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1 Surgery, University of Alabama at Birmingham, 35294-0019, Alabama, United States
2 Surgery, University of Alabama at Birmingham, Alabama, United States
3 Surgery, University of Alabama at Birmingham, Birmingham, Alabama, United States; Surgery, University of Alabama at Birmingham, 35294-0019, Alabama, United States
4 Center for Surgical Research, University of Alabama at Birmingham, Birmingham, Alabama, United States
* To whom correspondence should be addressed. E-mail: irshad.chaudry{at}ccc.uab.edu.
p38 mitogen-activated protein kinase (p38 MAPK) activates a number of heat shock proteins (hsps), including hsp27 and 
-crystallin in response to stress. The activation of hsp27 as well as -crystallin is known to protect organ/cells via increasing the stability of actin microfilaments. p38 MAPK also plays an important role in the regulation of apoptosis following cardiac injury. Although our previous studies have shown that 17-estradiol (E2) improves cardiovascular functions following trauma-hemorrhage, it remains unknown whether the salutary effects of E2 under those conditions are mediated via p38 MAPK. To study this, male (275-325 g) rats underwent soft tissue trauma and hemorrhage (mean BP 35-40 mmHg for ~ 90 min) followed by fluid resuscitation. At the onset of resuscitation, rats received intravenously either vehicle, E2 (1 mg/kg BW), E2 and p38 MAPK inhibitor SB203580 (2 mg/kg BW), or SB203580 alone and various parameters were measured at 2 h thereafter. The depressed cardiac functions following trauma-hemorrhage were restored to normal by E2 administration and this was accompanied with increases in cardiac p38 MAPK, hsp27 and -crystallin phosphorylation, but not Bcl-2 and activated caspase 3 expression. The E2-mediated improvement of cardiac function and increased p38 MAPK, hsp27 as well as -crystallin phosphorylation was abolished if SB203580 was administrated along with E2. These results suggest that the salutary effect of E2 on cardiac functions following trauma-hemorrhage is in part mediated via upregulation of p38 MAPK and subsequent hsp27 and -crystallin phosphorylation.
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