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LncVSM (AK098656) up/down-regulation in Vascular Smooth Muscle cells

ABSTRACT: Long non-coding RNAs (LncRNAs) in hypertensives and their mechanisms in regulating blood pressure still remain unexplored. The aim of present study is to construct the profiles of LncRNAs in blood of patients with essential hypertension and healthy controls. Methods and results, LncRNA microarray identified up-regulated, anddown-regulated LncRNAs, in hypertensives compared to their healthy controls. Among them, one vascular smooth muscle (VSM)-specific LncRNA AK096656 (LncVSM) was quantitated in plasma of patients with hypertension and their healthy controls using the real-time qRT-PCR. LncVSM shows specific expression in human arterial vascular smooth muscle cells (HASMCs) and promote its proliferation and migration. Expression profiles and Ingenuity Pathway Analysis (IPA) revealed that LncVSM activated Renin-Angiotensin Signaling (RAS). the overexpression of LncVSM would result hypertension related complications.

ORGANISM(S): Homo sapiens

PROVIDER: GSE75940 | GEO | 2015/12/12

SECONDARY ACCESSION(S): PRJNA305751

REPOSITORIES: GEO

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LncVSM (AK098656) up/down-regulation in Vascular Smooth Muscle cells

Project description:Long non-coding RNAs (LncRNAs) in hypertensives and their mechanisms in regulating blood pressure still remain unexplored. The aim of present study is to construct the profiles of LncRNAs in blood of patients with essential hypertension and healthy controls. Methods and results, LncRNA microarray identified up-regulated, anddown-regulated LncRNAs, in hypertensives compared to their healthy controls. Among them, one vascular smooth muscle (VSM)-specific LncRNA AK096656 (LncVSM) was quantitated in plasma of patients with hypertension and their healthy controls using the real-time qRT-PCR. LncVSM shows specific expression in human arterial vascular smooth muscle cells (HASMCs) and promote its proliferation and migration. Expression profiles and Ingenuity Pathway Analysis (IPA) revealed that LncVSM activated Renin-Angiotensin Signaling (RAS). the overexpression of LncVSM would result hypertension related complications. LncVSM (AK098656) transfection

2015-12-12 | E-GEOD-75940 | biostudies-arrayexpress

LncRNA expression profile and target gene prediction of calcification in human aortic smooth muscle cells induced by DPP4

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Project description:Background: Tissue remodeling induced by airway inflammation is a main trigger of pathogenesis in various chronic lung diseases like asthma, COPD, IPF, and pulmonary hypertension. The role of human airway smooth muscle cells (HASMCs) in this context is unclear. Hypothesis: HASMCs participate in linking inflammation with remodeling. Methods: The inflammatory responses of ex vivo-cultivated HASMCs to TNFÎ± were investigated by whole-genome-microarray analyses. Diferrential regulation of genes associated with airway inflammation and remodeling were verified by qRT-PCR and ELISA. Results: TNFa induced the expression of 18 cytokines/chemokines and five tissue remodeling genes involved in (severe/corticosteroid-insensitive) asthma, COPD, IPF and/or pulmonary hypertension. Conclusion: HASMCs participate in the interaction of inflammation and tissue remodeling. HASMCs might be considered as targets in therapies of chronic inflammatory lung diseases with regard to attenuating inflammation-induced remodeling processes leading to the development of emphysema or fibrosis. HASMCs of eight donors were left untreated of were stimulated with TNFa at 20 ng/ml. Total RNA was subjected after eight hours of stimulation to whole-human-genome oligo microarray analysis.

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Project description:RNA sequencing (RNA-seq) analysis revealed 31 novel lncRNAs in HCASMC, including a vascular cell-enriched lncRNA called SENCR (for Smooth muscle and Endothelial cell long Non-Coding RNA). RT-PCR and hybridization studies show SENCR exists in two isoforms and is transcribed antisense from the 5’ end of the FLI1 gene. Knockdown of SENCR has no effect on FLI1 mRNA or protein expression. Biochemical fractionation and RNA fluorescence in situ hybridization (FISH) studies indicate SENCR is a cytoplasmic lncRNA. RNA-seq experiments in HCASMC where SENCR is attenuated disclose decreased expression of Myocardin and many SMC contractile genes; conversely a pro-migratory gene signature is increased. RT-PCR and Western blotting validated several differentially expressed genes following SENCR knockdown. Loss-of-function studies in scratch wound and Boyden chamber assays support SENCR as an inhibitor of vascular cell migration. Total RNAs of 3 replicates of normal human coronary artery smooth muscle cells (Mock1, Mock2 and Mock3) were sequenced and analyzed for identification of novel lncRNAs. One of identified novel lncRNAs from that experiment is SENCR. To study its function, SENCR knock-down experiment were performed and then RNA-seq profiles of 3 replicates of both SENCR-knockdown samples and corresponding controls were compared.

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The inflammatory response of human airway smooth muscle cells

Project description:Background: Tissue remodeling induced by airway inflammation is a main trigger of pathogenesis in various chronic lung diseases like asthma, COPD, IPF, and pulmonary hypertension. The role of human airway smooth muscle cells (HASMCs) in this context is unclear. Hypothesis: HASMCs participate in linking inflammation with remodeling. Methods: The inflammatory responses of ex vivo-cultivated HASMCs to TNFα were investigated by whole-genome-microarray analyses. Diferrential regulation of genes associated with airway inflammation and remodeling were verified by qRT-PCR and ELISA. Results: TNFa induced the expression of 18 cytokines/chemokines and five tissue remodeling genes involved in (severe/corticosteroid-insensitive) asthma, COPD, IPF and/or pulmonary hypertension. Conclusion: HASMCs participate in the interaction of inflammation and tissue remodeling. HASMCs might be considered as targets in therapies of chronic inflammatory lung diseases with regard to attenuating inflammation-induced remodeling processes leading to the development of emphysema or fibrosis.

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