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Published on: December 2, 2022
Molecular interplay between microRNA-130a and PTEN in palmitic acid-mediated impaired function of endothelial
Xuemei Gu1, Xiao-Qian Wang1, Min-Jie Lin1
1Department of Endocrinology and Metabolism, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Abstract:
Metformin serves an important role in improving the functions of endothelial progenitor cells (EPCs). MicroRNAs (miRNAs), small non‑coding RNAs, have been investigated as significant regulators of EPC vascular functions. The present study investigated the molecular crosstalk between metformin and miRNA‑130a (miR‑130a) in the functions of EPCs exposed to palmitic acid (PA). Isolated EPCs were treated with metformin, PA, and metformin + PA, respectively. Cell Counting Kit‑8, Transwell and Matrigel assays were performed to detect the proliferation, migration and tube formation ability of EPCs following different treatments. The expression of miR‑130a, phosphatase and tensin homolog (PTEN) and phosphorylated‑AKT was analyzed by reverse transcription‑quantitative polymerase chain reaction and western blotting. The specific mechanism underlying the function of metformin in EPCs was further elucidated by transfecting miR‑130a mimics and inhibitor to overexpress and inhibit the expression of miR‑130a in EPCs, respectively. EPCs exhibited impaired functions of proliferation (P<0.01 compared with the control), migration (P<0.01 compared with the control) and tube formation (P<0.01 compared with the control) following treatment with PA, and the expression levels of miR‑130a and PTEN were decreased and increased, respectively. However, the presence of metformin, or the overexpression of miR‑130a using miR‑130a mimic alleviated the impairment of angiogenesis and proliferation, decreased the expression of PTEN and activated the phosphoinositide‑3 kinase/AKT pathway in EPCs exposed to PA. By contrast, downregulating the expression of miR‑130a with a miR‑130a inhibitor reversed the metformin‑mediated protection. These results demonstrate the beneficial effect of miR‑130a/PTEN on EPC functions, which can be regulated by metformin. The effects of metformin on improving PA‑induced EPC dysfunction are mediated by miR‑130a and PTEN, which may assist in the prevention and/or treatment of diabetic vascular disease.
Insights
Metformin improves endothelial progenitor cell (EPC) function by upregulating microRNA-130a (miR-130a) and activating the AKT pathway, counteracting palmitic acid-induced damage. This highlights miR-130a
Area of Science:
- Cardiovascular Biology
- Cellular and Molecular Medicine
- Endocrinology and Metabolism
Background:
- Endothelial progenitor cells (EPCs) are crucial for vascular health.
- Dysfunctional EPCs contribute to diabetic vascular complications.
- MicroRNAs (miRNAs) regulate EPC function, with miR-130a implicated in vascular processes.
Purpose of the Study:
- To investigate the role of metformin in modulating microRNA-130a (miR-130a) and its impact on EPC function under palmitic acid (PA) exposure.
- To elucidate the molecular mechanism by which metformin protects EPCs from PA-induced dysfunction.
Main Methods:
- EPCs were treated with metformin and/or palmitic acid (PA).
- Cell proliferation, migration, and tube formation were assessed using CCK-8, Transwell, and Matrigel assays.
- Expression levels of miR-130a, PTEN, and p-AKT were analyzed via RT-qPCR and Western blotting.
- miR-130a mimics and inhibitors were used to manipulate its expression.
Main Results:
- PA treatment impaired EPC proliferation, migration, and tube formation, decreasing miR-130a and increasing PTEN expression.
- Metformin or miR-130a mimic overexpression alleviated PA-induced EPC dysfunction.
- Metformin treatment decreased PTEN expression and activated the PI3K/AKT pathway.
- Inhibition of miR-130a reversed the protective effects of metformin.
Conclusions:
- Metformin protects EPCs from PA-induced dysfunction through the miR-130a/PTEN pathway.
- Metformin upregulates miR-130a, leading to PTEN downregulation and AKT pathway activation.
- This mechanism offers a potential therapeutic strategy for diabetic vascular disease.
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