Involvement of p38 MAPK and JNK in heat stress-induced cardioprotection.

Autor: Pantos C; Department of Pharmacology, University of Athens, 75 Mikras Asias Ave., 11527 Goudi, Athens, Greece. cpantos@cc.uoa.gr, Malliopoulou V, Mourouzis I, Moraitis P, Tzeis S, Thempeyioti A, Paizis I, Cokkinos A, Carageorgiou H, Varonos DD, Cokkinos DV
Jazyk: angličtina
Zdroj: Basic research in cardiology [Basic Res Cardiol] 2003 May; Vol. 98 (3), pp. 158-64.
DOI: 10.1007/s00395-003-0399-6
Abstrakt: The present study investigated whether heat stress-induced cardioprotection involves alterations in the pattern of p38 mitogen activated protein kinase (p38MAPK) and c-Jun NH2 - terminal kinase (JNK) activation during ischaemia - reperfusion in a model of isolated perfused rat heart. Wistar rats were subjected to whole-body hyperthermia at 42 degrees C for 15 min (HS), while untreated animals served as controls (CON). Twenty four hours later, CON and HS isolated hearts were perfused in a Langendorff mode and subjected to 20 min of zero-.ow global ischaemia followed by 45 min of reperfusion. Postischaemic recovery of left ventricular developed pressure at 45 min of reperfusion was expressed as % of the initial value (LVDP%). Activation of p38 MAPK and JNK was assessed by standard Western blotting techniques using a dual phospho-p38 MAPK and phospho-p46 JNK and p54 JNK antibodies. The levels of phospho-p38 MAPK at the end of reperfusion were not different in HS as compared to CON hearts. The levels of phospho-p46 JNK and p54 JNK were 1.4- and 1.6-fold less in HS than in CON hearts respectively, p < 0.05. LVDP% was 60.3 (s.e.m., 6.3) for HS and 42.9 (4.1) for CON, p < 0.05. In summary, heat stress pretreatment improves postischaemic recovery of function in isolated rat hearts and this is associated with suppressed JNK activation in response to ischaemia-reperfusion.
Databáze: MEDLINE
Externí odkaz: