LncRNA MIR503HG promotes hypertrophic scar progression via miR‐143‐3p‐mediated Smad3 expression.
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...
| Published in: | Wound Repair & Regeneration Vol. 29; no. 5; pp. 792 - 801 |
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| Main Authors: | , , , , , |
| Format: | pictorial research tables/charts Journal Article |
| Published: |
Wiley-Blackwell
Sep2021
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| Online Access: | View this record in EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=152209543&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 152209543 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 10671927 DPV jtl: Wound Repair & Regeneration issn: 10671927 maglogo: Y pubinfo: dt: Sep2021 vid: 29 iid: 5 pid: 480 pub: Wiley-Blackwell place: Malden, Massachusetts artinfo: ui: 152209543 149628804 152209543 152209543 10.1111/wrr.12913 152209543 ppf: 792 ppct: 9 formats: fmt: – @attributes: type: T – @attributes: type: C – @attributes: type: P tig: atl: LncRNA MIR503HG promotes hypertrophic scar progression via miR‐143‐3p‐mediated Smad3 expression. aug: au: Wei, Jun Wang, Zhiyong Zhong, Chaoyi Ding, Huarong Wang, Xiqiao Lu, Shuliang affil: Department of Plastic and Burn Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning Guangxi Zhuang Autonomous Region,, China sug: subj: Cicatrix, Hypertrophic Disease Progression Gene Expression RNA Pharmacodynamics Human Male Female Adult China Cell Culture Techniques Cell Proliferation Apoptosis Blotting, Western Polymerase Chain Reaction Methods Analysis of Variance Descriptive Statistics Adult: 19-44 years Male Female ab: 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. pubtype: Academic Journal doctype: pictorial research tables/charts Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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