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Testosterone down‐regulates sodium‐hydrogen exchanger isoform 8 (NHE8) expression
Author(s) -
Xu Hua,
Zhang Bo,
Li Jing,
Tong Weiqun,
Chen Huacong,
King Nolan,
Ghishan Fayez K
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1007.9
Subject(s) - endocrinology , medicine , testosterone (patch) , rna , gene expression , biology , hormone , western blot , messenger rna , estrogen , sodium–hydrogen antiporter , gene isoform , gene , andrology , sodium , chemistry , biochemistry , organic chemistry
NHE8 is the newest member of the sodium‐hydrogen exchanger family. It is expressed in intestinal and renal epithelial cells. We have shown that NHE8 is important for intestinal sodium absorption early in life and that its expression is regulated by many physiological factors. Since studies have shown that certain genes are regulated differently by gender, we investigated if NHE8 is one of these genes. Therefore, we compared NHE8 expression in male and female mice. RNA and brush‐border membrane protein were isolated from the intestinal mucosa of mice. Real‐time PCR was used to determine NHE8 mRNA levels, and Western blot was used to determine NHE8 protein levels. We performed the same experiments on Caco2 cells to study the effect of sex hormones on NHE8 expression. Our results showed that at four weeks of age, RNA and protein expression of NHE8 was similar between male and female mice, but at eight weeks of age, RNA and protein expression of NHE8 was significantly reduced by ~50% in male mice compared to female mice. In Caco2 cells, estrogen (100nM, 18 hours) had no effect whereas testosterone (100nM, 18 hours) inhibited NHE8 expression at RNA and protein levels that are comparable with the in vivo observations. In conclusion, our results suggest that NHE8 expression differs between male mice and female mice. The difference is likely due to testosterone's inhibitory effect. Our study was supported by NIH grant R01DK073638.