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Compensatory renal hypertrophy is mediated by a cell cycle-dependent mechanism
Baolian Liu1, Patricia A Preisig
1Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Kidney International
|October 10, 2002
Summary
Compensatory kidney growth after uninephrectomy is hypertrophic, not hyperplastic. This renal proximal tubule growth is driven by cell cycle-dependent mechanisms, not independent ones.
Area of Science:
- Nephrology
- Cell Biology
- Physiology
Background:
- Renal proximal tubule hypertrophy can occur via cell cycle-dependent or -independent mechanisms.
- Uninephrectomy (kidney removal) triggers compensatory growth in the remaining kidney.
Purpose of the Study:
- To determine if compensatory proximal tubule growth after uninephrectomy involves cell cycle-dependent or -independent mechanisms.
Main Methods:
- Studies were conducted in rats and mice following uninephrectomy or sham surgery.
- Hypertrophy was assessed by protein:DNA ratio; hyperplasia by BrdU incorporation.
- Cyclin-dependent kinase (CDK) activities (cdk4/cyclin D, cdk2/cyclin E) were measured.
Main Results:
- Compensatory growth was hypertrophic (increased protein:DNA ratio) with no change in BrdU incorporation in both species.
- CDK4/cyclin D activity increased in rats and mice.
- CDK2/cyclin E activity showed varied changes, and its inhibition did not prevent hypertrophy.
Conclusions:
- Uninephrectomy-induced compensatory proximal tubule growth is primarily hypertrophic.
- This growth is mediated by cell cycle-dependent mechanisms.