@article{3083582,
    title = "Involvement of p38 MAPK and JNK in heat stress-induced cardioprotection",
    author = "Pantos, C and Malliopoulou, V and Mourouzis, I and Moraitis, P and and Tzeis, S and Thempeyioti, A and Paizis, I and Cokkinos, A and and Carageorgiou, H and Varonos, DD and Cokkinos, DV",
    journal = "Basic Research in Cardiology",
    year = "2003",
    volume = "98",
    number = "3",
    pages = "158-164",
    publisher = "Dr. Dietrich Steinkopff Verlag GmbH and Co. KG",
    issn = "0300-8428, 1435-1803",
    doi = "10.1007/s00395-003-0399-6",
    keywords = "heat shock; ischaemia-reperfusion; JNK; rat; heart",
    abstract = "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
42degreesC 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-flow 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, beat stress pretreatment improves postischaemic
recovery of function in isolated rat hearts and this is associated with
sup. pressed JNK activation in response to ischaemia-reperfusion."
}