scholarly journals Rosiglitazone Inhibits Acyl-CoA Synthetase Activity and Fatty Acid Partitioning to Diacylglycerol and Triacylglycerol via a Peroxisome Proliferator-Activated Receptor- -Independent Mechanism in Human Arterial Smooth Muscle Cells and Macrophages

Diabetes ◽  
2007 ◽  
Vol 56 (4) ◽  
pp. 1143-1152 ◽  
Author(s):  
B. Askari ◽  
J. E. Kanter ◽  
A. M. Sherrid ◽  
D. L. Golej ◽  
A. T. Bender ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Fatty Acid ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Peroxisome Proliferator ◽  
Synthetase Activity ◽  
Arterial Smooth Muscle ◽  
Peroxisome Proliferator Activated Receptor ◽  
Independent Mechanism ◽  
Arterial Smooth Muscle Cells

scholarly journals NF-κB/p65 Competes With Peroxisome Proliferator-Activated Receptor Gamma for Transient Receptor Potential Channel 6 in Hypoxia-Induced Human Pulmonary Arterial Smooth Muscle Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Yan Wang ◽  
Naijian Li ◽  
Yingfeng Wang ◽  
Guobing Zheng ◽  
Jing An ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Transient Receptor Potential ◽  
Muscle Cells ◽  
Peroxisome Proliferator ◽  
Arterial Smooth Muscle ◽  
Peroxisome Proliferator Activated Receptor ◽  
Pulmonary Arterial ◽  
Arterial Smooth Muscle Cells ◽  
Pulmonary Arterial Smooth Muscle

Objective: Peroxisome proliferator-activated receptor gamma (PPARγ) has an anti-proliferation effect on pulmonary arterial smooth muscle cells (PASMCs) via the transient receptor potential channel (TRPC) and protects against pulmonary artery hypertension (PAH), whereas nuclear factor-kappa B (NF-κB) has pro-proliferation and pro-inflammation effects, which contributes to PAH. However, the association between them in PAH pathology remains unclear. Therefore, this study aimed to investigate this association and the mechanisms underlying TRPC1/6 signaling-mediated PAH.Methods: Human pulmonary arterial smooth muscle cells (hPASMCs) were transfected with p65 overexpressing (pcDNA-p65) and interfering plasmids (shp65) and incubated in normal and hypoxic conditions (4% O2 and 72 h). The effects of hypoxia and p65 expression on cell proliferation, invasion, apoptosis, [Ca2+]i, PPARγ, and TRPC1/6 expression were determined using Cell Counting Kit-8 (CCK-8), Transwell, Annexin V/PI, Fura-2/AM, and western blotting, respectively. In addition, the binding of p65 or PPARγ proteins to the TRPC6 promoter was validated using a dual-luciferase report assay, chromatin-immunoprecipitation-polymerase chain reaction (ChIP-PCR), and electrophoretic mobility shift assay (EMSA).Results: Hypoxia inhibited hPASMC apoptosis and promoted cell proliferation and invasion. Furthermore, it increased [Ca2+]i and the expression of TRPC1/6, p65, and Bcl-2 proteins. Moreover, pcDNA-p65 had similar effects on hypoxia treatment by increasing TRPC1/6 expression, [Ca2+]i, hPASMC proliferation, and invasion. The dual-luciferase report and ChIP-PCR assays revealed three p65 binding sites and two PPARγ binding sites on the promoter region of TRPC6. In addition, hypoxia treatment and shPPARγ promoted the binding of p65 to the TRPC6 promoter, whereas shp65 promoted the binding of PPARγ to the TRPC6 promoter.Conclusion: Competitive binding of NF-κB p65 and PPARγ to TRPC6 produced an anti-PAH effect.

scholarly journals Effects of vasopressin on ATP-sensitive and Ca2+-activated K+ channels of coronary arterial smooth muscle cells

1992 ◽  
Vol 58 ◽  
pp. 339
Author(s):  
Tetsuzo Wakatsuki ◽  
Yutaka Nakaya ◽  
Yukiko Miyoshi ◽  
Zeng Xiao-Rong ◽  
Masahiro Nomura ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
K Channels ◽  
Arterial Smooth Muscle Cells

Propagation of fast and slow intercellular Ca2+ waves in primary cultured arterial smooth muscle cells

Cell Calcium ◽  
2011 ◽  
Vol 50 (5) ◽  
pp. 459-467 ◽  
Author(s):  
Nadia Halidi ◽  
François-Xavier Boittin ◽  
Jean-Louis Bény ◽  
Jean-Jacques Meister
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells
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