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-ESTRADIOL ON T CELL SIGNALING AND CYTOKINE PRODUCTION AFTER TRAUMA-HEMORRHAGE ARE MEDIATED PRIMARILY VIA ESTROGEN RECEPTOR-
1 Center for Surgical Research, University of Alabama at Birmingham, Birmingham, Alabama, United States
2 Anesthesiology, Chang Gung University, Taoyuan, Taiwan - Republic of China
* To whom correspondence should be addressed. E-mail: irshad.chaudry{at}ccc.uab.edu.
Although 17
-estradiol administration following trauma-hemorrhage prevents the suppression in splenocyte cytokine production, it remains unknown whether the salutary effects of 17-estradiol are mediated via estrogen receptor (ER)-
or ER-. Moreover, it is unknown which signaling pathways are involved in salutary effects of 17-estradiol. Utilizing ER- or ER- specific agonist, we examined the role of ER- and ER- in E2-mediated restoration of T cell cytokine production following trauma-hemorrhage. Moreover, since MAPK, NF-
B and AP-1 are known to regulate T cell cytokine production, we also examined the activation of MAPK, NF-B and AP-1. Male rats underwent trauma-hemorrhage (mean arterial pressure 40 mmHg for 90 min) and fluid resuscitation. ER- agonist propyl pyrazole triol (PPT; 5 µg/kg), ER- agonist diarylpropionitrile (DPN; 5 µg/kg), 17-estradiol (50 µg/kg) or vehicle (10% DMSO) was injected subcutaneously during resuscitation. Twenty four hrs thereafter, splenic T cells were isolated, and their IL-2 and IFN-
production and MAPK, NF-B and AP-1 activation were measured. T cell IL-2 and IFN- production was decreased following trauma-hemorrhage and this was accompanied with a decrease in T cell MAPK, NF-B and AP-1 activation. PPT or 17-estradiol administration following trauma-hemorrhage normalized those parameters, while DPN administration had no effect. Since PPT, but not DPN administration following trauma-hemorrhage was as effective as 17-estradiol in preventing the T cell suppression, it appears that ER- plays a predominant role in mediating the salutary effects of 17-estradiol on T cells following trauma-hemorrhage and that such effects are likely mediated via normalization of MAPK, NF-B and AP-1 signaling pathways.
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