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World J Gastroenterol. Jan 7, 2014; 20(1): 175-182
Published online Jan 7, 2014. doi: 10.3748/wjg.v20.i1.175
Published online Jan 7, 2014. doi: 10.3748/wjg.v20.i1.175
Bile acid increases expression of the histamine-producing enzyme, histidine decarboxylase, in gastric cells
Hye Jin Ku, Hee Ju Park, Department of Pediatrics, College of Medicine, Pusan National University, Busan 601-721, South Korea
Hye Young Kim, Jae Hun Cheong, Department of Molecular Biology, College of Natural Sciences, Pusan National University, Busan 609-735, South Korea
Hyeong Hoe Kim, Department of Experimental Medicine, College of Medicine, Pusan National University, Busan 601-721, South Korea
Author contributions: All the authors contributed to this manuscript.
Supported by National Research Foundation of Korea grant funded by the Korea government, No. 2009-0093193
Correspondence to: Jae Hun Cheong, PhD, Department of Molecular Biology, College of Natural Sciences, Pusan National University, Busan 609-735, South Korea. molecule85@pusan.ac.kr
Telephone: + 82-51-5102277 Fax: +82-51-5139258
Received: July 14, 2013
Revised: September 16, 2013
Accepted: October 17, 2013
Published online: January 7, 2014
Processing time: 190 Days and 10.7 Hours
Revised: September 16, 2013
Accepted: October 17, 2013
Published online: January 7, 2014
Processing time: 190 Days and 10.7 Hours
Core Tip
Core tip: Histamine production and secretion in the stomach play critical roles in gastric acid secretion and in the pathogenesis of gastric diseases. Bile acids are tumor promoters, and higher levels of bile acids are found in patients with atrophic chronic gastritis and intestinal metaplasia. Increased histidine decarboxylase (HDC), which is a histamine producing enzyme, has been detected in intestinal-type gastric carcinoma. In this study, we provide new evidence that bile acids induce HDC expression in gastric cells and a series of specific transcription factors (farnesoid X receptor, small heterodimer partner, and caudal-type homeodomain transcription factor 1) play critical roles in bile acid-mediated HDC induction.