scholarly journals Differential roles of p38-MAPK and JNKs in mediating early protection or apoptosis in the hyperthermic perfused amphibian heart

2008 ◽  
Vol 211 (15) ◽  
pp. 2524-2532 ◽  
Author(s):  
C. Gaitanaki ◽  
M. Mastri ◽  
I.-K. S. Aggeli ◽  
I. Beis
Keyword(s):  
P38 Mapk ◽  
Amphibian Heart

scholarly journals CoCl2 induces protective events via the p38-MAPK signalling pathway and ANP in the perfused amphibian heart

2007 ◽  
Vol 210 (13) ◽  
pp. 2267-2277 ◽  
Author(s):  
C. Gaitanaki ◽  
T. Kalpachidou ◽  
I.-K. S. Aggeli ◽  
P. Papazafiri ◽  
I. Beis
Keyword(s):  
P38 Mapk ◽  
Signalling Pathway ◽  
Mapk Signalling Pathway ◽  
Mapk Signalling ◽  
Amphibian Heart

Hyperosmotic and thermal stresses activate p38-MAPK in the perfused amphibian heart

2002 ◽  
Vol 205 (4) ◽  
pp. 443-454 ◽  
Author(s):  
Ioanna-Katerina S. Aggeli ◽  
Catherine Gaitanaki ◽  
Antigone Lazou ◽  
Isidoros Beis
Keyword(s):  
P38 Mapk ◽  
Thermal Stresses ◽  
Final Concentration ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Immunohistochemical Studies ◽  
Kinase Phosphorylation ◽  
Rapid Activation ◽  
Amphibian Heart ◽  
Sb 203580

SUMMARY We assessed the activation of p38-MAPK (mitogen-activated protein kinase) by osmotic and thermal stresses in the isolated perfused amphibian (Rana ridibunda) heart. Hyperosmotic stress induced the rapid activation of the kinase. In particular, in the presence of 0.5 mol l–1 sorbitol, p38-MAPK was maximally phosphorylated (by approximately twelvefold) at 15 min, while excess of NaCl (206 mmol l–1 final concentration) or KCl (16 mmol l–1 final concentration) stimulated a less potent activation, maximised (by approximately eightfold and fourfold) within 2 min and 30 s, respectively, relative to control values. The effect of all three compounds examined was reversible, since the kinase phosphorylation levels decreased upon reperfusion of the heart with normal bicarbonate-buffered saline. Conversely, hypotonicity did not induce any p38-MAPK activation. Furthermore, both hypothermia and hyperthermia induced considerable phosphorylation of the kinase, by four- and 7.5-fold, respectively, relative to control values. Immunohistochemical studies elucidated the localisation pattern of phospho-p38-MAPK and also revealed enhanced atrial natriuretic peptide (ANP) immunoreactivity in osmotically stressed hearts. Interestingly, SB 203580 (1 μmol l–1) not only completely blocked the activation of p38-MAPK by all these interventions, but also abolished the enhanced ANP immunoreactivity induced by 0.5 mol l–1 sorbitol. These findings indicate the possible involvement of ANP in the mechanisms regulating responses under such stressful conditions.

scholarly journals Atrial Natriuretic Peptide mRNA Regulation by p38- MAPK in the Perfused Amphibian Heart

2005 ◽  
Vol 16 (4-6) ◽  
pp. 183-192 ◽  
Author(s):  
Athanassios Vassilopoulos ◽  
Catherine Gaitanaki ◽  
Panagiota Papazafiri ◽  
Isidoros Beis
Keyword(s):  
Atrial Natriuretic Peptide ◽  
P38 Mapk ◽  
Natriuretic Peptide ◽  
Mrna Regulation ◽  
Amphibian Heart ◽  
Atrial Natriuretic

Effects of various oxidants and antioxidants on the p38-MAPK signalling pathway in the perfused amphibian heart

2006 ◽  
Vol 291 (1-2) ◽  
pp. 107-117 ◽  
Author(s):  
Catherine Gaitanaki ◽  
Maria Papatriantafyllou ◽  
Konstantina Stathopoulou ◽  
Isidoros Beis
Keyword(s):  
P38 Mapk ◽  
Signalling Pathway ◽  
Mapk Signalling Pathway ◽  
Mapk Signalling ◽  
Amphibian Heart

α1- and β-adrenoceptor stimulation differentially activate p38-MAPK and atrial natriuretic peptide production in the perfused amphibian heart

2002 ◽  
Vol 205 (16) ◽  
pp. 2387-2397 ◽  
Author(s):  
Ioanna-Katerina S. Aggeli ◽  
Catherine Gaitanaki ◽  
Antigone Lazou ◽  
Isidoros Beis
Keyword(s):  
Atrial Natriuretic Peptide ◽  
P38 Mapk ◽  
Natriuretic Peptide ◽  
Mitogen Activated Protein Kinase ◽  
Dependent Manner ◽  
Mapk Activation ◽  
Adrenergic Agents ◽  
Kinase Phosphorylation ◽  
Amphibian Heart ◽  
Atrial Natriuretic

SUMMARY We investigated the activation of p38-MAPK by various adrenergic agents in the perfused Rana ridibunda heart. Phenylephrine (50 μmol l-1) rapidly induced the differential activation of all three mitogen-activated protein kinase (MAPK) subfamilies (ERK, JNKs and p38-MAPK)in this experimental system. Focusing on p38-MAPK response to phenylephrine,we found that the kinase phosphorylation reached maximal values at 30 s,declining thereafter to basal values at 15 min. p38-MAPK activation by phenylephrine was verified as exclusively α1-AR-mediated. Furthermore, SB203580 (1 μmol l-1) abolished the kinase phosphorylation by phenylephrine. Isoproterenol (50 μmol l-1)was also shown to activate p38-MAPK in a time- and temperature-dependent manner. A marked, sustained p38-MAPK activation profile was observed at 25°C, while at 18°C the kinase response to isoproterenol was modest. Isoproterenol effect on p38-MAPK stimulation was β-AR-mediated. Immunohistochemical studies revealed the enhanced presence of phosphorylated p38-MAPK and atrial natriuretic peptide (ANP) in both phenylephrine- and isoproterenol-stimulated hearts, a reaction completely blocked by the respective specific antagonists, or the specific p38-MAPK inhibitor SB203580. These findings indicate a functional correlation between p38-MAPK activation and ANP accumulation in the perfused amphibian heart.

Hyperosmotischer Stress induziert Interleukin 8 via p38 MAPK, Src-Kinase und EGRF in humanen Atemwegszellen

Pneumologie ◽  
2012 ◽  
Vol 66 (S 01) ◽  
Author(s):  
SM Loitsch ◽  
A Langanke ◽  
TOF Wagner ◽  
TO Hirche
Keyword(s):  
P38 Mapk ◽  
Src Kinase ◽  
Interleukin 8

MOLECULAR CONTROL OF ARTICULAR CARTILAGE DEGENERATION BY TRANSFORMING GROWTH FACTOR ALPHA

2008 ◽  
Vol 31 (4) ◽  
pp. 2
Author(s):  
Tom Appleton ◽  
Shirine Usmani ◽  
John Mort ◽  
Frank Beier
Keyword(s):  
Gene Expression ◽  
Articular Cartilage ◽  
Growth Factor ◽  
P38 Mapk ◽  
Transforming Growth Factor ◽  
Cartilage Degeneration ◽  
Signalling Pathways ◽  
Transforming Growth Factor Alpha ◽  
Factor Alpha ◽  
Articular Cartilage Degeneration

Background: Articular cartilage degeneration is a hallmark of osteoarthritis (OA). We previously identified increased expression of transforming growth factor alpha (TGF?) and chemokine (C-C motif) ligand 2 (CCL2) in articular cartilage from a rat modelof OA (1,2). We subsequently reported that TGF? signalling modified chondrocyte cytoskeletal organization, increased catabolic and decreased anabolic gene expression and suppressed Sox9. Due to other roles in chondrocytes, we hypothesized that the effects ofTGF? on chondrocytes are mediated by Rho/ROCK and MEK/ERK signaling pathways. Methods: Primary cultures of chondrocytes and articularosteochondral explants were treated with pharmacological inhibitors of MEK1/2(U0126), ROCK (Y27632), Rho (C3), p38 MAPK (SB202190) and PI3K (LY294002) to elucidate pathway involvement. Results: Using G-LISA we determined that stimulation of primary chondrocytes with TGF? activates RhoA. Reciprocally, inhibition of RhoA/ROCK but not other signalling pathways prevents modification of the actin cytoskeleton in responseto TGF?. Inhibition of MEK/ERKsignaling rescued suppression of anabolic gene expression by TGF? including SOX9 mRNA and protein levels. Inhibition of MEK/ERK, Rho/ROCK, p38 MAPK and PI3K signalling pathways differentially controlled the induction of MMP13 and TNF? gene expression. TGF? also induced expression of CCL2 specifically through MEK/ERK activation. In turn, CCL2 treatment induced the expression of MMP3 and TNF?. Finally, we assessed cartilage degradation by immunohistochemical detection of type II collagen cleavage fragments generated by MMPs. Blockade of RhoA/ROCK and MEK/ERK signalling pathways reduced the generation of type IIcollagen cleavage fragments in response to TGF? stimulation. Conclusions: Rho/ROCK signalling mediates TGF?-induced changes inchondrocyte morphology, while MEK/ERK signalling mediates the suppression ofSox9 and its target genes, and CCL2 expression. CCL2, in turn, induces the expression of MMP3 and TNF?, two potent catabolic factors known to be involved in OA. These pathways may represent strategic targets for interventional approaches to treating cartilage degeneration in osteoarthritis. References: 1. Appleton CTG et al. Arthritis Rheum 2007;56:1854-68. 2. Appleton CTG et al. Arthritis Rheum 2007; 56:3693-705.

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