Tissue‐specific Expression of Kir2.1, Clca3 and Aquaporin 4 in Adult and Embryonic Mouse Tissues

Gastric acid secretion occurs when activated parietal cells undergo a dynamic transformation in which tubulovesicles fuse with the apical membrane, resulting in proton secretion into the stomach via the H+/K+‐ATPase. Recent studies have shown that various channels and exchangers also may play a role in the regulation of acid secretion from parietal cells. However, it is unknown precisely when the expression of these genes is initiated in embryonic development, which may give clues as to the timing of early gastric acid secretion. The overall goal of this research was to analyze expression of potassium inward rectifying channel 2.1 (Kir2.1), calcium‐activated chloride channel–3 (Clca3), and the water channel aquaporin‐4 (Aqp4) in mouse adult and embryonic tissues. RT‐PCR was used to analyze expression of these genes in mouse embryos at various stages as well as in adult stomach, heart, small intestine, large intestine, spleen, brain, lung, testes, placenta, liver, skeletal muscle, kidney, skin, thymus, tongue, and eye. Preliminary results showed that Kir2.1 was expressed in the adult brain, heart, fundus, antrum, and spleen, but was not expressed at any of the embryonic stages tested (E11–E16). Clca3 was expressed in all adult tissues tested except for spleen, kidney, and liver, and was expressed in embryos at E11 and E16. Aqp4 was expressed in the brain, fundus, and placenta, and was expressed in embryos at E11 and E16. Further analysis will determine precisely when expression of these genes is initiated in embryonic development, allowing a more thorough understanding of the timing of acid secretion in mammalian development.