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1 Institute of Physiology, University of Regensburg, Regensburg, Germany
2 NIDDK, National Institutes of Health, Bethesda, MD, USA
3 Unit 36, INSERM, Paris, France
4 Institute of Anatomy, Charite, Berlin, Germany
* To whom correspondence should be addressed. E-mail: hayo{at}castrop.com.
To assess the feasibility of using the renin promoter for expressing Cre recombinase in JG cells only, we generated 5 independent transgenic mouse lines (designated hRen-Cre) expressing Cre recombinase under control of a 12.2 kb human renin promoter. In the kidneys of adult mice Cre mRNA (RT-PCR) was found in the renal cortex with Cre protein (immunohistochemistry) being localized in afferent arterioles, and to a lower degree in interlobular arteries. Cre mRNA levels were regulated in a renin-typical fashion by changes in oral salt intake, water restriction, or isoproterenol infusion, indicating the presence of key regulatory elements within 12.2 kb of the 5'-flanking region of the human renin gene. hRen-Cre mice were interbred with both the ROSA26-EGFP and ROSA26-lacZ reporter strains to assess renin promoter activity from Cre-mediated excision of a floxed stop-cassette and subsequent EGFP and 
-gal detecetion. In adult mice, -gal staining and EGFP was observed in afferent arterioles and interlobular arteries overlapping with Cre protein expression. In addition, intense -gal staining was found in cortical and medullary collecting ducts where Cre expression was minimal. In embryonic kidneys, -gal staining was detected in the developing collecting duct system beginning at day E12, showing substantial activity of the human renin promoter in the branching ureteric bud. Our data indicate that besides its well known activity in JG cells and renal vessels the human renin promoter is transiently active in the collecting duct system during kidney development complicating the use of this approach for JG cell-specific excision of floxed targets.
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