INDUCTION OF CALCYCLIN AFTER ISCHEMIC-INJURY TO RAT-KIDNEY

Citation
Ajp. Lewington et al., INDUCTION OF CALCYCLIN AFTER ISCHEMIC-INJURY TO RAT-KIDNEY, American journal of physiology. Renal, fluid and electrolyte physiology, 42(3), 1997, pp. 380-385
Citations number
26
Categorie Soggetti
Physiology
ISSN journal
03636127
Volume
42
Issue
3
Year of publication
1997
Pages
380 - 385
Database
ISI
SICI code
0363-6127(1997)42:3<380:IOCAIT>2.0.ZU;2-3
Abstract
Genes differentially expressed after acute renal ischemic injury were identified using differential display-polymerase chain reaction (DD-PC R). Messenger RNA for calcyclin, a member of the S100 family of calciu m-binding proteins, is increased in kidneys by 6 h following ischemic injury to rats compared with sham surgery. The level of calcyclin mRNA is increased 10-fold by 1 day postinjury and declines thereafter. In situ hybridization demonstrates little calcyclin mRNA in kidneys of sh am-operated rats. However, calcyclin protein is present in glomeruli a nd distal tubules (DT). Compared with kidneys from sham-operated contr ols, both calcyclin mRNA and protein expression are increased at 1-3 d ays following ischemic injury in the thick ascending limb of Henle, th e DT, and in damaged regenerating segments of proximal tubules. By 7 d ays postischemia there is a reduction in mRNA and protein expression. Calcyclin could play a role in the regulation of renal cell proliferat ion and regeneration in the recovery process after acute ischemic inju ry.