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Prospective, Randomized, and Controlled Study of a Human Umbilical Cord Mesenchymal Stem Cell Injection for Treating Diabetic Foot Ulcers
Published on: March 3, 2023
Long noncoding RNA XIST promotes cell proliferation and migration in diabetic foot ulcers through the miR-126-3p/EGFR
Wangbing Hong1, Zhenfang Xiong2, Xin Wang1
1Medical Center of Burn plastic and wound repair, The 1st Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China.
Background:
The prevalence of diabetic foot ulcers (DFUs) has caused serious harm to human health. To date, a highly effective treatment is lacking. Long noncoding RNA X-inactive specific transcript (lncRNA XIST) has been the subject of mounting research studies, all of which have found that it serves as a protective factor against certain diseases; however, its function in DFUs is not entirely understood. This study was performed to determine the importance of the lncRNA XIST in the pathogenesis and biological function of DFUs.
Methods:
Diabetic ulcer skin from rats was analysed using haematoxylin-eosin (HE), Masson's trichrome, and immunohistochemistry (IHC) staining. The differences in the expression of genes and proteins were examined with real-time quantitative polymerase chain reaction (RT-qPCR) and Western blotting. Next, the interaction was verified with a dual luciferase gene reporter assay. In addition, CCK-8, Transwell, and wound healing assays were used to assess the proliferation and migration of HaCaT cells.
Results:
The lncRNA XIST and epidermal growth factor receptor (EGFR) were downregulated, while microRNA-126-3p (miR-126-3p) was increased in diabetic ulcer rat skin tissues and high glucose-induced HaCaT cells. In addition, we found that the lncRNA XIST binds to miR-126-3p and that EGFR is directly targeted by miR‑126‑3p. Silencing XIST contributed to upregulated miR-126-3p expression, thus lowering EGFR levels and inhibiting the proliferative and migratory abilities of high glucose-treated HaCaT cells; however, the miR-126-3p inhibitor and overexpression of EGFR reversed this effect.
Conclusion:
Decreased lncRNA XIST expression inhibits the proliferative and migratory abilities of high glucose-induced HaCaT cells by modulating the miR-126-3p/EGFR axis, causing delayed wound healing.
Insights
Diabetic foot ulcers (DFUs) involve decreased long noncoding RNA XIST, which impairs cell growth and migration. Restoring the miR-126-3p/EGFR axis can improve DFU healing.
Area of Science:
- Molecular Biology
- Biochemistry
- Cell Biology
Background:
- Diabetic foot ulcers (DFUs) pose a significant health challenge with limited effective treatments.
- Long noncoding RNA XIST (lncRNA XIST) shows protective roles in various diseases, but its function in DFUs is unclear.
- This study investigates the role of lncRNA XIST in the pathogenesis and biological mechanisms of DFUs.
Purpose of the Study:
- To elucidate the role of lncRNA XIST in diabetic foot ulcer development.
- To understand the molecular interactions involving lncRNA XIST, microRNA-126-3p, and epidermal growth factor receptor in DFUs.
- To identify potential therapeutic targets for improving DFU wound healing.
Main Methods:
- Analysis of diabetic ulcer rat skin tissues using HE, Masson's trichrome, and IHC staining.
- Gene and protein expression analysis via RT-qPCR and Western blotting.
- Cellular assays (CCK-8, Transwell, wound healing) to assess HaCaT cell proliferation and migration, with interaction verification via dual luciferase assay.
Main Results:
- lncRNA XIST and EGFR were downregulated, while miR-126-3p was upregulated in DFU tissues and high glucose-induced cells.
- lncRNA XIST directly binds to miR-126-3p, and miR-126-3p targets EGFR.
- Silencing lncRNA XIST inhibited cell proliferation and migration by upregulating miR-126-3p and downregulating EGFR, effects reversed by miR-126-3p inhibition or EGFR overexpression.
Conclusions:
- Reduced lncRNA XIST expression exacerbates DFU by inhibiting HaCaT cell proliferation and migration.
- The miR-126-3p/EGFR axis is a key pathway modulated by lncRNA XIST in high glucose conditions.
- Targeting the lncRNA XIST/miR-126-3p/EGFR pathway holds promise for enhancing DFU wound healing.
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