In vitro modulation of tubular cyst regression in murine polycystic kidney disease. Kidney Int 1989 Dec;36(6):960-8
Date
12/01/1989Pubmed ID
2557482DOI
10.1038/ki.1989.288Scopus ID
2-s2.0-0024852999 (requires institutional sign-in at Scopus site) 26 CitationsAbstract
Recent studies in a murine model of genetically-determined polycystic kidney disease, the CPK mouse, have suggested that alterations in renal Na-K ATPase activity in concert with tubular epithelial hyperplasia have pathogenic import in proximal tubular cyst formation. In the current study, we therefore studied the relative roles of Na-K ATPase activity, tubular epithelial hyperplasia, and basal lamina alterations during in vitro modulation of proximal tubular cyst regression during serum-free organ culture of newborn CPK kidneys. Under basal in vitro conditions, regression of CPK proximal tubular cysts was demonstrated in association with progressive decreases in Na-K ATPase activity and tubular epithelial hyperplasia. The pattern of proximal tubular cyst regression was modified by: a) Na-K ATPase activity induction with triiodothyronine, which promoted proximal tubular cystogenesis; and b) Na-K ATPase activity inhibition with ouabain, which blocked the effects of T3 on the process of cyst formation. Modulation of proximal tubular cystogenesis by Na-K ATPase induction and inhibition were accomplished without significant changes in proximal tubular epithelial hyperplasia or expression of basal lamina components. We conclude that increased Na pump activity may have a significant role in proximal tubular cyst formation and progressive enlargement in the CPK mouse.
Author List
Avner ED, Sweeney WE Jr, Ellis DAuthor
Ellis D. Avner MD Professor in the Pediatrics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsEpithelium
Hyperplasia
Kidney Tubules
Mice
Mice, Inbred Strains
Organ Culture Techniques
Polycystic Kidney Diseases
Sodium Channels
Sodium-Potassium-Exchanging ATPase
