title: Expression of GH receptor, IGF-I receptor and IGF-I mRNA in the kidney and liver of rats recovering from unilateral renal ischemia.
abstract: The role of the growth-hormone (GH), insulin-like growth factor-I (IGF-I) axis in the kidney has been extensively studied in recent years. To further elucidate the role for GH and IGF-I in renal regeneration, the expression of the GH-rec, IGF-I-rec and IGF-I mRNA was studied in the post-ischemic regenerating kidney and in the liver of the same rats, using a solution hybridization assay. Rats were subjected to 90 min of unilateral renal ischemia followed by reperfusion. The kidneys and livers were collected 1, 3 and 7 days after injury. Five animals were operated on in each group. An additional five animals were sham-operated and killed on day 4. In the kidney, significant alterations were found in the expression of mRNAs for the GH-rec and the IGF-rec. The GH-rec mRNA decreased significantly at day 1 (P < 0.01) to less than one-fifth of the initial value, and normalized at days 3 and 7. The IGF-rec mRNA levels increased more than three-fold at day 3 (P < 0.01) and more than five-fold at day 7 (P < 0.01). In the kidneys there was no significant alteration in the IGF-I mRNA level. In the liver, significant alteration in the level of the GH-rec mRNA was found, while the levels of IGF-rec and the IGF-I mRNA did not change significantly. The levels of GH-rec mRNA increased two-fold at day 3 (P < 0.05), while the levels were unchanged at days 1 and 7. In the early phase of renal regeneration, there is a sharp decrease in the expression of GH-rec mRNA in the kidney. This suggests that there are no direct effects on renal tissue mediated by GH in this situation. There is a significant increase in the intrarenal IGF-I-rec mRNA levels from day 3, suggesting an increased need for IGF-I during regeneration. In the liver, the concentration of GH-mRNA is increased significantly at day 3. These data show on alterations that suggest a role for these factors in renal regeneration.
authors.affiliation: Department of Internal Medicine, Research Center for Endocrinology and Metabolism, University of Göteborg, Sweden.
authors.forename: G L
authors.initials: GL
authors.lastname: Matejka
mesh_terms: D000818:Animals; D003289:Convalescence; D005786:Gene Expression Regulation; D013006:Growth Hormone / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000096:biosynthesis* / Q000235:genetics; D007511:Ischemia / Q000378:metabolism*; D007668:Kidney / Q000098:blood supply / Q000378:metabolism* / Q000502:physiology; D008099:Liver / Q000378:metabolism*; D008297:Male; D009693:Nucleic Acid Hybridization; D012333:RNA, Messenger / Q000096:biosynthesis* / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D017526:Receptor, IGF Type 1 / Q000096:biosynthesis* / Q000235:genetics; D011986:Receptors, Somatotropin / Q000096:biosynthesis* / Q000235:genetics; D012038:Regeneration; D015424:Reperfusion; D012260:Ribonucleases / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D011986:Receptors, Somatotropin; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone; D017526:Receptor, IGF Type 1; D012260:Ribonucleases