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1 Division of Research and Education, Scott & White Hospital, Temple, TX, USA
2 Department of Clinical Medicine, University of Rome, "La Sapienza", Polo Pontino, Latina, Italy
3 Division of Gastroenterology, Tohoku University School of Medicine, 1-1 Seiryo, Aobaku, Sendai, Japan
4 Department of Gastroenterology, Polytechnic University of Marche, Ancona, Italy Ancono, Italy
5 Central Texas Veterans Health Care System, Temple, TX, USA
6 Department of Medical Physiology, The Texas A&M University System Health Science Center, College of Medicine, Temple, TX, USA
7 Central Texas Veterans Health Care System, Temple, TX, USA; Department of Medicine and Medical Physiology, The Texas A&M University System Health Science Center, College of Medicine, Temple, TX, USA; Department of Medical Physiology, The Texas A&M University System Health Science Center, College of Medicine, Temple, TX, USA
* To whom correspondence should be addressed. E-mail: Galpini{at}tamu.edu.
Loss of parasympathetic innervation after vagotomy impairs cholangiocyte proliferation, which is associated with depressed cAMP levels, impaired ductal secretion, and enhanced apoptosis. Agonists that elevate cAMP levels prevent cholangiocyte apoptosis and restores cholangiocyte proliferation and ductal secretion. No information exists regarding the role of adrenergic innervation in the regulation of cholangiocyte functions. In the present studies, we investigated the role of adrenergic innervation on cholangiocyte proliferative and secretory responses to bile duct ligation (BDL). Adrenergic denervation by treatment with 6-OHDA during BDL decreased cholangiocyte proliferation and secretin-stimulated ductal secretion with concomitant increased apoptosis, which was associated with depressed cholangiocyte cAMP levels. Chronic administration of forskolin (an adenylyl cyclase activator) or beta 1 and beta 2 adrenergic receptors agonists (clenbuterol or dobutamine) prevented the decrease in cholangiocyte cAMP levels, maintained cholangiocyte secretory and proliferative activities and decreased cholangiocyte apoptosis due to adrenergic denervation. This was associated with enhanced phosphorylation of Akt. The protective effects of clenbuterol, dobutamine and forskolin on 6-OHDA-induced changes in cholangiocyte apoptosis and proliferation were partially blocked by chronic in vivo administration of wortmannin. In conclusion, we propose that adrenergic innervation plays a role in the regulation of biliary mass and cholangiocyte functions during BDL by modulating intracellular cAMP levels.
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