Abstract
The induction of polycystic kidney disease (PKD) by glucocorticoids in newborn mice behaves as a "threshold" trait, with prevalence of PKD varying in different inbred strains after exposure to an inducing steroid. C3H mice (low threshold for PKD) demonstrated greater specific dexamethasone binding than DBA mice (high threshold) on the second day of life. Treatment with methylprednisolone acetate (MPA), a cyst-inducing steroid, down regulated dexamethasone binding earlier than in DBA mice. C3H mice demonstrated greater whole kidney homogenate Na-K ATPase activity than DBA mice within 24h of MPA injection. Specific renal glucocorticoid binding may be a regulator of threshold for murine glucocorticoid induced PKD. Our findings support in vitro evidence that glucocorticoid induced Na-K ATPase activity during critical periods of nephron development is an important regulatory point of this model.
| Original language | English |
|---|---|
| Pages (from-to) | 181-184 |
| Number of pages | 4 |
| Journal | Journal of Steroid Biochemistry and Molecular Biology |
| Volume | 39 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - Aug 1991 |
Bibliographical note
Funding Information:Acknowledgements--We gratefully acknowledge the technical assistance of Susanna McCarthy in animal care and Na-K ATPase assays, and Janie¢ Martin and Sanjay Sareen in preparation of this manuscript. This work was supported by operating grants from the Kidney Foundation of Canada.
ASJC Scopus Subject Areas
- Endocrinology, Diabetes and Metabolism
- Biochemistry
- Molecular Medicine
- Molecular Biology
- Endocrinology
- Clinical Biochemistry
- Cell Biology
PubMed: MeSH publication types
- Journal Article
- Research Support, Non-U.S. Gov't
