The Oxygen Radical Generator Pyrogallol Impairs Cardiomyocyte Contractile Function Via a Superoxide and p38 MAP Kinase-Dependent Pathway: Protection by Anisodamine and Tetramethylpyrazine

2004 ◽  
Vol 4 (4) ◽  
pp. 375-384 ◽  
Author(s):  
Lucy B. Esberg ◽  
Jun Ren
Keyword(s):  
Map Kinase ◽  
Contractile Function ◽  
Oxygen Radical ◽  
P38 Map Kinase ◽  
Dependent Pathway

TNF-α and serum induce SKALP/elafin gene expression in human keratinocytes by a p38 MAP kinase-dependent pathway

2000 ◽  
Vol 292 (4) ◽  
pp. 180-187 ◽  
Author(s):  
R. Pfundt ◽  
M. Wingens ◽  
M. Bergers ◽  
M. Zweers ◽  
M. Frenken ◽  
...  
Keyword(s):  
Gene Expression ◽  
Map Kinase ◽  
Human Keratinocytes ◽  
P38 Map Kinase ◽  
Tnf Α ◽  
Dependent Pathway

Na+-glucose cotransport triggers ezrin phosphorylation via a P38 MAP kinase-dependent pathway

2003 ◽  
Vol 124 (4) ◽  
pp. A312-A313
Author(s):  
Ham Shiue ◽  
Sara Palkon ◽  
Huiren Zhao ◽  
Patrick Cullinan ◽  
Janis K. Burkhardt ◽  
...  
Keyword(s):  
Map Kinase ◽  
P38 Map Kinase ◽  
Dependent Pathway

Temporary blockade of contractility during reperfusion elicits a cardioprotective effect of the p38 MAP kinase inhibitor SB-203580

2005 ◽  
Vol 288 (6) ◽  
pp. H2726-H2734 ◽  
Author(s):  
Tomohiko Sumida ◽  
Hajime Otani ◽  
Shiori Kyoi ◽  
Takayuki Okada ◽  
Hiroyoshi Fujiwara ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Infarct Size ◽  
Map Kinase ◽  
Kinase Inhibitor ◽  
Contractile Function ◽  
P38 Map Kinase ◽  
Blue Dye ◽  
Kinase Inhibition ◽  
Sb 203580

p38 MAP kinase activation is known to be deleterious not only to mitochondria but also to contractile function. Therefore, p38 MAP kinase inhibition therapy represents a promising approach in preventing reperfusion injury in the heart. However, reversal of p38 MAP kinase-mediated contractile dysfunction may disrupt the fragile sarcolemma of ischemic-reperfused myocytes. We, therefore, hypothesized that the beneficial effect of p38 MAP kinase inhibition during reperfusion can be enhanced when contractility is simultaneously blocked. Isolated and perfused rat hearts were paced at 330 rpm and subjected to 20 min of ischemia followed by reperfusion. p38 MAP kinase was activated after ischemia and early during reperfusion (<30 min). Treatment with the p38 MAP kinase inhibitor SB-203580 (10 μM) for 30 min during reperfusion, but not the c-Jun NH2-terminal kinase inhibitor SP-600125 (10 μM), improved contractility but increased creatine kinase release and infarct size. Cotreatment with SB-203580 and the contractile blocker 2,3-butanedione monoxime (BDM, 20 mM) or the ultra-short-acting β-blocker esmorol (0.15 mM) for the first 30 min during reperfusion significantly reduced creatine kinase release and infarct size. In vitro mitochondrial ATP generation and myocardial ATP content were significantly increased in the heart cotreated with SB-203580 and BDM during reperfusion. Dystrophin was translocated from the sarcolemma during ischemia and reperfusion. SB-203580 increased accumulation of Evans blue dye in myocytes depleted of sarcolemmal dystrophin during reperfusion, whereas cotreatment with BDM facilitated restoration of sarcolemmal dystrophin and mitigated sarcolemmal damage after withdrawal of BDM. These results suggest that treatment with SB-203580 during reperfusion aggravates myocyte necrosis but concomitant blockade of contractile force unmasks cardioprotective effects of SB-203580.

Nanohydroxyapatite increases BMP-2 expression via a p38 MAP kinase dependent pathway in periodontal ligament cells

2013 ◽  
Vol 58 (8) ◽  
pp. 1021-1028 ◽  
Author(s):  
Mizuki Suto ◽  
Eiji Nemoto ◽  
Sousuke Kanaya ◽  
Risako Suzuki ◽  
Masahiro Tsuchiya ◽  
...  
Keyword(s):  
Map Kinase ◽  
Periodontal Ligament ◽  
P38 Map Kinase ◽  
Periodontal Ligament Cells ◽  
Dependent Pathway
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