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• W2105571225 abstract "p38 mitogen-activated protein kinase (MAPK) activates a number of heat shock proteins (HSPs), including HSP27 and α B -crystallin, in response to stress. Activation of HSP27 or α B -crystallin is known to protect organs/cells by increasing the stability of actin microfilaments. Although our previous studies showed that 17β-estradiol (E 2 ) improves cardiovascular function after trauma-hemorrhage, whether the salutary effects of E 2 under those conditions are mediated via p38 MAPK remains unknown. Male rats (275–325 g body wt) were subjected to soft tissue trauma and hemorrhage (35–40 mmHg mean blood pressure for ∼90 min) followed by fluid resuscitation. At the onset of resuscitation, rats were injected intravenously with vehicle, E 2 (1 mg/kg body wt), E 2 + the p38 MAPK inhibitor SB-203580 (2 mg/kg body wt), or SB-203580 alone, and various parameters were measured 2 h thereafter. Cardiac functions that were depressed after trauma-hemorrhage were returned to normal levels by E 2 administration, and phosphorylation of cardiac p38 MAPK, HSP27, and α B -crystallin was increased. The E 2 -mediated improvement of cardiac function and increase in p38 MAPK, HSP27, and α B -crystallin phosphorylation were abolished with coadministration of SB-203580. These results suggest that the salutary effect of E 2 on cardiac function after trauma-hemorrhage is in part mediated via upregulation of p38 MAPK and subsequent phosphorylation of HSP27 and α B -crystallin." @default.
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• W2105571225 date "2007-06-01" @default.
• W2105571225 modified "2023-09-28" @default.
• W2105571225 title "Role of p38 mitogen-activated protein kinase pathway in estrogen-mediated cardioprotection following trauma-hemorrhage" @default.
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• W2105571225 doi "https://doi.org/10.1152/ajpheart.01303.2006" @default.
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• W2105571225 hasPublicationYear "2007" @default.
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