad3 were explored with a dual-luciferase reporter assay. Cell proliferation, apoptosis, and invasion were measured by CCK-8 assay, flow cytometry and transwell assay, respectively. The protein level of Smad3 was tested via Western blotting. MIR503HG was upregulated and miR-143-3p was downregulated in HS versus normal skin tissues. The knockdown of MIR503HG and the overexpression of miR-143-3p suppressed the proliferation and invasion of hHSF, and promoted cell apoptosis. MIR503HG bound to miR-143-3p while miR-143-3p directly targeted Smad3 to inhibit its expression. Suppression of miR-143-3p and overexpression of Smad3, respectively, reversed these effects of knockdown of MIR503HG and overexpression of miR-143-3p on hHSFs. Our research supports a model in which the MIR503HG/miR-143-3p/Smad3 axis serves as a critical regulator of HS, highlighting a promising therapeutic option for HS.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Cicatrix, Hypertrophic
/
MicroRNAs
/
RNA, Long Noncoding
Limits:
Humans
Language:
En
Journal:
Wound Repair Regen
Journal subject:
DERMATOLOGIA
Year:
2021
Document type:
Article
Affiliation country:
China