Parietal cell-selective Slc26a9 deletion in mice results in gastric mucosal immune disorders, which is the key event to development of autoimmune gastritis

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Introduction: Autoimmune gastritis (AIG) is the basis of gastric malignancy, including neuroendocrine tumor (NET) and gastric cancer. We reported that Slc26a9 is highly expressed in parietal cells (PCs), and its deficiency caused gastric cancer.

Aim(s): The present study was undertaken to study a potential role of Slc26a9 downregulation in the development of AIG.

Materials and methods: Slc26a9fl/fl mice were crossed with H+-K+-Atp4b-Cre to produce the PCs-specific Slc26a9 knockout in Slc26a9fl/fl/Atp4b-Cre mice in a mixed genomic background. Flow cytometry analysis, histopathological and immunohistochemical (IHC) analysis with specific markers were performed in Slc26a9fl/fl and Slc26a9fl/fl/Atp4b-Cre mice.

Conference:

Presenting Author: Liu X

Authors: Deng Z, Chen J, Ma Z, Tuo B, Li T,

Keywords: slc26a9, Autoimmune gastritis, gastric neuroendocrine cell,