Epidermal growth factor inhibits na-pi cotransport in weaned and
suckling rats.
Arar, Mazen, Ihsan Elshihabi, Hubert K. Zajicek And, Moshe Levi, (with
The Technical Assistance Of Myrna Gonzales, and Paul Wilson).
1Department of Pediatrics, University of Texas Health Science
Center at San Antonio, San Antonio, Texas 78284, and 2 Department of
Internal Medicine, University of Texas Southwestern Medical Center at
Dallas and Veterans Affairs Medical Center, Dallas, Texas 75216.
APStracts 5:0166F, 1998.
In the present study we determined the effect of epidermal growth
factor (EGF, 100(mg/100kg body weight) on sodium gradient-dependent
phosphate transport (Na-Pi cotransport) regulation in suckling (12d
old) and weaned (24d old) rats. Weaned rats had higher proximal
tubular brush border membrane vesicle (BBMV) Na-Pi cotransport sodium
gradient-dependent phosphate (Na-Pi) transport activity (2325+/-3516
in weaned versusvs 130+/-922 pmol/10 sec/mg protein in suckling,
p<0.05). Chronic treatment with EGF induced inhibition of BBMV Na
-Pi cotransport in both suckling (130+/-229 versusvs 104+/-167 pmol/10
sec/mg protein, p<0.05) and weaned rats (232+/-1635 versusvs 145+/
-920 pmol/10 sec/mg protein, p<0.005). The inhibitory effect was
selective for Na-Pi cotransport as there was no inhibition of Na
-Glucose cotransport. Weaned rats had Western blot analysis indicated
a higher abundance of BBMV NaPi-2 protein in weaned than in suckling
animals rats (increase of 54%, p<0.001)). Weaned rats and also had
a 2-fold increase in NaPi-2 mRNA. The EGF induced inhibition of Na-Pi
transport was paralleled by decreases in NaPi-2 protein abundance in
both weaned (decrease of 26%, p<0.01) and suckling (decrease of
27%, p<0.01) animals. In contrast, there were no changes in NaPi-2
mRNA abundance. We conclude that proximal tubule BBMV Na-Pi
cotransport activity, NaPi-2 mRNAprotein, and NaPi-2 proteinmRNA
abundance are higher in weaned than in suckling rats. EGF inhibits
Na-Pi cotransport activity in BBMV isolated from suckling and weaned
rats and this inhibition is mediated via a decrease in NaPi-2 protein
abundance, in the absence of a with no change in NaPi-2 mRNA.
Received 24 September 1997; accepted in final form 18 September
1998.
APS Manuscript Number F307-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 20 October 1998