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Renin Gene (renin + gene)

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Life Sciences	83%

Selected Abstracts

Plasma renin in mice with one or two renin genes

ACTA PHYSIOLOGICA, Issue 4 2004
P. B. Hansen
Abstract Aim:, In the present study we have investigated whether the presence of a second renin gene exerts an overriding influence on plasma renin such that mice with two renin genes have consistently higher renin levels than mice with only one renin gene. Methods:, Plasma renin was determined as the rate of angiotensin I generation using a radioimmunoassay (RIA) kit with (plasma renin concentration, PRC) or without (plasma renin activity, PRA) the addition of purified rat angiotensinogen as substrate. Results:, In male 129SvJ, DBA/2 and Swiss Webster mice, strains possessing both Ren-1 and Ren-2, PRC (ng Ang I mL,1 h,1) averaged 178 ± 36, 563 ± 57 and 550 ± 43 while PRA was 2.9 ± 0.5, 3.6 ± 0.8 and 7.8 ± 1.2. In male C57BL/6, C3H and BALB/c mice that express only Ren-1, PRC averaged 426 ± 133, 917 ± 105 and 315 ± 72, and PRA was 3.4 ± 1.0, 6.9 ± 1.7 and 4.5 ± 1.2. In the two renin gene A1AR,/, mice compared with the one renin gene A1AR+/+, PRC averaged 538 ± 321 and 415 ± 159 while PRA averaged 3.2 ± 1.1 and 4.4 ± 1.4 ng Ang I mL,1 h,1. Aldosterone levels showed no significant differences between one renin (C57BL/6, C3H and BALB/c) and two renin (129SvJ, DBA/2 and Swiss Webster) gene mice. Furthermore, by quantitative real-time polymerase chain reaction (RT-PCR) we found no correlation between the number of renin genes and whole kidney renin mRNA levels from one and two renin gene mice. Conclusion:, Our data show that baseline plasma renin is not systematically higher in mice with two renin genes than in one renin gene mice. Thus, the presence of a second renin gene does not seem to be a major determinant of differences in PRC between different mouse strains. [source]

Candidate cis -elements for human renin gene expression in the promoter region

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2004
Tadashi Konoshita
Abstract The regulation of renin gene expression, the rate-limiting enzyme of the system, is thought to be fundamental to the total system. Previously, we mapped six putative cis -elements in the promoter region of the human renin gene with nuclear proteins from human chorionic cells and human renal cortex by DNase I protection assay (footprint A,F). Each footprint contains Ets motif like site (A), HOXñPBX recognition sequence (B), unknown sequence as DNA binding consensus (C), CRE (D), COUP-TFII (ARP-1) motif like site (E), and AGE3 like site (F). Footprint D has been characterized by means of functional studies as the genuine human renin gene CRE interacting with CREB in cooperation with the site of footprint B. To obtain further clues to the specific expression in the promoter region, these putative cis -elements were conducted to a consensus-specific binding assay to compare renin-producing and non-renin-producing cells by EMSA and electromobility super-shift assay. Different sequence-specific DNA/protein binding was obtained among the different cell lines with footprint B site, with COUP-TFII (ARP-1) motif like site and possibly with footprint F site. The results implicate these putative cis -elements and each corresponding trans -factor in the specific expression of the human renin gene in the promoter region. Further functional characterization of these elements would provide important data for a better understanding of human renin gene expression. © 2004 Wiley-Liss, Inc. [source]

Renin: from ,pro' to promoter

BIOESSAYS, Issue 5 2003
Brian J. Morris
Renin is the rate-limiting enzyme in a cascade that leads to production of angiotensin II, which is perhaps our most important regulator of salt and water balance and blood pressure. In this personal perspective, I describe how I entered the renin field 33 years ago by discovering that proteases increased the level of renin activity in biological fluids, so revealing the existence of a ,pro' form of the molecule. This led me on a journey that encapsulated all of the major milestones in molecular discovery for renin. These included (1) the elucidation of the steps in renin biosynthesis, (2) the cloning of renin cDNA and its gene, (3) demonstration of the structure of the renin protein, (4) using the renin gene in the first genetic studies in hypertension, (5) finding the mechanism by which the major controller, cyclic AMP, regulates the promoter, (6) showing that a strong enhancer and its weak promoter control this physiologically regulatable gene in accord with the variegation (on/off switching) model, and (7) being the first to identify molecules involved in posttranscriptional control. The renin molecule, its gene and molecular control are now very well understood, but more fine details on the topic of renin continue to emerge to delight ,reninologists' and others. BioEssays 25:520,527, 2003. © 2003 Wiley Periodicals, Inc. [source]

FLUORESCENCE ACTIVATED CELL SORTING OF TRANSIENTLY TRANSFECTED As4.1 CELLS SHOWS RENIN ENHANCER DIRECTS ON/OFF SWITCHING OF RENIN PROMOTER IN VITRO

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2008
Brian J MorrisArticle first published online: 27 FEB 200
SUMMARY 1The proximal promoter of the renin gene is weak and its activity is influenced by a strong, far-upstream enhancer. This and the ability of renin expression in renal afferent arteriolar cells to be ,recruited' under chronic stimulation is consistent with the on/off switching (variegation) model of gene expression. If true, this would provide an example in which variegation controls a physiologically regulable gene. 2The present study tested the hypothesis that renin promoter activity may accord with the variegation model, at least in individual juxtaglomerular (mouse As4.1) cells in vitro. 3As4.1 cells were transiently transfected with constructs containing the mouse renin (Ren-1c) enhancer adjacent to the Ren-1c promoter and a linked reporter gene encoding enhanced green fluorescent protein (EGFP). The EGFP signal from individual cells was monitored by fluorescence activated cell sorting. 4In the presence of the renin enhancer there was 10-fold higher EGFP expression in transfected cells compared with cells transfected with EGFP constructs containing the promoter alone. There was, moreover, an 8-fold increase in the number of EGFP expressing cells. However, EGFP expression in individual transfected cells was similar in the presence or absence of the enhancer. 5Results from the in vitro system used suggest that the Ren-1c enhancer does not regulate the rate of promoter activity, but rather increases the probability of achieving an active transcriptional state. Limitations of these findings are discussed. [source]