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

Project description: Not available

| 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

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

To examine vascular smooth muscle cells (VSMC) under four conditions

Project description:Vascular calcification is a hallmark of atherosclerosis and end-stage renal disease (ESRD). However, the molecular mechanism of vascular calcification is poorly understood. Diabetes mellitus is increasingly recognized as the most important cause for atherosclerosis and ESRD. Emerging evidence supports the concept that vascular calcification resembles the process of osteogenesis, in which the vascular smooth muscle cells (VSMC) undergo osteochondrogenic differentiation. Recently, we have established an in vitro calcification system with primary mouse VSMC. With the use of osteogenic stimuli, we induced trans-differentiation of primary mouse VSMC into bone-like cells. Interestingly stroptozotocin (STZ), O-GlcNAcase inhibitor and a drug that has been used to induce diabetes in mice, was able to induce calcification of VSMC and the expression of the osteogenic transcription factor Runx2, suggesting glycosylation may be involved in regulation of Runx2. We have reported an essential role of Runx2 in oxidative stress-induce VSMC calcification and have recently generated a tissue specific mouse with Runx2 ablation in smooth muscle cells. Therefore, we will use STZ and other relevant reagents in the glucose synthesis/metabolism pathways as stimuli for VSMC calcification to characterize the glycogene profiles during VSMC calcification. Results from VSMC of Runx2 knockout mice will be compared with those from control mice to determine the regulation of calcification-associated glycogenes by Runx2 in response to STZ. These studies will provide foundation for further mechanistic studies and may lead to identification of novel strategies and targets for diabetes-induced vascular calcification. To examine vascular smooth muscle cells (VSMC) under two conditions: 1) wild-type VSMC differentiated into bone-like cells with osteogenic media, 2) wild-type VSMC treated with STZ and osteogenic media

2011-09-05 | E-GEOD-31928 | biostudies-arrayexpress

Cavenderia fasciculata strain:SH3

Project description:Cavenderia fasciculata strain:SH3 Genome sequencing and assembly

| PRJNA40189 | ENA

MIA gene family-related signaling in oral squamous cell carcinoma cells

Project description:Melanoma inhibitory activity (MIA) gene family is novel tumor-associated molecules. Although MIA gene family has several tumor progressive and/or suppressive functions, the detailed relevant signaling partners are unclear and investigated. In this study, we investigated the detailed MIA gene family-associated signaling using human oral squamous cell carcinoma cells.

2016-07-01 | GSE80347 | GEO

BACH1 Deficiency Prevents Neointima Formation and Maintains the Differentiated Phenotype of Vascular Smooth Muscle Cell by Regulating Chromatin Accessibility

Project description:Chromatin accessibility is important for cell fate determination in differentiation and multiple pathophysiological processes. Here, we report a transcription factor BACH1, facilitates the recruitment of G9a and YAP, maintains the state of H3K9me2 and decreases the chromatin accessibility at the promoter of VSMC marker genes, thereby repressing their expression and contributing to dedifferentiated VSMC phenotype. Moreover, VSMC-specific loss of BACH1 in mice inhibited the transformation of VSMC from contractile to synthetic phenotype and VSMC proliferation and attenuated the neointimal hyperplasia in wire-injured femoral arteries.

2023-05-31 | GSE184391 | GEO

PARP1 regulates VSMC phenotypic switch and neointima via Myocardin

Project description:We applied the transcriptome profiling (RNA-seq) for high-throughput profiling of genes changes in VSMC dedifferentiation. Rat primary VSMCs were divided into 3 groups, control, PDGF-BB, PDGF-BB+PJ34,and mRNA sequence were performed. We found that PDGF-BB could upregualted the genes involved in cell proliferation and migration, and downregulated the VSMC contractile genes, all of which could be reversed by PARP inhibitor PJ34. Then we knockdowned the co-factor Myocardin in VSMCs, and found the above effects of PJ34 were nearly abolished.Our study first provided the transcription changes by RNA-seq in VSMC dedifferentiation, and demonstrated the key roles of PARP1 and the PARylation process in VSMC phenotypic switch.

2018-09-20 | GSE103995 | GEO

MIA-PaCa2 cells transfected with silencer RNA against HuR and YAP1

Project description:Purpose: To determine biological impact between silencing HuR and YAP1, in MIA-PaCa2. Methods: Expression profiling of MIA-PaCa2 cells knocked-down for HuR and YAP1 and control cells transfected with scramble siRNA.

2022-06-07 | GSE167525 | GEO

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