Differential expression, abundance, and regulation of na+
-phosphate cotransporter genes in murine kidney.
Tenenhouse, Harriet S., St[acute]ephane Roy, Jos[acute]ee Martel, and
Claude Gauthier.
Medical Research Council Genetics Group, McGill University-Montreal
Children's Hospital Research Institute, Departments of Pediatrics and
Biology, McGill University, Montreal, Quebec H3H 1P3, Canada
APStracts 5:0122F, 1998.
Three classes of high affinity Na+-Pi cotransporters are expressed in
mammalian kidney. These include Npt1 (type I), Npt2 (type II) and the
cellular receptors for gibbon ape leukemia virus (Glvr-1) and
amphotropic murine retrovirus (Ram-1) (type III). We defined the
tissue distribution as well as the relative renal abundance of Npt1,
Npt2, Glvr-1 and Ram-1 mRNAs and examined the effects of low Pi diet,
the Hyp mutation and growth hormone (GH) on their renal expression by
ribonuclease protection assay. In normal mouse kidney, Npt1, Npt2,
Glvr-1 and Ram-1 accounted for 15 + 1.0, 84 + 1.0, 0.5 + 0.2 and 0.5
+ 0.3 percent of total Na+-Pi cotransporter mRNAs, respectively.
Evidence was obtained for low abundance Npt1 mRNA expression in liver
and Npt2 mRNA expression in intestine whereas Glvr-1 and Ram-1 mRNAs
were also detected in bone, intestine, heart and liver. Npt2 mRNA was
localized to proximal tubules in the renal outer cortex whereas Glvr
-1 transcripts were detected throughout the kidney by in situ
hybridization. The Hyp mutation elicited a significant reduction in
renal Npt1 and Npt2 mRNAs (78 + 8 and 57 + 3 percent of normal,
respectively), whereas neither low Pi diet nor GH influenced the
renal abundance of Npt1 and Npt2 transcripts. Renal Glvr-1 mRNA
expression was significantly increased in Hyp mice and GH-treated
mice (145 + 6 and 165 + 5 percent of control, respectively) while the
renal abundance of Ram-1 transcript was unaffected by either the Hyp
mutation, low Pi diet or GH treatment. In summary, we demonstrate
that Npt2 is the predominant Na+-Pi cotransporter in mouse kidney,
that Npt2 and Glvr-1 have distinct patterns of renal expression, and
that the Hyp mutation modulates the renal expression of Npt1, Npt2
and Glvr-1 mRNAs. Our results suggest that increased renal Glvr-1
mRNA may contribute to GH stimulation of renal Na+-Pi cotransport.
Received 8 May 1998; accepted in final form 2 July 1998.
APS Manuscript Number F111-8.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 30 July 1998