TY - JOUR
TI - Involvement of p38 MAPK and JNK in heat stress-induced cardioprotection
AU - Pantos, C
AU - Malliopoulou, V
AU - Mourouzis, I
AU - Moraitis, P and
AU - Tzeis, S
AU - Thempeyioti, A
AU - Paizis, I
AU - Cokkinos, A and
AU - Carageorgiou, H
AU - Varonos, DD
AU - Cokkinos, DV
JO - Basic Research in Cardiology
PY - 2003
VL - 98
TODO - 3
SP - 158-164
PB - Dr. Dietrich Steinkopff Verlag GmbH and Co. KG
SN - 0300-8428, 1435-1803
TODO - 10.1007/s00395-003-0399-6
TODO - heat shock; ischaemia-reperfusion; JNK; rat; heart
TODO - 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.
ER -