Abstract
We have examined the response of the renal insulin-like growth factor (IGF-I) axis to acute ischemic injury in the rat Key findings included a decrease in IGF-I mRNA and peptide levels, a decrease in GH receptor gene plus protein expression and a decrease in the IGF binding proteins except for IGF binding protein 1. Administration of GH to compensate for the reduced GH receptor binding corrected the IGF-I mRNA levels suggesting a relative GH deficiency. Interestingly, IGF-I receptor mRNA levels were unchanged while plasma membrane IGF-I receptor number increased two fold. This appeared to be due to a redistribution of receptors to a 'membrane location. IGF-I receptor autophosphorylation and tyrosine kinase activity were intact despite severe uremia for up to 6 days. We propose that this increase of functional IGF-I receptors following acute tubular necrosis will sensitize the kidney to the administration of exogenous IGF-I.
Original language | English (US) |
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Pages (from-to) | 343-348 |
Number of pages | 6 |
Journal | Renal Failure |
Volume | 20 |
Issue number | 2 |
DOIs | |
State | Published - 1998 |
Keywords
- Acute renal failure
- Insulin-like growth factor
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine
- Nephrology