The role of AT1 receptor, Ras and NAD(P)H oxidase on p38 MAPK phosphorylation by angiotensin II stimulation in primary cultured vascular smooth muscle cells

2012 ◽  
Vol 37 (4) ◽  
pp. 407-416
Author(s):  
Serkan Caglar ◽  
Arzu Cetin ◽  
Fatih Uzuner ◽  
Alper Tokay ◽  
Mustafa Kirca ◽  
...  
1998 ◽  
Vol 39 (4) ◽  
pp. 561-561 ◽  
Author(s):  
Chikara Satoh ◽  
Noboru Fukuda ◽  
Atsushi Kubo ◽  
Hirobumi Kishioka ◽  
Mari Nakayama ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Si-yu Zeng ◽  
Jing-fei Luo ◽  
Hai-yan Quan ◽  
Yun-bin Xiao ◽  
Yu-huan Liu ◽  
...  

Objectives. Protein arginine methyltransferase 2 (PRMT2) protects against vascular injury-induced intimal hyperplasia; however, little is known about the role of PRMT2 in angiotensin II (Ang II)-induced VSMCs proliferation and inflammation. This research aims to determine whether PRMT2 inhibits Ang II-induced proliferation and inflammation of vascular smooth muscle cells (VSMCs). Materials and Methods. PRMT2 overexpression was used to elucidate the role of PRMT2 in Ang II-induced VSMCs proliferation and inflammation. Western blotting and reverse transcriptional PCR were adopted to detect protein and mRNA expression severally. Cell viability was evaluated by 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay and cell cycle distribution by flow cytometry. Results. Ang II significantly reduced mRNA and protein levels of PRMT2 in VSMCs in time-dependent and dose-dependent manner. Results of PRMT2 overexpression indicated that PRMT2 inhibited proliferation of VSMCs stimulated with 100 nmol/L Ang II for 24 hours. Furthermore, overexpression of PRMT2 reduced Ang II-induced production of proinflammatory cytokines such as interleukin 6 (IL-6) and interleukin 1β (IL-1β) in VSMCs. Conclusions. These findings suggest that PRMT2 alleviates Ang II-induced VSMCs proliferation and inflammation, providing a new mechanism about how Ang II mediated VSMCs proliferation and inflammation.


Cytokine ◽  
2002 ◽  
Vol 18 (4) ◽  
pp. 206-213 ◽  
Author(s):  
Young D Jung ◽  
Fan Fan ◽  
David J McConkey ◽  
Marina E Jean ◽  
Wenbiao Liu ◽  
...  

Author(s):  
Vanessa Truong ◽  
Madhu B Anand-Srivastava ◽  
Ashok K Srivastava

Cyclic adenosine monophosphate response element (CRE) binding protein (CREB) is a nuclear transcription factor that regulates the transcription of several genes containing the CRE sites in their promoters. CREB is activated by phosphorylation on a key serine residue, Ser 311, in response to a wide variety of extracellular stimuli including angiotensin II (Ang II). Ang II is an important vasoactive peptide and mitogen for vascular smooth muscle cells (VSMC) that in addition to regulating the contractile response in VSMC also plays an important role in phenotypic switch of vascular smooth muscle cells (VSMC) from contractile to a synthetic state. The synthetic VSMC are known to exhibit proliferative and migratory properties due to hyperactivation of Ang II-induced signaling events. Ang II has been shown to induce CREB phosphorylation/activation and transcription of genes implicated in proliferation, growth and migration. Here, we have highlighted some key studies that have demonstrated an important role of CREB in Ang II-mediated gene transcription, proliferation, hypertrophy and migration of VSMC.


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