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

Autor: Dennis Varonos, Panagiotis Moraitis, Ioannis Paizis, Anastasia Thempeyioti, Iordanis Mourouzis, Hariclia Carageorgiou, Stylianos Tzeis, Dennis V. Cokkinos, Constantinos Pantos, Vassiliki Malliopoulou, Alexandros D. Cokkinos
Rok vydání: 2003
Předmět:
Zdroj: Basic Research in Cardiology. 98:158-164
ISSN: 1435-1803
0300-8428
DOI: 10.1007/s00395-003-0399-6
Popis: 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, p0.05. LVDP% was 60.3 (s.e.m., 6.3) for HS and 42.9 (4.1) for CON, p0.05. 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: OpenAIRE
Externí odkaz: