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The cytosolic calcium ([Ca2+]cyt) is one of the most important cell signaling that can modulate gastrointestinal (GI) epithelial secretion and promote GI mucosal wound repair. The GI mucosal bicarbonate secretion is the main mechanism of mucosal protection. Our research team has been working in this field and provided solid evidence for the important role of Ca2+ signaling in the regulation of GI epithelial secretion and the underlying molecular mechanisms. In this review, we attempt to systemically review the current status of our knowledge on the role of Ca2+ signaling in the regulation of intestinal bicarbonate secretion and in the upper GI epithelial protection. We expect that novel targets could be identified for drug development to better protect GI mucosa and treat mucosal injury with the advance in this filed.

// Xin Yang 1 , Yanjun Guo 1 , Jialin He 1 , Fenglian Zhang 1 , Xuemei Sun 1 , Shiming Yang 1 and Hui Dong 1, 2 1 Department of Gastroenterology, Xinqiao Hospital, Third Military Medical University, Chongqing, P.R. China 2 Division of Gastroenterology, Department of Medicine, School of Medicine, University of California, San Diego, California, USA Correspondence to: Hui Dong, email: h_uidong@163.com Keywords: estrogen, estrogen receptors, HCO 3 - secretion, Cl - secretion Received: April 15, 2017 Accepted: May 22, 2017 Published: May 31, 2017 ABSTRACT Gastrointestinal (GI) epithelial ion transport is physiologically important in many aspects of humans, such as in maintaining fluid balance of whole body, and also plays a role in the development and progression of common GI disease. Estrogen and estrogen receptors have been shown to modulate the activity of epithelial ion secretion in GI tract. This review aims to address the current state of knowledge about the role of estrogen and estrogen receptors in modulation of GI epithelial secretion and to elucidate the underlying mechanisms. We highlight the recent findings regarding the importance of estrogen and estrogen receptors in GI epithelia protection and body fluid balance by modulation of gastrointestinal epithelial HCO 3 - and Cl - secretion, especially current information about the regulatory mechanisms of duodenal HCO 3 - secretion based on our study in this field. Since there are no reviews on this topic but only few papers to address the main issues, we hope to timely provide new perspectives for the association between estrogen and GI disease.