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Transcriptional changes upon overexpression of seven candidate miRNAs in human saphenous vein smooth muscle cells. [HSVSMC]

ABSTRACT: Transcriptional changes upon overexpression of seven candidate miRNAs in human saphenous vein smooth muscle cells. [HSVSMC]

PROVIDER: PRJNA1063639 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27504400_1.fastq.gz	Fastqsanger.gz
	SRR27504400_2.fastq.gz	Fastqsanger.gz
	SRR27504401_1.fastq.gz	Fastqsanger.gz
	SRR27504401_2.fastq.gz	Fastqsanger.gz
	SRR27504402_1.fastq.gz	Fastqsanger.gz

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Transcriptional changes upon overexpression of seven candidate miRNAs in human saphenous vein endothelial cells. [HSVEC]

Project description:Proliferation of vascular smooth muscle cells (vSMCs) following injury is a crucial factor contributing to pathological vascular remodelling. MicroRNAs (miRNAs) are powerful gene regulators and attractive therapeutics agents. Here, we aim to systemically identify and characterise miRNAs with therapeutic potential in targeting aberrant vSMC proliferation. We performed a high-throughput in vitro screen using a library of 2042 human miRNA-mimics for their impact on VSMC proliferation and identified seven novel antiproliferative miRNAs i.e miR-1827, miR-4774-3p, miR-5681b, miR-449b-5p, miR-491-3p, miR-323a-3p, and miR-892b.Overexpression of these 7 miRNAs affects proliferation of vSMCs from different vascular beds. Focusing on vein graft failure, a condition in which miRNA based therapeutics can be applied to the graft ex-vivo, we showed that these miRNAs reduced human saphenous vein SMC (HSVSMC) proliferation without inducing apoptosis or senescence, and five of them also significantly decreased migration.In contrast to HSVSMC, miRNA overexpression on saphenous vein endothelial cells (ECs) led to no or lower decrease of proliferation for the seven miRNAs. We performed RNA-seq on HSVEC overexpressing the seven miRNAs and showed a limited response of ECs to the miRNA overexpression.

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Transcriptional changes upon overexpression of seven candidate miRNAs in human saphenous vein smooth muscle cells. [HSVSMC]

Project description:Proliferation of vascular smooth muscle cells (vSMCs) following injury is a crucial factor contributing to pathological vascular remodelling. MicroRNAs (miRNAs) are powerful gene regulators and attractive therapeutics agents. Here, we aim to systemically identify and characterise miRNAs with therapeutic potential in targeting aberrant vSMC proliferation. We performed a high-throughput in vitro screen using a library of 2042 human miRNA-mimics for their impact on VSMC proliferation and identified seven novel antiproliferative miRNAs i.e miR-1827, miR-4774-3p, miR-5681b, miR-449b-5p, miR-491-3p, miR-323a-3p, and miR-892b.Overexpression of these 7 miRNAs affects proliferation of vSMCs from different vascular beds. Focusing on vein graft failure, a condition in which miRNA based therapeutics can be applied to the graft ex-vivo, we showed that these miRNAs reduced human saphenous vein SMC (HSVSMC) proliferation without inducing apoptosis or senescence, and five of them also significantly decreased migration.We performed RNA sequencing on HSVSMC overexpressing each of these 7 miRNAs. This analysis showed that each miRNA overexpression affects a core cell cycle gene network. However, this effect is mediated by distinct miRNA targets.

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Transcriptional changes upon overexpression of candidate miRNAs in human saphenous vein endothelial cells and human saphenous vein smooth muscle cells.

Project description:Transcriptional changes upon overexpression of candidate miRNAs in human saphenous vein endothelial cells and human saphenous vein smooth muscle cells.

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Transcriptional changes upon overexpression of seven candidate miRNAs in human saphenous vein endothelial cells. [HSVEC]

Project description:Transcriptional changes upon overexpression of seven candidate miRNAs in human saphenous vein endothelial cells. [HSVEC]

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Project description:Vein graft failure is driven by early neointima l proliferation involving vascular smooth muscle cell (VSMC) proliferation, inflammation, and extracellular matrix remodeling. To elucidate the spatial and transcriptional landscape of this process, we performed spatial transcriptomic profiling of ex vivo cultured human saphenous vein segments at baseline (Day 0) and after 7 days in organ culture. Integration of spatial gene expression with histological features revealed distinct zones of VSMC transdifferentiation, inflammatory activation, and extracellular matrix reorganization. This dataset provides a resource for investigating molecular mechanisms underlying early human vein graft adaptation and neointimal proliferation.

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Project description:Vein graft failure is a major limitation of coronary and peripheral bypass surgery, driven by neointima proliferation and smooth muscle cell (SMC) phenotypic modulation. To investigate the early molecular events underlying this process, we cultured segments of human saphenous veins ex vivo for seven days. Bulk RNA sequencing and 10x Visium spatial transcriptomics were performed on paired fresh (Day 0) and cultured (Day 7) samples. Differential gene expression analysis revealed significant downregulation of contractile SMC markers and cytoskeletal genes, and upregulation of extracellular matrix (ECM), inflammatory, and stress-response pathways. Integration of both datasets highlighted coordinated suppression of SMC contractile phenotype and activation of matrix remodeling programs, consistent with early neointima development. These results provide a multi-omics resource defining molecular transitions that drive human vein graft remodeling.

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