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Am J Physiol Heart Circ Physiol (July 29, 2005). doi:10.1152/ajpheart.00682.2005
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Submitted on June 23, 2005
Accepted on July 26, 2005

PGC-1 UPREGULATION VIA ESTROGEN RECEPTORS: A COMMON MECHANISM OF SALUTARY EFFECTS OF ESTROGEN AND FLUTAMIDE ON HEART FUNCTION FOLLOWING TRAUMA-HEMORRHAGE

Ya-Ching Hsieh1, Shaolong Yang1, Mashkoor A Choudhry1, Huang-Ping Yu1, Loring W Rue1, Kirby I Bland1, and Irshad H Chaudry1*

1 Surgery, University of Alabama at Birmingham, Birmingham, AL, USA

* To whom correspondence should be addressed. E-mail: Irshad.Chaudry{at}ccc.uab.edu.

Flutamide, an androgen receptor antagonist, is thought to improve cardiovascular functions by blocking the androgen receptor following trauma-hemorrhage (T-H). Although 17{beta}-estradiol (E2) and flutamide improve cardiac function following T-H, it is unknown whether E2 and flutamide produce their salutary effect via the same or different mechanism. We hypothesized that both E2 and flutamide mediate their effects via estrogen receptor (ER)-mediated upregulation of PGC-1 [peroxisome proliferator-activated receptor (PPAR{gamma}) coactivator-1]. PGC-1, a key regulator of cardiac mitochondrial function, induces mitochondrial genes by activating transcription factors such as nuclear respiratory factor (NRF)-2 which regulate mitochondrial proteins (i.e., mitochondrial transcription factor A (Tfam), cytochrome c oxidase subunit IV (COX IV), and {beta}-ATP synthase). Adult male rats underwent T-H (5 cm midline incision, hemorrhage (BP 40 mmHg for ~ 90 min) and resuscitation. At the onset of resuscitation, rats received vehicle, flutamide (25 mg/kg), or E2 (50 µg/kg), respectively. Another group received the ER antagonist ICI 182,780 (3 mg/kg) with or without flutamide. Flutamide or E2 administration following T-H restored the depressed cardiac functions. Moreover, E2 and flutamide normalized cardiac PGC-1, NRF-2, Tfam, COX IV, {beta}-ATP synthase expressions, mitochondrial ATP, cytochrome c oxidase activity, mitochondrial DNA (mito DNA)-encoded gene COX I. However, if the ER antagonist ICI 182,780 was administered with flutamide, the flutamide-mediated PGC-1 upregulation was totally abolished. These results indicate that both E2 and flutamide upregulate PGC-1 via ER. Thus, PGC-1 upregulation appears to be the common mechanism by which E2 and flutamide mediate their salutary effects on cardiac function following T-H.




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