scholarly journals Selective inhibition of ATPase activity during contraction alters the activation of p38 MAP kinase isoforms in skeletal muscle

2013 ◽  
Vol 114 (6) ◽  
pp. 1445-1455 ◽  
Author(s):  
Jeffrey J. Brault ◽  
Natalie M. Pizzimenti ◽  
John N. Dentel ◽  
Robert W. Wiseman
2009 ◽  
Vol 587 (13) ◽  
pp. 3363-3373 ◽  
Author(s):  
Melissa A. Chambers ◽  
Jennifer S. Moylan ◽  
Jeffrey D. Smith ◽  
Laurie J. Goodyear ◽  
Michael B. Reid

2003 ◽  
Vol 71 (11) ◽  
pp. 6672-6675 ◽  
Author(s):  
Kazuto Matsunaga ◽  
Hiroyuki Yamaguchi ◽  
Thomas W. Klein ◽  
Herman Friedman ◽  
Yoshimasa Yamamoto

ABSTRACT A possible involvement of the mitogen-activated protein (MAP) kinase cascade in the inhibition of macrophage interleukin-12 (IL-12) production by Legionella pneumophila infection was examined. The results of MAP kinase inhibition by p42/44 and p38 MAP kinase inhibitors and of p42/44 MAP kinase activity assays indicate that L. pneumophila infection of macrophages causes a selective inhibition of lipopolysaccharide-induced IL-12 production by activating the p42/44 MAP kinase cascade. In addition, it was also revealed that the p38 MAP kinase may be important for the production of IL-12 but not for the inhibition caused by L. pneumophila infection.


2001 ◽  
Vol 536 (1) ◽  
pp. 273-282 ◽  
Author(s):  
Mei Yu ◽  
Eva Blomstrand ◽  
Alexander V. Chibalin ◽  
Anna Krook ◽  
Juleen R. Zierath

2002 ◽  
Vol 283 (6) ◽  
pp. H2282-H2287 ◽  
Author(s):  
Michael P. Massett ◽  
Zoltan Ungvari ◽  
Anna Csiszar ◽  
Gabor Kaley ◽  
Akos Koller

Protein kinase C (PKC) and mitogen-activated protein (MAP) kinases have been implicated in the modulation of agonist-induced contractions of large vessels. However, their role in pressure- and agonist-induced constrictions of skeletal muscle arterioles, which have a major role in regulating peripheral resistance, is not clearly elucidated. Thus constrictions of isolated rat gracilis muscle arterioles (∼80 μm in diameter) to increases in intraluminal pressure and to norepinephrine (NE) or angiotensin II (ANG II) were assessed in the absence or presence of chelerythrine, PD-98058, and SB-203580 (inhibitors of PKC, p42/44 and p38 MAP kinase pathways, respectively). Arteriolar constriction to NE and ANG II were significantly reduced by chelerythrine (by ∼90%) and unaffected by SB-203580, whereas PD-98058 decreased only ANG II-induced constrictions (by ∼60%). Pressure-induced increases in wall tension (from 0.1 to 0.7 N/m) resulted in significant arteriolar constrictions (50% maximum) that were abolished by chelerythrine without altering smooth muscle intracellular Ca2+ concentration ([Ca2+]i) (fura 2 microfluorimetry). PD-98058 and SB-203580 significantly decreased the magnitude of myogenic tone (by 20% and 60%, respectively) and reduced the sensitivity of the myogenic mechanism to wall tension, causing a significant rightward shift in the wall tension-myogenic tone relationship without affecting smooth muscle [Ca2+ i]. MAP kinases were demonstrated with Western blotting. Thus in skeletal muscle arterioles 1) PKC is involved in both myogenic and agonist-induced constrictions , 2) PD-98058-sensitive p42/44 MAP kinases modulate both wall tension-dependent and ANG II-induced constrictions, whereas 3) a SB-203580-sensitive p38 MAP kinase pathway seems to be specifically involved in the mechanotransduction of wall tension.


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