RNA-Seq analysis HDAC9 knockdown effect on vascular smooth muscle cells
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ABSTRACT:
PROVIDER: PRJNA950380 | ENA |
REPOSITORIES: ENA
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Project description:Vascular smooth muscle cells (VSMCs) phenotype switch has been thought to be critical to the development of thoracic aneurysm/dissection. To investigate the function HDAC9 in the regulation of VSMCs phenotype switch, we used siRNA knockdown of HDAC9 in human aortic smooth muscle cells (HASMC)we established Human aortic smooth muscle cells (HASMCs).
2024-12-31 | GSE228573 | GEO
Project description:Patients with heterozygous missense mutations in the ACTA2 or MYH11 genes are known to exhibit thoracic aortic aneurysm (TAA) and a risk of early onset aortic dissection. However, less common phenotypes involving arterial obstruction are also observed, including coronary and cerebrovascular stenotic disease. Recently an epigenetic complex containing the histone deacetylase HDAC9 and the long noncoding RNA, MALAT1 was implicated in pathologic vascular smooth muscle cell phenotypic changes in aneurysmal disease, however its involvement in stenotic disease has not been explored. Herein we implicate the HDAC9-MALAT1 complex in transcriptional silencing of contractile associated gene products, known to undergo downregulation in stenotic lesions. Furthermore, neointimal formation was inhibited in Hdac9 or Malat1 deficient mice with preservation of contractile protein expression. Pharmacologic targeting of the complex through either MALAT1 antisense oligonucleotides or inhibition of the methyltransferase EZH2 reduced neointimal formation. In conclusion, we report the implication of the HDAC9-MALAT1 complex in stenotic disease and demonstrate that pharmacologic therapy based on epigenetic targets can ameliorate arterial obstruction in an experimental system.
2021-09-01 | GSE120394 | GEO
Project description:HDAC9 Complex Inhibition Improves Smooth Muscle Dependent Arterial Stenosis
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Project description:Vascular smooth muscle cells (VSMCs) phenotype switch has been thought to be critical to the development of thoracic aneurysm/dissection. To investigate the function EZH2 in the regulation of VSMCs phenotype switch, we established mouse vascular smooth muscle cells in which each target gene has been knocked down by siRNA.
2023-12-16 | GSE227177 | GEO
Project description:Vascular smooth muscle cells (VSMCs) phenotype switch has been thought to be critical to the development of thoracic aneurysm/dissection. To investigate the function SIRT6 in the regulation of VSMCs phenotype switch, we established mouse vascular smooth muscle cells in which each target gene has been knocked down by siRNA.
2024-12-11 | GSE246209 | GEO
Project description:RNA-Seq analysis Ezh2 knockdown effect on vascular smooth muscle cells
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Project description:RNA-Seq analysis SIRT6 knockdown effect on vascular smooth muscle cells
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Project description:The full length of LncVSM transfected into Vascular Smooth Muscle cells to down-regulation for screening differential expression prolifes of LncVSM effecting.The empty vector transfected Vascular Smooth Muscle cells as controls. Eight Samples analyzed.
2016-01-12 | E-GEOD-76720 | biostudies-arrayexpress
Project description:YAP/TAZ in vascular smooth muscle
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Project description:Rho-associated kinase (ROCK) and zipper-interacting protein kinase (ZIPK) have been implicated in diverse physiological functions, including smooth muscle contraction, cell proliferation, cell adhesion, apoptosis, cell migration and inflammation. Many aspects of regulation via ROCK and ZIPK, however, remain unclear. In this study, we utilized an siRNA approach to knock down ROCK1 and ZIPK in cultured human arterial smooth muscle cells. Microarray analysis was performed, using a whole-transcript expression chip, to identify changes in gene expression profiles induced by ROCK1 and ZIPK knockdown. ROCK1 knockdown affected the expression of 553 genes (355 down-regulated and 198 up-regulated), while ZIPK knockdown affected the expression of 390 genes (219 down-regulated and 171 up-regulated). A high incidence of up- and down-regulation of transcription regulator genes was observed in both ROCK1 and ZIPK knockdowns. Other markedly affected groups included transporters, kinases, peptidases, transmembrane and G protein-coupled receptors, growth factors, phosphatases and ion channels. Three microRNAs (mir-145, mir-199 and mir-622) were up-regulated by ROCK1 knockdown, whereas ZIPK knockdown had no effect on microRNA expression. 76 differentially expressed genes were common to ROCK1 and ZIPK knockdown, of which 41 were down-regulated and 26 up-regulated by both treatments, while the other 9 genes were differentially up/down-regulated. Ingenuity Pathway Analysis identified five pathways shared between the two knockdowns, which are mainly involved in cell cycle regulation. Marked differences in the effects of ROCK1 and ZIPK knockdown on the genes involved in cell cycle regulation suggested that ROCK1 and ZIPK regulate the cell cycle by different mechanisms. ROCK1, but not ZIPK knockdown significantly reduced the viability of vascular SMC. ROCK1 knockdown also affected several cytokine signaling pathways with up-regulation of 5 and down-regulation of 4 cytokine genes, in contrast to ZIPK knockdown, which affected the expression of only two cytokine genes (both down-regulated). IL-6 gene expression and secretion of IL-6 protein were up-regulated by ROCK1 knockdown, whereas ZIPK knockdown reduced IL-6 mRNA expression and IL-6 protein secretion and ROCK1 protein expression, suggesting that ROCK1 may inhibit IL-6 secretion. IL-1β mRNA and protein levels were increased in response to ROCK1 knockdown. Finally, ROCK1 but not ZIPK knockdown inhibited proliferation of vascular smooth muscle cells. We conclude that ROCK1 and ZIPK have diverse, but predominantly distinct regulatory functions in vascular smooth muscle cells. Human coronary artery smooth muscle cells were transfected with siRNA targeting ROCK1 or ZIPK or with negative control siRNA that does not target any gene product. 48 h later, total RNA was isolated, reverse transcribed, amplified, labeled with the Ambion WT Express kit and hybridized to Human Gene 1.0 ST arrays (Affymetrix) at 45 oC for 16 h. The probe arrays were washed and stained on an Affymetrix GeneChip Fluidics-450 and scanned on an Affymetrix GeneChip Scanner 3000 7G System. Triplicates were prepared under all three conditions for microarray analysis.
2015-05-15 | E-GEOD-56819 | biostudies-arrayexpress