Differential mRNA expression of insulin-like growth factor system during renal injury and hypertrophy

被引:33
作者
Hise, MK
Li, L
Mantzouris, N
Rohan, RM
机构
[1] UNIV MARYLAND, SCH MED, DEPT INTERNAL MED, DIV NEPHROL, BALTIMORE, MD 21201 USA
[2] UNIV MARYLAND, SCH MED, DEPT OBSTET & GYNECOL, DIV REPROD ENDOCRINOL, BALTIMORE, MD 21201 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL FLUID AND ELECTROLYTE PHYSIOLOGY | 1995年 / 269卷 / 06期
关键词
messenger ribonucleic acid; acute kidney failure; carrier proteins;
D O I
10.1152/ajprenal.1995.269.6.F817
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The cellular effects of insulin-like growth factor I (IGF-I) are modified by a family of binding proteins (IGFBPs) that act as reservoirs in serum for the growth factor and are produced locally by tissues, including the kidney. Because regulation of these proteins may influence renal repair, either directly or by their interactions with IGF-I, we studied gene expression during the recovery from renal failure induced by folic acid and during the compensatory increase in renal function following uninephrectomy (UNX). Expression of IGF-I, the IGF-I receptor (IGF-IR), and all six IGFBPs was detected using an ribonuclease protection assay. IGFBP-5 was the most abundant binding protein mRNA present in kidney, whereas IGFBP-2 and -6 were the least abundant. During regeneration following folic acid-induced acute renal failure, IGF-I, IGFBP-3, and IGFBP-5 mRNAs declined in abundance approximately two- to threefold. On the other hand, IGF-IR, IGFBP-1, and IGFBP-2 were increased (similar to 2-, 6-, and 6-fold, respectively) in the first 24 h. IGFBP-1 mRNA remained elevated for at least 3 days. Despite the known increase in cellular RNA content following UNX, little difference in specific expression of mRNAs was observed. Because IGFBP-1 has been shown to stimulate cell migration and has previously been localized to the distal nephron, the site of greatest injury in the folic acid model, these data are compatible with the notion that this protein may function either directly to affect cellular repair or act as a reservoir for IGF-I under conditions of cellular damage.
引用
收藏
页码:F817 / F824
页数:8
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