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Transcriptome analysis of human coronary artery smooth muscle cells under pro-differentiation and pro-dedifferentiation treatments

ABSTRACT: This study explores the transcriptomic landscape of human coronary artery smooth muscle cells (HCASMCs) in response to stimuli that promote differentiation (Repsox) or dedifferentiation (PDGF-BB, IL-1b). Our RNA sequencing analysis identifies DNA damage-inducible transcript 4 (DDIT4) as a key regulator of vascular smooth muscle cell (VSMC) phenotypic switching, showing its significant upregulation in synthetic phenotypes and downregulation in contractile phenotypes. This dataset provides a resource for understanding the transcriptional programs governing VSMC plasticity in the context of vascular remodeling and atherosclerotic disease.

ORGANISM(S): Homo sapiens

PROVIDER: GSE311133 | GEO | 2026/06/06

REPOSITORIES: GEO

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Project description:Vascular calcification is a complex process and has been associated with aging, diabetes, chronic kidney disease (CKD). Although there have been several studies studying the role of miRNAs (miRs) in bone osteogenesis, little is known about the role of miRs in vascular calcification and their role in the pathogenesis of vascular abnormalities. Matrix vesicles (MV) are known to play an important role in initiating vascular smooth muscle cell (VSMC) calcification. In the present study, we performed miRNA microarray analysis to identify the dysregulated miRs between MV and VSMC derived from CKD rats to understand the role of post-transcriptional regulatory networks governed by these miRNAs in vascular calcification and to uncover the differential miRNA content of MV. The percentage of miRNA to total RNA was increased in MV compared to VSMC. Comparison of expression profiles of miRNA by microarray demonstrated 33 miRs to be differentially expressed with the majority (~ 57%) of them down-regulated. Target genes controlled by differentially expressed miRNAs were identified utilizing two different complementary computational approaches Miranda and Targetscan to understand the functions and pathways that may be affected due to the production of MV from calcifying VSMC thereby contributing to the regulation of genes by miRs. We found several processes including vascular smooth muscle contraction, response to hypoxia and regulation of muscle cell differentiation to be enriched. Signaling pathways identified included MAP-kinase and wnt signaling that have previously been shown to be important in vascular calcification. In conclusion, our results demonstrate that miRs are concentrated in MV from calcifying VSMC, and that important functions and pathways are affected by the miRs dysregulation between calcifying VSMC and the MV they produce. This suggests that miRs may play a very important regulatory role in vascular calcification in CKD by controlling an extensive network of post-transcriptional targets. Compare miRNA from matrix vesicles to miRNA from vascular smooth muscle cells that gave rise to the matrix vesicles from 3 sets of MV and VSMC derived from 3 normal and 3 CKD rats

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Transcriptome analysis of human coronary artery smooth muscle cells under pro-differentiation and pro-dedifferentiation treatments

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