Characterization of the molecular mechanisms of the coupling between intracellular loops of prostacyclin receptor with the C-terminal domain of the Gαs protein in human coronary artery smooth muscle cells

2006 ◽  
Vol 454 (1) ◽  
pp. 80-88 ◽  
Author(s):  
Lihai Zhang ◽  
Murat Bastepe ◽  
Harald Jüppner ◽  
Ke-He Ruan
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Molecular Mechanisms ◽  
Muscle Cells ◽  
Human Coronary Artery ◽  
Terminal Domain ◽  
Prostacyclin Receptor ◽  
Intracellular Loops

Functional Characterization of Cysteinyl Leukotriene CysLT2 Receptor on Human Coronary Artery Smooth Muscle Cells

2001 ◽  
Vol 287 (5) ◽  
pp. 1088-1092 ◽  
Author(s):  
Masazumi Kamohara ◽  
Jun Takasaki ◽  
Mitsuyuki Matsumoto ◽  
Shun-ichiro Matsumoto ◽  
Tetsu Saito ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Functional Characterization ◽  
Muscle Cells ◽  
Human Coronary Artery ◽  
Cysteinyl Leukotriene

scholarly journals Quantitative trait loci mapped for TCF21 binding, chromatin accessibility and chromosomal looping in coronary artery smooth muscle cells reveal molecular mechanisms of coronary disease loci

2020 ◽  
Author(s):  
Quanyi Zhao ◽  
Michael Dacre ◽  
Trieu Nguyen ◽  
Milos Pjanic ◽  
Boxiang Liu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Molecular Mechanisms ◽  
Disease Risk ◽  
Muscle Cells ◽  
Chromatin Accessibility ◽  
Human Coronary Artery ◽  
Chromosomal Structure ◽  
Functional Variants

AbstractBackgroundTo investigate the epigenetic and transcriptional mechanisms of coronary artery disease (CAD) risk, as well as the functional regulation of chromatin structure and function, we have created a catalog of genetic variants associated with three stages of transcriptional cis-regulation in primary human coronary artery vascular smooth muscle cells (HCASMC).ResultsTo this end, we have used a pooling approach with HCASMC lines to map regulatory variation that mediates binding of the CAD associated transcription factor TCF21 with ChIPseq studies (bQTLs), variation that regulates chromatin accessibility with ATACseq studies (caQTLs), and chromosomal looping with HiC methods (clQTLs). We show significant overlap of the QTLs, and their relationship to smooth muscle specific genes and the binding of smooth muscle transcription factors. Further, we use multiple analyses to show that these QTLs are highly associated with CAD GWAS loci and correlated to lead SNPs in these loci where they show allelic effects. We have verified with genome editing that identified functional variants can regulate both chromatin accessibility and chromosomal looping, providing new insights into functional mechanisms regulating chromatin state and chromosomal structure. Finally, we directly link the disease associated TGFβ1-SMAD3 pathway to the CAD associated FN1 gene through a response QTL that modulates both chromatin accessibility and chromosomal looping.ConclusionsTogether, these studies represent the most thorough mapping of multiple QTL types in a highly disease relevant primary cultured cell type, and provide novel insights into their functional overlap and mechanisms that underlie these genomic features and their relationship to disease risk.

Abciximab Inhibits the Migration and Invasion Potential of Human Coronary Artery Smooth Muscle Cells

2000 ◽  
Vol 32 (12) ◽  
pp. 2195-2206 ◽  
Author(s):  
Rüdiger Blindt ◽  
Anja-Katrin Bosserhoff ◽  
Ute Zeiffer ◽  
Nicole Krott ◽  
Peter Hanrath ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Migration And Invasion ◽  
Human Coronary Artery ◽  
Invasion Potential

scholarly journals Effect of Paclitaxel+Hirudin on the TLR4-MyD88 Signaling Pathway During Inflammatory Activation of Human Coronary Artery Smooth Muscle Cells and Mechanistic Analysis

2018 ◽  
Vol 50 (4) ◽  
pp. 1301-1317 ◽  
Author(s):  
Hongmei Li ◽  
Xian Wang ◽  
Anlong Xu
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Dependent Manner ◽  
Human Coronary Artery ◽  
Post Intervention ◽  
Inflammatory Activation ◽  
Myd88 Pathway

Background/Aims: Approximately 10%-20% of patients with acute cardiovascular disease who have received coronary intervention suffer restenosis and high inflammation. The stent compound paclitaxel+hirudin was prepared for the treatment of post-intervention restenosis. This study aimed to explore the anti-inflammatory and anti-restenosis mechanisms of paclitaxel+hirudin with regard to the TLR4/MyD88/NF-κB pathway. Methods: Human coronary artery smooth muscle cells (HCASMCs) at 4-6 generations after in vitro culture were used as a model. Lipopolysaccharide (LPS) was used as an inducer to maximally activate the TLR4/MyD88/NF-κB inflammation pathway. After MyD88 knockdown and selective blocking of MyD88 degradation with epoxomicin, the effects of paclitaxel+hirudin stenting on key sites of the TLR4/MyD88/NF-κB pathway were detected using ELISA, Q-PCR, and western blot analysis. Results: LPS at 1 μg/mL for 48 h was the optimal modeling condition for inflammatory activation of HCASMCs. Paclitaxel+hirudin inhibited the levels of key proteins and the gene expression, except for that of the MyD88 gene, of the TLR4-MyD88 pathway. The trend of the effect of paclitaxel+hirudin on the pathway proteins was similar to that of MyD88 knockdown. After epoxomicin intervention, the inhibitory effects of paclitaxel+hirudin on the key genes and proteins of the TLR4-MyD88 pathway were significantly weakened, which even reached pre-intervention levels. Paclitaxel+hirudin affected the MyD88 protein in a dosage-dependent manner. Conclusion: The paclitaxel+hirudin compound promotes MyD88 degradation in the TLR4/MyD88/NF-κB pathway to reduce the activity of TLR4 and NF-κB p65 and to weaken the LPS-initiated inflammatory reactions of IL-1β, IL-6, and TNF-α.

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