AI Article Synopsis
- HCO3(-) secretion is crucial for protecting the duodenum from acid injury, but the specific transporter responsible for this process is still unknown.
- Recent research has identified several anion exchangers, including DRA, pendrin, and the less understood PAT1.
- Investigations show that PAT1 functions as a Cl(-)/HCO3(-) exchanger, is mainly expressed in the small intestine, and is localized in the brush border membranes of duodenal villus cells.
Article Abstract
HCO3(-) secretion is the most important defense mechanism against acid injury in the duodenum. However, the identity of the transporter(s) mediating apical HCO3(-) secretion in the duodenum remains unknown. A family of anion exchangers, which include downregulated in adenoma (DRA or SLC26A3), pendrin (PDS or SLC26A4), and the putative anion transporter (PAT1 or SLC26A6) has recently been identified. DRA and pendrin mediate Cl(-)/base exchange; however, the functional identity and distribution of PAT1 (SLC26A6) is not known. In these studies, we investigated the functional identity, tissue distribution, and membrane localization of PAT1. Expression studies in Xenopus oocytes demonstrated that PAT1 functions in Cl(-)/HCO3(-) exchange mode. Tissue distribution studies indicated that the expression of PAT1 is highly abundant in the small intestine but is low in the colon, a pattern opposite that of DRA. PAT1 was also abundantly detected in stomach and heart. Immunoblot analysis studies identified PAT1 as a approximately 90 kDa protein in the duodenum. Immunohistochemical studies localized PAT1 to the brush border membranes of the villus cells of the duodenum. We propose that PAT1 is an apical Cl(-)/HCO3(-) exchanger in the small intestine.
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| http://dx.doi.org/10.1152/ajpgi.00338.2001 | DOI Listing |
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