scholarly journals β2-Adrenergic Receptor-induced p38 MAPK Activation Is Mediated by Protein Kinase A Rather than by Gior Gβγ in Adult Mouse Cardiomyocytes

2000 ◽  
Vol 275 (51) ◽  
pp. 40635-40640 ◽  
Author(s):  
Ming Zheng ◽  
Sheng-Jun Zhang ◽  
Wei-Zhong Zhu ◽  
Bruce Ziman ◽  
Brian K. Kobilka ◽  
...  
Cell ◽  
1991 ◽  
Vol 67 (4) ◽  
pp. 723-730 ◽  
Author(s):  
Takashi Okamoto ◽  
Yoshitake Murayama ◽  
Yujiro Hayashi ◽  
Masaki Inagaki ◽  
Etsuro Ogata ◽  
...  

Nature ◽  
10.1038/36362 ◽  
1997 ◽  
Vol 390 (6655) ◽  
pp. 88-91 ◽  
Author(s):  
Yehia Daaka ◽  
Louis M. Luttrell ◽  
Robert J. Lefkowitz

2002 ◽  
Vol 277 (34) ◽  
pp. 31249-31256 ◽  
Author(s):  
A. Musa Zamah ◽  
Martha Delahunty ◽  
Louis M. Luttrell ◽  
Robert J. Lefkowitz

2010 ◽  
Vol 4 (5) ◽  
pp. 721-729
Author(s):  
Hamid Yaghooti ◽  
Mohsen Firoozrai ◽  
Soudabeh Fallah ◽  
Mohammad Reza Khorramizadeh

Abstract Background: Adenosine is known as a protective and anti-inflammatory nucleoside. Angiotensin II is the main hormone of the renin-angiotensin system. It is associated with endothelial permeability, recruitment, and activation of the immune cells through induction of inflammatory mediators. Matrix metalloproteinase-9 (MMP-9) plays an important role in inflammatory processes mediated by macrophages. Objectives: Investigate whether adenosine pretreatment modulates angiotensin II-induced MMP-9 expression and activation of signaling molecules. Methods: Human monocytic U-937 cells were treated with either adenosine or angiotensin II alone or angiotensin II following a pretreatment with adenosine. Supernatants were analyzed for MMP-9 activity by zymography method. MMP-9 gene expression was analyzed using real-time PCR. Activation of inflammatory mediators IκB-α, NF-κB, JNK, p38 MAPK, and STAT3 were analyzed by a multi-target ELISA kit. Association of Protein kinase A (PKA) in adenosine effects was studied by pre-incubation with H89, a selective PKA inhibitor. Results: Treatment of the cells with angiotensin II significantly increased MMP-9 production (p <0.05). Adenosine pretreatment did not attenuate this angiotensin II effect. Angiotensin II treatment induced NF-κB, JNK and p38 activation. Pretreatment with adenosine prior to angiotensin II stimulation showed a 40% inhibitory effect on p38 induction (p <0.05). This effect was reversed by PKA inhibition. Conclusion: The present data confirmed that monocytic MMP-9 was a target gene for angiotensin II. Adenosine pretreatment did not inhibit MMP-9 increase in response to angiotensin II. However, it showed a potential inhibitory effect on angiotensin II inflammatory signaling.


2003 ◽  
Vol 13 (6) ◽  
pp. 367-374 ◽  
Author(s):  
Narayanan Parameswaran ◽  
Carolyn Hall ◽  
Laura McCabe ◽  
William Spielman

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