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Physiol. Genomics (November 8, 2005). doi:10.1152/physiolgenomics.00133.2005
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Submitted on June 8, 2005
Accepted on November 4, 2005

Gene Expression Profiling of Gastrin Target Genes in Parietal Cells

Renu N Jain1, Cynthia S Brunkan1, Catherine S Chew2, and Linda C Samuelson1*

1 Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA
2 Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA, USA

* To whom correspondence should be addressed. E-mail: lcsam{at}umich.edu.

Previous studies demonstrated that mice with a null mutation in the gene encoding the hormone gastrin have impaired gastric acid secretion. Hence, the aim of this study was to evaluate changes in the acid-secreting parietal cell in gastrin-deficient (GAS-KO) mice. Analysis of several transcripts encoding parietal cell proteins involved in gastric acid secretion showed reduced abundance in the GAS-KO stomach, including H+, K+-ATPase alpha and beta subunits, KCNQ1 potassium channel, aquaporin 4 water channel and creatine kinase B, which were reversed by gastrin infusion for 1 week. Although mRNA and protein levels of LIM and SH3 domain-containing protein 1 (LASP-1) were not greatly changed in the mutant, there was a marked reduction in phosphorylation, consistent with its proposed role as a cAMP signal adaptor protein associated with acid secretion. A more comprehensive analysis of parietal cell gene expression in GAS-KO mice was performed using the Affymetrix U74AV2 chip with RNA from parietal cells purified by flow cytometry to >90%. Comparison of gene expression in GAS-KO and wild type mice identified 47 transcripts that differed by ≥2-fold, suggesting that gastrin affects parietal cell gene expression in a specific manner. The differentially expressed genes included several genes in signaling pathways, with a substantial number (20%) known to be target genes for Wnt and Myc.




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