Pharmacological and genetic evidence that cathepsin B is not the physiological activator of rodent prorenin
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M. David Percival
Abstract
Renin is the first enzyme in the renin-angiotensin-aldosterone system which is the principal regulator of blood pressure and hydroelectrolyte balance. Previous studies suggest that cathepsin B is the activator of the prorenin zymogen. Here, we show no difference in plasma renin activity, or mean arterial blood pressure between wild-type and cathepsin B knockout mice. To account for potential gene compensation, a potent, selective, reversible cathepsin B inhibitor was developed to determine the role of cathepsin B on prorenin processing in rats. Pharmacological inhibition of cathepsin B in spontaneously hypertensive and double transgenic rats did not result in a reduction in renal mature renin protein levels or plasma renin activity. We conclude that cathepsin B does not play a significant role in this process in rodents.
©2010 by Walter de Gruyter Berlin New York
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Articles in the same Issue
- Minireview
- Physiology and pathophysiology of the RANKL/RANK system
- Genes and Nucleic Acids
- Murine aldo-keto reductase family 1 subfamily B: identification of AKR1B8 as an ortholog of human AKR1B10
- Characterization of plant miRNAs and small RNAs derived from potato spindle tuber viroid (PSTVd) in infected tomato
- Protein Structure and Function
- Characterization of a mutant R11H αB-crystallin associated with human inherited cataract
- Secretion of hepatoma-derived growth factor is regulated by N-terminal processing
- Twin arginine translocation (Tat)-dependent protein transport: the passenger protein participates in the initial membrane binding step
- Kinetic and structural characterization of bacterial glutaminyl cyclases from Zymomonas mobilis and Myxococcus xanthus
- Membranes, Lipids, Glycobiology
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- Molecular Medicine
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- Cell Biology and Signaling
- Acute and long-term effects of metformin on the function and insulin secretory responsiveness of clonal β-cells
- Proteolysis
- Increase of SARS-CoV 3CL peptidase activity due to macromolecular crowding effects in the milieu composition
- Pharmacological and genetic evidence that cathepsin B is not the physiological activator of rodent prorenin
- Acknowledgement
- Acknowledgement
