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Enhancer-associated LncRNA-ITGA2 promotes vascular smooth muscle remodeling by mediating ITGA2 promoter-enhancer interactions [RNA-seq]

ABSTRACT: To characterize the effects of PDGF-BB on long non-coding RNA (lncRNA) expression in vascular smooth muscle cells (VSMCs). Primary human VSMCs were cultured and treated with PDGF (20 ng/mL) or vehicle control (Veh) for 24 hours. Then we conducted lncRNA-seq and observed an increased in LncRNA-ITGA2 transcript reads following PDGF-BB treatment. This result is consistent with our microarray findings.

ORGANISM(S): Homo sapiens

PROVIDER: GSE290463 | GEO | 2025/12/31

REPOSITORIES: GEO

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Enhancer-associated LncRNA-ITGA2 promotes vascular smooth muscle remodeling by mediating ITGA2 promoter-enhancer interactions

Project description:In this study, multiomics profiling, including CUT&Tag, promoter capture Hi-C (PCHi-C), and microarray, identified LncRNA-ITGA2 as a novel elncRNA that was highly expressed in PDGF-induced proliferative human VSMCs. Notably, LncRNA-ITGA2 was significantly increased in both plasma and coronary atherosclerotic tissues of patients with coronary artery disease (CAD) compared with control subjects. Loss- and gain-of-function studies revealed that LncRNA-ITGA2 potently increased PDGF-induced VSMC proliferation and migration. Moreover, LncRNA-ITGA2 overexpression enhanced neointimal hyperplasia in vivo in a mouse carotid artery injury model, exhibiting its partial functional conservation. RNA-sequencing and CRISPR-Cas9 gene-editing technology revealed integrin α2 (ITGA2) as a downstream target of LncRNA-ITGA2 in VSMCs. Mechanistically, promoter-enhancer interactions were detected by PCHi-C at the ITGA2 locus after PDGF-BB treatment. Chromatin immunoprecipitation sequencing (ChIP-Seq) and chromatin isolation by RNA purification (ChIRP)-qPCR showed that LncRNA-ITGA2 directly bound to the Enhancer-ITGA2 and increased H3K27 acetylation in both the Enhancer-ITGA2 and Promoter-ITGA2. In addition, we demonstrated, by ChIRP-MS and RNA immunoprecipitation, that LncRNA-ITGA2 interacted with the DNA binding-protein NONO (non-pou domain containing octamer-binding protein), which also bound to the ITGA2 promoter, as verified by the ChIP-qPCR assay. Ultimately, the knockout cell lines of NONO, LncRNA-ITGA2, and its promoter confirmed the above regulatory mechanism.

2024-12-31 | GSE248192 | GEO

Enhancer-associated LncRNA-ITGA2 promotes vascular smooth muscle remodeling by mediating ITGA2 promoter-enhancer interactions [CUT&TAG]

Project description:The proliferation and migration of VSMCs significantly contribute to vascular remodeling. Recent studies have suggested that enhancer-associated long noncoding RNAs (elncRNAs) play crucial roles in regulating gene expression and cell fate. However, the specific elncRNAs implicated in VSMC dysfunction and their regulatory mechanisms remain poorly understood. This study used multiomics profiling, including CUT&Tag, promoter capture Hi-C (PCHi-C), and microarray analysis, to identify LncRNA-ITGA2 as a novel elncRNA highly expressed in PDGF-induced proliferative human VSMCs. We used CUT&Tag technology to identify enhancer regions labeled by H3K4me1, and overlap lncRNA gene loci in LNCipedia database to identify enhancer-associated long noncoding RNAs (elncRNAs). By integrating the CUT&Tag data of H3K4me1 and H3K27ac, the dynamic regulatory network of enhancers was systematically analyzed, providing a key epigenetic basis for subsequent functional studies and target discovery.

2025-12-31 | GSE290462 | GEO

Enhancer-associated LncRNA-ITGA2 promotes vascular smooth muscle remodeling by mediating ITGA2 promoter-enhancer interactions

Project description:We investigated the function of Lnc-RNA-ITGA2, which comprises a single exon and is located on chromosome 5 within the first intronic region of the ITGA2 gene, as critical regulator of VSMC phenotypes in vitro.

2025-12-31 | GSE290748 | GEO

Enhancer-associated LncRNA-ITGA2 promotes vascular smooth muscle remodeling by mediating ITGA2 promoter-enhancer interactions

Project description:Enhancer-associated LncRNA-ITGA2 promotes vascular smooth muscle remodeling by mediating ITGA2 promoter-enhancer interactions

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Disfunction of arachidonic acid metabolism in vascular smooth muscle cells contributes to restenosis

Project description:We applied the transcriptome profiling (RNA-seq) for high-throughput profiling of genes changes in the phenotypic switch of VSMCs. Rat primary VSMCs were divided into 3 groups, control, PDGF-BB, PDGF-BB+PTUPB,and mRNA sequence were performed. We found that Cell cycle related genes and cellular senescence related genes were significantly upregulated by PDGF-BB and significantly reversed by PTUPB. Subsequently, we deleted PTTG1 as a key gene for PTUPB to reverse phenotypic switching in VSMCs. Our study provided the transcription changes by RNA-seq in VSMC phenotypic switch, and found that PTUPB played a crucial role in correcting the dysregulation of sEH/COX-2 derived ARA metabolism in VSMC phenotypic switch

2023-09-01 | GSE241545 | GEO

Microarray expression profile and bioinformatics analysis of circular RNAs in the phenotypic switching of rat vascular smooth muscle cells: a preliminary study

Project description:In order to further study the role of circular RNA in the phenotypic transformation of vascular smooth muscle cells (VSMCs), the differential expression profile of circRNA in the phenotypic transition of VSMCs induced by platelet-derived growth factor-BB (PDGF-BB) was screened using chip technology. Vascular smooth muscle cells from rat thoracic aorta were induced with 20ng/ml PDGF-BB as the experimental group and compared with the control group. After induction for 24 hours, the differentially expressed circRNA was screened by circular RNA chip.

2021-12-17 | GSE190952 | GEO

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Project description:Objective: Vascular smooth muscle cell (VSMC) phenotypic switching is critical for normal vessel formation, vascular stability, and healthy brain aging. Phenotypic switching is regulated by mediators including platelet derived growth factor (PDGF)-BB, insulin-like growth factor (IGF-1), as well as transforming growth factor-β (TGF-β) and endothelin-1 (ET-1), but much about the role of these factors in microvascular VSMCs remains unclear. Methods: We used primary rat microvascular VSMCs to explore PDGF-BB- and IGF-1-induced phenotypic switching. Results: PDGF-BB induced an early proliferative response, followed by formation of polarized leader cells and rapid, directionally coordinated migration. In contrast, IGF-1 induced cell hypertrophy, and only a small degree of migration by unpolarized cells. TGF-β and ET-1 selectively inhibit PDGF-BB-induced VSMC migration primarily by repressing migratory polarization and formation of leader cells. Contractile genes were downregulated by both growth factors, while other genes were differentially regulated by PDGF-BB and IGF-1. Conclusions: These studies indicate that PDGF-BB and IGF-1 stimulate different types of microvascular VSMC phenotypic switching characterized by different modes of cell migration. Our studies are consistent with a chronic vasoprotective role for IGF-1 in VSMCs in the microvasculature while PDGF is more involved in VSMC proliferation and migration in response to acute activities such as neovascularization. Better understanding of the nuances of the phenotypic switching induced by these growth factors is important for our understanding of a variety of microvascular diseases.

2025-12-09 | GSE312686 | GEO

Microassay analysis of the lncRNAs expression profile in human aortic vascular smooth muscle cells(hAoSMCs) treated with PDGF-BB at 24 h.

Project description:Atherosclerosis is the most important mechanism of cardiovascular and cerebrovascular diseases and has become one of the most serious diseases that threaten human health. Vascular smooth muscle cells (VSMCs) are the main cellular components that constitute the structure of the blood vessel wall. The excessive proliferation and migration are pivotal pathological basis of atherosclerosis, in-stent restenosis, pulmonary hypertension and other vascular proliferative diseases. PDGF-BB is a potent proliferative agent for VSMCs, but the specific mechanism of PDGF-BB signaling pathway involved in biological processes such as proliferation and migration of VSMCs is not elusive.

2023-10-22 | GSE186313 | GEO

Deletion of Smooth Muscle ZFP36 Promotes Neointimal Hyperplasia in Mice

Project description:Platelet-derived growth factor (PDGF-BB) released from the injured intima induces the proliferation and migration of vascular smooth muscle cells (VSMCs), which is the key mechanism of neointimal hyperplasia. Zinc finger 36 (ZFP36), a widespread RNA-binding protein, is important for pathological processes in many diseases. In this study we investigated the role of ZFP36 in VSMCs proliferation, migration and neointimal hyperplasia in mice. We generated smooth muscle-specific Zfp36 knockout (Zfp36SMKO) mice, and established restenosis mouse models by ligation of left carotid artery in Zfp36SMKO mice. We showed that the expression levels of ZFP36 were significantly decreased in human atherosclerotic coronary arteries and murine injured carotid arteries compared with controls. Compared to control Zfp36fl/fl mice, Zfp36SMKO mice displayed accelerated neointimal hyperplasia. In cultured mouse VSMCs, PDGF-BB (20 ng/mL) significantly downregulated ZFP36 expression through KLF4 binding site in Zfp36 promoter. We revealed that ZFP36 could bind to the mRNA of cell migration-inducing protein (CEMIP) and promoted its degradation in VSMCs, thereby reducing the expression of CEMIP protein. Knockdown of Cemip inhibited VSMCs proliferation and migration induced by Zfp36 knockout, thereby suppressing neointimal hyperplasia in Zfp36SMKO mice. We conclude that vascular smooth muscle ZFP36 has a protective effect against neointimal hyperplasia by reducing CEMIP expression. ZFP36 is downregulated by vascular injury and PDGF-BB treatment, which promotes VSMCs proliferation and migration and neointima formation. The results suggest that targeting ZFP36 may represent a novel therapeutic strategy for preventing or treating neointimal hyperplasia and related cardiovascular diseases.

2025-05-29 | GSE286906 | GEO

Rat vascular smooth muscle cells LC-MS/MS

Project description:Crotonylation of histones is discovered of late as one of post-translational modification that can regulate gene expression. However, the function of crotonylation on non-histone proteins in vascular smooth muscle cells (VSMC) is unclear. Here, we aim to use modification and proteomic analysis to find the cellular characteristic of crotonylated non-histone proteins and the crosstalk with ubiquitinated proteins in vascular smooth muscle cell (VSMC) phenotypic remodeling. We performed modification and proteomic analysis of VSMCs before and after stimulated with platelet-derived growth factor-BB (PDGF-BB). The crotonylated and ubiquitinated pan-antibody was used to enrich the protein and then subjected to high-throughput mass spectrometry analysis. The enrichment analysis was performed within differentially modified proteins in regards to GO terms, KEGG and protein domain.

2022-05-19 | PXD029070 | Pride

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