ArticleJournal of cellular and molecular medicine2020
The microRNA miR-134-5p induces calcium deposition by inhibiting histone deacetylase 5 in vascular smooth muscle cells.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Hypophosphatemia as a Potential Class Effect of Histone Deacetylase Inhibitors: Evidence from Disproportionality Analysis and Mendelian Randomization Analysis of Drug Targets.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Transcription factor GTF2I regulates osteoclast differentiation through mediating miR-134-5p and MAT2A expressions.Journal of cell communication and signaling · 2025Article
- Review
- The role of miR-134-5p in 7-ketocholesterol-induced human aortic endothelial dysfunction.EXCLI journal · 2024Article
- MicroRNA regulation of phenotypic transformations in vascular smooth muscle: relevance to vascular remodeling.Cellular and molecular life sciences : CMLS · 2023Review
- Circular RNA circSmoc1-2 regulates vascular calcification by acting as a miR-874-3p sponge in vascular smooth muscle cells.Molecular therapy. Nucleic acids · 2022Article
- Article
- The microRNA miR-134-5p induces calcium deposition by inhibiting histone deacetylase 5 in vascular smooth muscle cells.Journal of cellular and molecular medicine · 2020Article
- Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review.Frontiers in cell and developmental biology · 2020Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium deposition in vascular smooth muscle cells (VSMCs) is a form of ectopic ossification in blood vessels. It can result in rigidity of the vasculature and an increase in cardiac events. Here, we report that the microRNA miR-134-5p potentiates inorganic phosphate (Pi)-induced calcium deposition in VSMCs by inhibiting histone deacetylase 5 (HDAC5). Using miRNA microarray analysis of Pi-treated rat VSMCs, we first selected miR-134-5p for further evaluation. Quantitative RT-PCR confirmed that miR-134-5p was increased in Pi-treated A10 cells, a rat VSMC line. Transfection of miR-134-5p mimic potentiated the Pi-induced increase in calcium contents. miR-134-5p increased the amounts of bone runt-related transcription factor 2 (RUNX2) protein and bone morphogenic protein 2 (BMP2) mRNA in the presence of Pi but decreased the expression of osteoprotegerin (OPG). Bioinformatic analysis showed that the HDAC5 3'untranslated region (3'UTR) was one of the targets of miR-134-5p. The luciferase construct containing the 3'UTR of HDAC5 was down-regulated by miR-134-5p mimic in a dose-dependent manner in VSMCs. Overexpression of HDAC5 mitigated the calcium deposition induced by miR-134-5p. Our results suggest that a Pi-induced increase of miR-134-5p may cause vascular calcification through repression of HDAC5.
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