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Altered Expression of Renal Sodium‐Phosphate Cotransporter in Mice with Chemically Induced Colitis
Author(s) -
Uno Jennifer K,
Mah Amanda T,
Tooley James E,
Xu Hua,
Kiela Pawel R,
Ghishan Fayez K
Publication year - 2007
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.21.6.a1320-c
Subject(s) - endocrinology , medicine , colitis , cotransporter , chemistry , kidney , inflammation , homeostasis , inflammatory bowel disease , reabsorption , bone remodeling , downregulation and upregulation , sodium , biochemistry , disease , organic chemistry , gene
Reduced bone mass is a common complication of IBD, although the mechanisms contributing to osteopenia are incompletely understood. Skeletal integrity is the result of PO 4 − and Ca 2+ accessibility and the balanced activity of osteoblasts and osteoclasts. While the detrimental effects of inflammation on osteoblasts and osteoclasts are well studied, little is known about alterations in phosphate homeostasis in an inflammatory state. To determine changes in phosphate handling which may contribute to the bone loss observed in individuals with IBD, we studied the expression of renal and intestinal sodium phosphate cotransporters in a mouse model of chemically‐induced colitis. NaPi‐2a and NaPi‐2b expression was evaluated by real‐time PCR, immunohistochemistry and western blotting in kidney and intestine of 6 week old mice administered intrarectally with TNBS or PBS. While no changes were observed for intestinal NaPi‐2b, expression of NaPi‐2a protein in the renal proximal tubules was significantly decreased in TNBS colitis, with no significant change in mRNA expression. Furthermore, expression of NaPi‐2a protein was restored to control values in animals treated with neutralizing anti‐TNFα antibody. These results indicate that in acute chemically induced colitis, renal Pi reabsorption is adversely affected and thus, altered renal phosphate handling may contribute to the abnormal bone metabolism associated with IBD. Supported by R01‐DK33209 .