Anatomical relationships in the patterns of insulin-like growth factor (IGF)-I, IGF binding protein-1, and IGF-I receptor gene expression in the rat kidney.

Endocrinology ◽  
1992 ◽  
Vol 130 (6) ◽  
pp. 3237-3245 ◽  
Author(s):  
E Chin ◽  
J Zhou ◽  
C Bondy
Endocrinology ◽  
1997 ◽  
Vol 138 (3) ◽  
pp. 938-946 ◽  
Author(s):  
Burkhard Tönshoff ◽  
David R. Powell ◽  
Dongling Zhao ◽  
Susan K. Durham ◽  
Michael E. Coleman ◽  
...  

1997 ◽  
Vol 272 (5) ◽  
pp. F661-F667 ◽  
Author(s):  
R. M. Rohan ◽  
T. G. Unterman ◽  
L. Liu ◽  
M. K. Hise

We studied the renal expression of the insulin-like growth factor (IGF) system to gain a better perspective of its potential role in the hyperplastic adaptation of the distal nephron to potassium deficiency. Rats were pair fed 1% or 0.002% potassium diets for periods up to 10 days. IGF-I mRNA was diminished in potassium-deficient rats within 4 days, whereas mRNA for IGF binding protein-1 (IGFBP-1), a collecting duct-associated protein, was increased by day 7. At day 10 mRNA for IGFBP-1 in potassium-deficient animals averaged 2.07 +/- 0.53 (mean +/- SD, relative densitometry units) compared with 0.89 +/- 0.26 in control rats (n = 4, P = 0.002). Conversely, IGFBP-3, a binding protein whose mRNA has been localized to the interstitial compartment, averaged 2.40 +/- 0.02 in potassium-deficient rats and 4.77 +/- 0.05 in controls (n = 4, P < 0.03) at day 10 of treatment. Immunohistochemistry performed using a specific IGFBP-1 antibody revealed hyperplasia of distal nephron segments along with an increase in IGFBP-1 in potassium-depleted rats. These data suggest that IGFBP-1 may play an important role in the control of cellular adaptations in the hypokalemic rat kidney either directly by influencing cell migration or indirectly by localizing IGF-I to the distal nephron.


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