RNAseq analysis of primary differentiated rat aorta tissue compared to proliferative cultured cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE127794 | GEO | 2019/06/18
REPOSITORIES: GEO
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Project description:Smooth muscle cells (SMCs) are important in a number of physiological systems and organs, including the cardiovascular system. The hallmark property of differentiated SMCs is the ability to contract, but contractile SMCs themselves show a range of phenotypes allowing prolonged tonic contraction in vascular smooth muscle or rapid phasic contraction in tissues such as bladder. Another distinctive characteristic, in contrast with terminally differentiated striated muscle cells, is that SMCs exhibit phenotypic plasticity. Vascular SMCs are able to modulate their phenotype along a continuum between a contractile phenotype, characteristic of healthy blood vessels, and a more proliferative âsyntheticâ phenotype, so-named for the enhanced synthesis and secretion of extracellular matrix components. Synthetic phenotype cells are found in a number of pathological situations such as atherosclerosis and arterial injury. We used mouse exon-junction (MJAY) arrays to gain insights into both the global contribution of alternative splicing events in re-shaping the transcriptome of dedifferentiating mouse aorta and bladder SMCs, and into the underlying regulatory mechanisms of the alternative splicing program. Affymetrix splice junction arrays (MJAY) were used to profile changes in both alternative splicing and transcript levels during the phenotypic modulation of smooth muscle cells when placed in culture. RNA extracted from intact aorta and bladder smooth muscle tissue was used for differentiated samples. For dedifferentiated, proliferative samples smooth muscle cells were enzymatically dispersed and grown in tissue culture for a week. Triplicate RNA samples were prepared from smooth muscle tissue of mouse aorta and bladder (differentiated) and from smooth muscle cells from each tissue cultured for 7 days (proliferative). The samples allowed comparison of alternative splicing (and other transcriptome) changes between differentiated and proliferative smooth muscle cell samples from two distinct types of smooth muscle cell, as well as allowing direct comparison of aorta (tonic smooth muscle) and bladder (phasic smooth muscle).
2016-07-01 | E-MTAB-4841 | biostudies-arrayexpress
Project description:RNAseq analysis of primary differentiated rat aorta tissue compared to proliferative cultured cells
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Project description:This SuperSeries is composed of the following subset Series:; GSE13835: Smooth muscle cells in atherosclerosis-prone and resistant regions of the aorta of C57Bl/6 mice at age of 4 months; GSE13836: Smooth muscle cells in atherosclerosis-prone and resistant regions of the aorta of apoE-/- mice at age of 4 months Experiment Overall Design: Refer to individual Series
2009-05-27 | E-GEOD-13865 | biostudies-arrayexpress
Project description:We compared the global gene expression profiles of C57BL/6 mice aortas with the profiles of cultured vascular smooth muscle cells (vSMC) from the same mice, and determined whether gene responses to dioxin exposure in the vSMCs would be predictive of responses in the aorta.
2003-10-29 | E-MEXP-23 | biostudies-arrayexpress
Project description:We used microarrays to characterize the global changes in gene expression within the ascending aorta of mice due to conditional disruption of TGF-β signaling in smooth muscle and/or due to heterozygous fibrillin-1 mutation.
2013-05-31 | GSE36778 | GEO
Project description:Pharmacological activation of the transcription factor PPAR gamma lowers blood pressure and improves glucose tolerance in humans. In contrast, naturally occurring mutations (e.g., P467L, V290M) in the ligand binding domain of PPAR gamma in humans leads to severe insulin resistance and early-onset hypertension. Experimental evidence, including whole genome expression profiling, suggests that these mutant versions of PPAR gamma act in a dominant negative manner. Because PPAR gamma is expressed in a variety of cell types and tissues, we generated a transgenic mouse model (SP467L) specifically targeting dominant negative PPAR gamma to the vascular smooth muscle cells in order to determine the action of PPAR gamma in the blood vessel independent of its systemic metabolic actions. In the data set provided herein, we examined the gene expression profile in thoracic aorta from SP467L mice and their control littermates using the Affymetrix mouse exon 1.0 ST array. We generated transgenic mice specifically targeting expression of mutant dominant negative human PPAR gamma (P467L) to vascular smooth muscle using a smooth muscle-specific promoter (smooth muscle myosin heavy chain or SMMHC). Thoracic aortas were isolated from 7 male transgenic mice and 5 non-transgenic littermate controls. Total RNA was prepared using conventional methods and quality was assessed using the Bioanalyzer 2100 (Agilent Technologies). For the microarray hybridizations, each sample corresponded to aorta derived from one mouse. All procedures were conducted at the University of Iowa DNA Core facility using standard Affymetrix protocols. In brief, approximately 50 ng of total RNA was used as input to a two-step amplification procedure (NuGen, http://www.nugeninc.com/) to generate biotin-labeled RNA fragments for hybridization to the Affymetrix mouse exon 1.0 ST array.
2012-10-03 | E-GEOD-37195 | biostudies-arrayexpress
Project description:To investigate the function of PRDM6 in smooth muscle cells during outflow tract development, we have isolated the ascending aorta and the ductus arteriosus (DA) separatly from the E18.5 Wnt1Cre;PRDM6f/f mouse (PRDM6 KO) and PRDM6f/f mouse (Control) and compared the gene expression profile of the four groups of samples
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Project description:We used microarrays to characterize the global changes in gene expression within the ascending aorta of mice due to conditional disruption of TGF-M-NM-2 signaling in smooth muscle and/or due to heterozygous fibrillin-1 mutation. Myh11-CreERT2.Tgfbr2f/f (abbreviated as Cre.Tgfbr2) mice were cross-bred to Fbn1C1039G/+ (abbreviated as Fbn1C/+) mice and treated with vehicle or tamoxifen for 5 d starting at 4 wk of age to generate 4 groups of animals: 1) Cre.Tgfbr2-Veh: controls with intact TGF-M-NM-2 signaling and wild-type fibrillin-1 expression; 2) Cre.Tgfbr2-Tmx: conditional disruption of Tgfbr2 in smooth muscle with wild-type fibrillin-1 expression; 3) Fbn1C1039G.Cre.Tgfbr2-Veh: heterozygous expression of mutant fibrillin-1 with intact TGF-M-NM-2 signaling; and 4) Fbn1C1039G.Cre.Tgfbr2-Tmx: conditional disruption of Tgfbr2 in smooth muscle with heterozygous expression of mutant fibrillin-1. The animals were euthanized at 6 weeks of age and their ascending aortas (from above the coronary arteries to the first arch branch) were collected and total RNA was extracted.
2013-05-31 | E-GEOD-36778 | biostudies-arrayexpress
Project description:When aortic cells are under stress, such as increased hemodynamic pressure, they adapt to the environment by modifying their functions, allowing the aorta to maintain its strength. To understand the regulation of this adaptive response, we examined the transcriptomic and epigenomic programs in aortic smooth muscle cells (SMCs) during the adaptive response to angiotensin II (AngII) infusion and determined its importance in protecting against aortic aneurysm and dissection.
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Project description:Bicuspid aortic valve (BAV) is the most common congenital cardiovascular disease in general population and is frequently associated with the development of thoracic aortic aneurysm (TAA). There is no effective strategy to intervene with TAA progression due to an incomplete understanding of the pathogenesis. In this study, protein analyses of human aortic tissues showed the insufficient expression of NOTCH1 and impaired mitochondrial dynamics in BAV-TAA. To verify it, we constructed aorta-on-a-chip to replicate the rhythmic tensile on human aorta, on which human aortic smooth muscle cells (HAoSMCs) endured a microenvironment of biomimetic strain unattainable in animal models. HAoSMCs with NOTCH1-knockdown exhibited reduced contractile phenotype and were accompanied by attenuated mitochondrial fusion. Furthermore, we identified that mitochondrial fusion activators (leflunomide and teriflunomide) or mitochondrial fission inhibitor (Mdivi-1) rescued the mitochondrial dysfunction in HAoSMCs from BAV-TAA patients. These findings suggest that impaired mitochondrial dynamics could be a potential therapeutic target for BAV-TAA.
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