English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Purpose: To determine the effect of miR-485-5p on keratinocyte proliferation and migration. Methods: Human primary keratinocytes (HaCaT cells) were treated with different concentrations of transforming growth factor-β1 (TGF)-β1. miR-485-5p expression levels were determined using quantitative reverse transcription-polymerase chain reaction (qRT-PCR). MTT (3-[4,5-dimethylthiazol-2yl]-2,5 diphenyl tetrazolium bromide) and wound healing assays were performed to investigate the regulatory effects of miR-485-5p on cell viability and migration of HaCaT cells. Downstream target gene expression of miR-485-5p was determined using a luciferase activity assay. Results: In HaCaT cells, miR-485-5p was timeand dose-dependently downregulated by TGF-β1 treatment (p < 0.05). Forced expression of miR-485-5p decreased cell viability and migration of HaCaT cells (p < 0.05). Knockdown of miR-485-5p enhanced HaCaT cell viability and migration. Integrin subunit alpha-5 (ITGA5) was predicted and verified to be a downstream target of miR-485-5p in HaCaT cells. Overexpression of ITGA5 attenuated the miR-485-5p-induced decrease of HaCaT cell viability and migration (p < 0.05). Conclusion: MiR-485-5p reduces cell proliferation and migration of keratinocytes through the regulation of ITGA5. This mechanism provides a potential therapeutic strategy for skin wound healing.

MicroRNA-485-5p reduces keratinocyte proliferation and migration by regulating ITGA5 expression in skin wound healing