Ren-1 and Ren-2 loci are expressed in mouse kidney.

Field, Loren J.; Gross, Kenneth W.

doi:10.1073/pnas.82.18.6196

Cited by 84 publications

(44 citation statements)

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“…Renin mRNA from both renin genes has been shown to be essentially proportional in the renal cortex. 7 Pentz et al 19 deletions lead to a 50% reduction in total renin mRNA. 4 In Sv-129 mice, when the Ren-2 gene was deleted by gene targeting, there was no abnormal morphology and no change in blood pressure.…”

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

“…6 mRNA derived from the two renin genes accumulates in the kidney of two-gene strains in approximately equal levels, 7 and homozygous deletion of Ren-1 d reduces total renin mRNA by 50% within the kidney. 7 However, in mice with two renin genes, Ren-1 d gene expression is reported to be higher (70% to 80% of total), and is thought to be the source of the renin activated in JG cell granules and released constitutively in response to classic renin-stimulating pathways. 8 Using chronically uninephrectomized inbred mice, similar with the exception that they had either one or two renin genes, Wang et al 9 reported that mice with two renin genes had much higher plasma renin concentration (PRC) than mice with only one renin gene.…”

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Cardiovascular and Renal Phenotype in Mice With One or Two Renin Genes

et al. 2004

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Abstract-We compared the phenotype of two common mouse models, C-57BL/6J (C57), which carries only the Ren-1 c gene, and 129/SvJ (Sv-129), with both Ren 1 d and Ren-2. We hypothesized two renin gene Sv-129 would have increased blood pressure and the renin-angiotensin system would be more influential in regulating renal function compared with one renin gene mice. Sv-129 consistently had higher blood pressure than C-57, whether conscious (128 versus 108 mm Hg, PϽ0.001) or anesthetized (102 versus 88 mm Hg, PϽ0.001). Plasma renin concentration in both conscious and anesthetized C-57 mice was 3-to 4-fold higher than in Sv-129 (PϽ0.05), whereas renal cortical renin content was 2.5-fold higher (PϽ0.005). Renal blood flow and renal vascular resistance were the same in C-57 and Sv-129. Exogenous angiotensinogen produced identical pressor and renal vasoconstrictor responses in both strains. Blocking AT 1 receptors with losartan reduced blood pressure by 19 mm Hg in both strains. Nitric oxide synthase inhibition by L-NAME increased blood pressure by 29 mm Hg in C-57 and 35 mm Hg in Sv-129 mice, but the decrease in renal blood flow was 30% less in C-57 (PϽ0.025). We conclude that Sv-129 mice with two renin genes have higher blood pressure but lower plasma and renal renin than C-57 mice with one renin gene. Renin substrate may limit angiotensin II production in the mouse. In Sv-129, the influence of nitric oxide on renal but not systemic resistance may be exaggerated. Renin from Ren-2 may act independently of normal renin control mechanisms. Key Words: angiotensin Ⅲ angiotensinogen Ⅲ endothelium Ⅲ mouse Ⅲ nitric oxide Ⅲ nitric oxide synthase Ⅲ renin T he potent vasoconstrictor hormone angiotensin II (AngII) is the active product of the renin-angiotensin system. AngII is typically produced through the rate-limiting cleavage of the substrate angiotensinogen by the enzyme renin.

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Cardiovascular and Renal Phenotype in Mice With One or Two Renin Genes

et al. 2004

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“…Studies aimed at defining the DNA sequences involved in the control of both Ren-1C/D and Ren-2 expression have been hampered by the unavailability of a renin-producing cell line for DNA transfection. The renin-producing cells of the juxtaglomerular apparatus represent only 0.1% of the kidney cell population (4). However, a Ren-2 transgene comprising the transcriptional unit plus 2.5kb of upstream and 3kb of downstream sequence is sufficient to direct expression to both the kidney and SMG in transgenic mice.…”

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confidence: 99%

Differential extra-renal expression of the mouse renin genes

Miller¹,

Carter²,

Brooks³

et al. 1989

Nucl Acids Res

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We have used RNase-protection analyses to study renin gene expression in one-and two-gene mouse strains. The RNase-protection assay is capable of discriminating between the transcripts from the different renin genes. In a two-gene strain containing Ren-1D and Ren-2, we demonstrate transcriptional activity from Ren-ID in kidney, submandibular gland (SMG), testes, liver, brain and heart. Ren-2 is clearly expressed in kidney, SMG and testes. Similar analyses of one gene strains (containing show expression in kidney, SMG, testes, brain and heart. We cannot detect renin mRNA in the liver of these mice.Ren-1C and Ren-1D thus display quite different tissue-specificities. In order to determine whether the different tissue-specificities of the highly homologous Ren-lC and Ren-1D genes are due to different trans-acting factors in the different mouse strains or to different cis-acting DNA elements inherent to the genes, we introduced a Ren-11D transgene (Ren-l*) into a background strain containing only the Ren-1C gene. The transgene exhibits the same tissue-specificity as the Ren-1D gene of two-gene strains suggesting the presence of different cis-acting DNA elements in Ren-1C and Ren-1D. INTRODUCTIONThe aspartyl protease renin catalyses the initial and rate-limiting step in the conversion of angiotensinogen to the vasoactive hormone angiotensin II and thus plays a key role in the regulation of blood pressure (1). The primary site of renin biosynthesis is the juxtaglomerular apparatus of the kidney.

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“…3,4 In addition, a limited spectrum of extrarenal sites of tissue-renin production, including the adrenal gland, testes, ovaries, coagulating gland, liver, and submandibular gland (SMG), has also been identified. 5 The most dramatic difference in Ren-1 and Ren-2 expression has been noted in the SMG.…”

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Evaluating a Model of an NRE Mediated Tissue-Specific Expression of Murine Renin Genes

et al. 2001

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Abstract-We have used comparative sequence analysis to evaluate a putative silencer element that has been proposed to be involved in the differential tissue-expression of the murine renin genes: Ren-1 and Ren-2. In the mouse, these genes share a similar pattern of tissue-specific renin expression. One significant difference is seen in the submandibular gland (SMG) where renin expression from the Ren-2 locus is 100-fold greater than the expression from the Ren-1 locus. One model proposes that this differential expression arises from the interplay among a negative regulatory element and a cAMP responsive element, their respective binding factors, and the disruption of the negative regulatory element by an insertion (M2) that is found in Ren-2 but not in Ren-1. enin is an important regulatory enzyme involved in blood pressure maintenance and electrolyte homeostasis. It catalyzes the first reaction in the production of angiotensin II, a potent vasoactive hormone that is directly involved in both the circulating and tissue-specific renin-angiotensin systems. Many inbred strains of mice, such as DBA/2, which are derived from M. domesticus and M. musculus, possess an additional copy of the renin gene. This second locus arose as a tandem duplication to Ren-1. 1,2 Precisely the same duplication event is observed in the closely related subspecies M. hortulanus and M. spretus. 3 In these mouse species, the 2 renin genes, Ren-1 and Ren-2, share overlapping but nonidentical patterns of tissue-specific expression.The primary site of synthesis for circulating renin in all mouse strains is the kidney. Multiple alleles from both Ren-1hortulanus allele) and Ren-2 (Ren-2 d ϭ Renin-2 DBA/2J allele, Ren-2 h ϭ Renin-2 M. hortulanus allele) are expressed at approximately equal levels in the kidneys from 1-or 2-gene strains of mice. 3,4 In addition, a limited spectrum of extrarenal sites of tissue-renin production, including the adrenal gland, testes, ovaries, coagulating gland, liver, and submandibular gland (SMG), has also been identified. 5 The most dramatic difference in Ren-1 and Ren-2 expression has been noted in the SMG. In 2-gene strains of mice (DBA2/J and M. hortulanus), Ren-2 expression is Ͼ100-fold higher than expression of Ren-1 transcripts. Overall, the Ren-2 d and Ren-2 h alleles show a similar expression pattern as judged by the examination of a number of tissues, including SMG, kidney, testes, coagulating gland, and liver. Ren-1 d and Ren-1 h also share a similar pattern of renin expression, differing only in the increased expression of Ren-1 h in the liver relative to Ren-1 d . 5 Dzau and his colleagues 6 -9 have proposed that the similarities seen for Ren-2 and Ren-1 expression in the kidney, versus the differences seen in the SMG of DBA/2J, result from the complex interplay among a negative regulatory element (NRE), a cAMP responsive element (CRE), and their

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Ren-1 and Ren-2 loci are expressed in mouse kidney.

Cited by 84 publications

References 19 publications

Cardiovascular and Renal Phenotype in Mice With One or Two Renin Genes

Cardiovascular and Renal Phenotype in Mice With One or Two Renin Genes

Differential extra-renal expression of the mouse renin genes

Evaluating a Model of an NRE Mediated Tissue-Specific Expression of Murine Renin Genes

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