Extracellular Superoxide Changes Intracellular ROS And NAD(P)H Lifetime As Well As Intracellular Signaling Via ERK1/2 To Upregulate A Redox Sensitive Transcription Factor, Egr-1 In Pulmonary Artery Smooth Muscle Cells

2011 ◽  
Author(s):  
Eva N. Grayck ◽  
Emily Gibson ◽  
Radu Moldovan ◽  
Tanya Hartney ◽  
Moshe Levi
Keyword(s):  
Transcription Factor ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Intracellular Signaling ◽  
Muscle Cells ◽  
Intracellular Ros ◽  
Pulmonary Artery Smooth Muscle

Signal transduction pathways of IL-1β-mediated iNOS in pulmonary vascular smooth muscle cells

2001 ◽  
Vol 281 (4) ◽  
pp. L816-L823 ◽  
Author(s):  
Jonathan D. Finder ◽  
Jennifer L. Petrus ◽  
Andrew Hamilton ◽  
Raphael T. Villavicencio ◽  
Bruce R. Pitt ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Intracellular Signaling ◽  
Muscle Cells ◽  
Dominant Negative ◽  
Janus Kinase ◽  
Dominant Negative Mutant ◽  
Pulmonary Artery Smooth Muscle

Interleukin (IL)-1β is an important early mediator of inflammation in pulmonary artery smooth muscle cells. We previously reported that a geranylgeranyltransferase inhibitor elevated basal levels of inducible nitric oxide synthase (iNOS) and enhanced IL-1β-mediated induction, suggesting that Rac or Rho small G proteins are candidates for antagonism of such induction. In this study, overexpression of constitutively active Rac1 or its dominant negative mutant did not affect IL-1β induction of iNOS. Alternatively, treatment with Clostridium botulinum C3 exoenzyme, which ADP-ribosylates Rho, was associated with superinduction of iNOS, suggesting an inhibitory role for Rho. IL-1β activated the three mitogen-activated protein kinase (extracellular signal-regulated kinases 1 and 2, c-Jun NH2-terminal kinase/stress-activated protein kinase, and p38) and the Janus kinase (JAK)-signal transducer and activator of transcription pathways. The former two pathways were not associated with IL-1β-mediated iNOS induction, whereas the latter two appeared to have inhibitory roles in iNOS expression. These data suggest that a broad intracellular signaling response to IL-1β in rat pulmonary artery smooth muscle cells results in elevated levels of iNOS that is opposed by the geranylgeranylated small G protein Rho as well as the p38 and JAK2 pathways.

scholarly journals AML1-like Transcription Factor Induces Serine Elastase Activity in Ovine Pulmonary Artery Smooth Muscle Cells

1998 ◽  
Vol 83 (3) ◽  
pp. 252-263 ◽  
Author(s):  
Dennis A. Wigle ◽  
Karen E. Thompson ◽  
Shmuel Yablonsky ◽  
Syed H. E. Zaidi ◽  
Claire Coulber ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Elastase Activity ◽  
Pulmonary Artery Smooth Muscle

Hypoxic Growth of Bovine Pulmonary Artery Smooth Muscle Cells

CHEST Journal ◽  
1998 ◽  
Vol 114 (1) ◽  
pp. 29S-30S ◽  
Author(s):  
Edward C. Dempsey ◽  
Mita Das ◽  
Maria G. Frid ◽  
Yongjian Xu ◽  
Kurt R. Stenmark
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Pulmonary Artery Smooth Muscle

Upregulation of profilin, cofilin-2 and LIMK2 in cultured pulmonary artery smooth muscle cells and in pulmonary arteries of monocrotaline-treated rats

2006 ◽  
Vol 44 (5) ◽  
pp. 275-282 ◽  
Author(s):  
Yan-Ping Dai ◽  
Shaner Bongalon ◽  
Honglin Tian ◽  
Samuel D. Parks ◽  
Violeta N. Mutafova-Yambolieva ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Pulmonary Arteries ◽  
Muscle Cells ◽  
Pulmonary Artery Smooth Muscle
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