James L. Boyer, M.D.

Ensign Professor of Medicine
Director, Liver Center
Section of Digestive Diseases, Department of Internal Medicine
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Research Interests

Our laboratory has a long standing interest in the basic physiology of bile formation and the pathophysiologic mechanisms underlying mechanisms of cholestasis. Bile formation is one of the unique functions of the liver and is impaired in many forms of cholestatic liver injury. Our early studies established that the hepatocyte is a polarized secretory cell where transport mechanisms are organized on plasma membrane domains like a classic epithelium (Physiologic Reviews 60:303-326, 1980). This concept has led to the identification and characterization of a number of membrane transport proteins both at the functional level and through molecular cloning techniques that determine the secretion of bile (Physiologic Reviews 83:633-671, 2003). Current studies focus on adaptive responses of hepatobiliary transporters to cholestasis and involve both studies of nuclear receptor transcriptional and post-transcriptional regulators. Trainees utilize a variety of fundamental techniques ranging from general cell biologic and molecular biologic procedures to advanced morphologic approaches including fluorescent and confocal scanning microscopy. This research is supported by NIH grants and core facilities provided by an NIH Liver Center.

Selected Publications

• Trauner M, and Boyer JL. 2003. Bile salt transporters: molecular characterization, function, and regulation. Physiol. Rev. Apr;83(2):633-71.
• Bohan A, Chen W-S, Denson LA, Held MA and Boyer JL. 2003. Tumor Necrosis Factor a-dependent Up-regulation of Lrh-1 and Mrp3(Abcc3) Reduces Liver Injury in Obstructive Cholestasis. J. Biol. Chem.278(38):36688-36698.
• Mennone A, Verkman AS, and Boyer JL. 2002. Unimpaired osmotic water permeability and fluid secretion in bile duct epithelia of AQP1 null mice. Am. J. Physiol. 283 :G739-G746.
• Denson LA, Bohan A, Held MA, and Boyer JL. 2002. Organ-specific alterations in RAR alpha:RXR alpha abundance regulate rat Mrp2 (Abcc2) expression in obstructive cholestasis. Gastroenterology 123 (2):599-607.
• Wang L, Soroka CJ, and Boyer JL. 2002. The role of bile salt export pump mutations in progressive familial intrahepatic cholestasis type II. J. Clin. Invest.110:965-972.
• Bohan A and Boyer JL. 2002. Mechanisms of Hepatic Transport of Drugs: Implications for Cholestatic Drug Reactions. Semin. Liver Dis.22: 123-136.
• Boyer JL. 2002. Milestones in Liver Disease. A commentary: Sperber I. Secretion of organic anions in the formation of urine and bile [Pharmacol. Rev. 1959;11:109-134]. J. Hepatol. 36: 4-7.
• Lee J, Azzaroli F, Wang L, Soroka C, Gigliozzi A, Setchell KDR, Kramer W, and Boyer JL. 2001. Adaptive Regulation of Bile Salt Transporters in Kidney and Liver in Obstructive Cholestasis in the Rat. Gastroenterology 121: 1473-1484.
• Wang W, Seward D, Li L, and Boyer JLJanuary 15, 2008 together mediate organic solute and steriod transport in the liver of a marine vertebrate. Proc. Natl. Acad. Sci. U.S.A.98: 9431-9436.
• Cai S-Y, Wang L, Ballatori N , and Boyer JL. 2001. Bile salt export pump is highly conserved during vertebrate evolution and its expression is inhibited by PFIC type II mutations. Am. J. Physiol. Gastrointest. Liver Physiol. 281: G316-G322.
• Soroka CJ, Lee JM, Azzaroli F, and Boyer JL. 2001. Cellular localization and up-regulation of multidrug resistance-associated protein 3 in hepatocytes and cholangiocytes during obstructive cholestasis in rat liver. Hepatology 33: 783-791.
• Boyer JL. 2001. Advancing the bile-ology of cholestatic liver disease. Hepatology 33: 758-759.
• Mennone A, Biemesderfer D, Negoianu D, Yang C-L, Abbiati T, Schultheis PJ, Shull GE, Aronson PS, and Boyer JL. 2001. Role of sodium/hydrogen exchanger isoform NHE3 in fluid secretion and absorption in mouse and rat cholangiocytes. Am. J. Physiol. Gastrointest. Liver Physiol. 280: G247-G254.
• Cho WK, Mennone A, and Boyer JL. 2001. Isolation of functional polarized bile duct units from mouse liver. Am. J. Physiol. Gastrointest. Liver Physiol. 280: G241-G246.
• Lee J and Boyer JL. 2000. Molecular alterations in hepatocyte transport mechanisms in acquired cholestatic liver disorders. Semin. Liver Dis. 20: 373-384.
• Gigliozzi A, Fraioli F, Sundaram P, Lee J, Mennone A, Alvaro D, and Boyer JL. 2000. Molecular identification and functional characterization of Mdr1a in rat cholangiocytes. Gastroenterology 119: 1113-1122.
• Schlosser SF, Azzaroli F, Dao T, Hingorani R, Crispe IN, and Boyer JL. 2000. Induction of murine hepatocyte death by membrane-bound CD95 (Fas/APO-1)-ligand: Characterization of an in vitro system. Hepatology32: 779-785.
• Lee JM, Trauner M, Soroka CJ, Stieger B, Meier PJ, and Boyer JL. 2000. Expression of the bile salt export pump is maintained after chronic cholestasis in the rat. Gastroenterology118: 163-172.
• Ballatori N, Rebbeor NF, Connolly GC, Seward DJ, Lenth BE, Henson JH, Sundaram P, and Boyer JL. 2000. Bile salt excretion in skate liver is mediated by a functional analog of Bsep/Spgp, the bile salt export pump. Am. J. Physiol. Gastrointest. Liver Physiol. 278: G57-G63.
• Trauner M, Meier PJ, and Boyer JL. 1998. Molecular pathogenesis of cholestasis. N. Engl. J. Med.339: 1217-1227.

Contact

Campus Address
Yale University School of Medicine
333 Cedar Street (1080 LMP)
P. O. Box 208019
New Haven, CT 06510

Office Location
One Gilbert Street
TAC Bldg., Room #S241C
New Haven, CT 06519

E-mail
james.boyer@yale.edu

Office Phone
203-785-5279

Fax
203-785-7273