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MIA SH3 Domain ER Export Factor 3 deficiency prevents neointimal formation by restoring BAT-like PVAT and decreasing VSMC proliferation and migration

ABSTRACT: MIA SH3 Domain ER Export Factor 3 deficiency prevents neointimal formation by restoring BAT-like PVAT and decreasing VSMC proliferation and migration

PROVIDER: PRJNA776870 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16678364.fastq.gz	Fastqsanger.gz
	SRR16678365.fastq.gz	Fastqsanger.gz
	SRR16678366.fastq.gz	Fastqsanger.gz
	SRR16678367.fastq.gz	Fastqsanger.gz

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Similar Datasets

MIA SH3 Domain ER Export Factor 3 Deficiency Prevents Neointimal Formation by Restoring BAT-Like PVAT and Decreasing VSMC Proliferation and Migration.

Project description:Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) and excessive accumulation of dysfunctional PVAT are hallmarks of pathogenesis after angioplasty. Recent genome-wide association studies reveal that single-nucleotide polymorphism (SNP) in MIA3 is associated with atherosclerosis-relevant VSMC phenotypes. However, the role of MIA3 in the vascular remodeling response to injury remains unknown. Here, we found that expression of MIA3 is increased in proliferative VSMCs and knockdown of MIA3 reduces VSMCs proliferation, migration, and inflammation, whereas MIA3 overexpression promoted VSMC migration and proliferation. Moreover, knockdown of MIA3 ameliorates femoral artery wire injury-induced neointimal hyperplasia and increases brown-like perivascular adipocytes. Collectively, the data suggest that MIA3 deficiency prevents neointimal formation by decreasing VSMC proliferation, migration, and inflammation and maintaining BAT-like perivascular adipocytes in PVAT during injury-induced vascular remodeling, which provide a potential therapeutic target for preventing neointimal hyperplasia in proliferative vascular diseases.

| S-EPMC8631732 | biostudies-literature

MIA SH3 Domain ER Export Factor 3 deficiency prevents neointimal formation by restoring BAT-like PVAT and decreasing VSMC proliferation and migration

Project description:RNA-sequencing data of HASMC transfected with MIA3 siRNA or scramble siRNA.

2021-11-03 | GSE186951 | GEO

Genome-wide gene expression analysis on tibialis anterior muscle from nebulin SH3 domain deleted (Neb∆SH3) mice

Project description:Genome-wide gene expression analysis on tibialis anterior muscle from 2-month-old nebulin SH3 domain deleted (Neb∆SH3) mice compared to wildtype.

2013-09-23 | GSE47801 | GEO

Novel Roles of Nrf3-Trim5 Axis in Vascular Smooth Muscle Cell Dysfunctions and Neointimal Hyperplasia

Project description:Neointimal hyperplasia (NIH), driven by vascular smooth muscle cell (VSMC) dysfunction, is a key factor in vascular diseases like atherosclerosis and restenosis. While Nrf3 is known to regulate VSMC differentiation, its role in NIH remains unclear. Using transcriptomic data, Nrf3 knockout mice (global), we assessed Nrf3’s impact on VSMC function and NIH. We identified Trim5, a gene linked to coronary artery disease, as a downstream target of Nrf3, which promotes autophagy in VSMCs and injured arteries, enhancing VSMC dysfunction and NIH. Nrf3 overexpression increased VSMC proliferation, migration, and inflammation, while deletion or knockdown had the opposite effects. Nrf3-/- and Nrf3ΔSMC mice showed reduced VSMC accumulation and attenuated NIH after vascular injury. These findings highlight Nrf3 as a novel modulator of VSMC dysfunction and injury-induced NIH, with potential for therapeutic targeting of the Nrf3-Trim5 axis to treat NIH-related vascular diseases.

2024-12-02 | GSE281869 | GEO

Inhibition of PARP 1 Protects Against Hyperglycemic-induced Neointimal Hyperplasia by Upregulating TFPI-2 Activity

Project description:To investigate the function and potential mechanism of PARP-1 poly(ADP-ribose) polymerase 1 (PARP1) in diabetic neointimal hyperplasia. Type 1 diabetes mellitus was induced using streptozotocin (STZ) in wild-type mice and PARP1-/- mice, and ligation of the left carotid artery was performed to induce neointimal hyperplasia. Ligated carotid arteries from diabetic mice developed more extensive neointimal hyperplasia and showed greater proliferation and migration than arteries from nondiabetic mice. The augmented remodeling response was absent in diabetic mice deficient in PARP1. PARP1 deficiency reduces diabetic neointimal hyperplasia by upregulating tissue factor pathway inhibitor (TFPI)-2, which acted as a suppressor of vascular smooth muscle cell (VSMCs) proliferation and migration. The underlying mechanisms involve PARP1 that acts as a negative transcription factor by enhancing TFPI-2 promoter DNA methylation. Our studies demonstrated for the first time that Inhibition of PARP1 alleviates neointimal hyperplasia in diabetes by up-regulating TFPI-2 expression and blocking VSMC proliferation and migration. The development of PARP1 inhibitors might serve to limit mainly proliferative and migratory processes in restenosis-prone diabetic patients

2019-11-30 | GSE141193 | GEO

Genome-wide gene expression analysis on tibialis anterior muscle from nebulin SH3 domain deleted (Neb∆SH3) mice

Project description:Genome-wide gene expression analysis on tibialis anterior muscle from 2-month-old nebulin SH3 domain deleted (Neb∆SH3) mice compared to wildtype. Total RNA was obtained from biological triplicates of tibialis anterior muscle from 2-month-old nebulin SH3 domain deleted (Neb∆SH3) mice compared to wildtype.

2013-09-23 | E-GEOD-47801 | biostudies-arrayexpress

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Defining the lineage of thermogenic perivascular adipose tissue [Thoracic PVAT]

Project description:Brown adipose tissue can expend large amounts of energy and thus increasing its amount or activity is a promising therapeutic approach to combat metabolic disease. In humans, major deposits of brown fat cells are found intimately associated with large blood vessels, corresponding to perivascular adipose tissue (PVAT). However, the cellular origins of PVAT are poorly understood. We applied single cell transcriptomic analyses, ex vivo adipogenesis assays, and genetic fate mapping to determine the identity of perivascular adipocyte progenitors. In mice, we found that thoracic PVAT develops from a fibroblastic lineage, consisting of progenitor cells (Pdgfra+; Ly6a+; Pparg-) and preadipocytes (Pdgfra+; Ly6a+; Pparg+). Progenitor and preadipocyte cells in PVAT shared transcriptional similarity with analogous cell types in white adipose tissue, pointing towards a conserved hierarchical structure of adipose lineage cells. Interestingly, the aortic adventitia of adult animals contained a novel population of adipogenic smooth muscle cells (SMCs) (Myh11+; Pdgfra-; Pparg+) that contributed to perivascular adipocyte formation. Similarly, human PVAT contained presumptive fibroblastic and SMC-like adipocyte progenitors, as revealed by single nucleus RNAseq. Taken together, these studies define distinct populations of progenitor cells for thermogenic PVAT, providing a foundation for developing strategies to augment brown fat activity.

2021-04-01 | GSE166355 | GEO

Differences in PVAT mRNA profiles of recipient mice transplanted with splenocytes

Project description:Recent investigations raise the possibility that senescent immune cells may fuel vascular damage by perivascular adipose tissue (PVAT) dysfunction, as immune cell infiltration in PVAT increases substantially in the development of vascular disease compared to the healthy state and leads to changes in PVAT-derived effector cytokine levels that comprise vascular biology.Though evidence revealed possible cross-talk among immune cells, PVAT and vasculature, it is less clear if senescent immune cells or a particular cell subset may induce PVAT dysfunction and further impair vascular biology during type 2 diabtes (T2DM). NLRP3 inflammasome plays a critical role in inflammatory response as a major component of innate immunity, it provides a molecular platform that responds to a variety of stimuli, initiating sterile inﬂammation cascade.Furthermore, there is evidence that NLRP3 inflammasome can be activated by sensing danger-associated molecular patterns (DAMPs), which in turn promotes age-related thymic demise and T cell senescence, implicating its potential role in immunosenescence. Here, we employed WT and Nlrp3 KO mice to develop T2DM, and implanted the splenocytes isolated from WT, Nlrp3 KO, WT-T2DM, Nlrp3 KO-T2DM mice that were modeled for 4 months to 3-month-old WT mice. Then, we explored the differentially expressed genes of PVAT in recipient mice implanted with splenocytes and evaluate immune infiltration of PVAT.

2023-08-31 | GSE242021 | GEO

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