Identity of the renin cell is mediated by cAMP and chromatin remodeling: an in vitro model for studying cell recruitment and plasticity

Pentz, Ellen S.; López, María Luisa S. Sequeira; Cordaillat, Magali; Gómez, R. Ariel

doi:10.1152/ajpheart.01152.2007

Cited by 69 publications

(110 citation statements)

References 47 publications

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“…We have previously shown that the cAMP/CBP/p300/CREB pathway is fundamental in the control of renin synthesis and release. 4,22 A similar analysis was also performed for the renin enhancer ( Figure 6B) that begins at Ϫ2500 for the mouse and Ϫ11,015 for the human, and, in each case, extends about 275 bases further 5Ј. The presence of an estrogen response element (V$EREF) is intriguing.…”

Section: Transcriptional Control Of the Renin Phenotypementioning

confidence: 84%

“…4 We isolated YFP ϩ cells from the kidney of newborn and adult mice, and from adult mice subjected to a physiologic challenge that elicits the retransformation of arteriolar smooth muscle cells (aSMCs) to the renin phenotype, and compared their gene profiles to those from multiple cell types of the nephron at variousstagesofdevelopment(Figure1B). 5 Finally,todefinewhether the set of genes expressed by the renin cell located at the pole of the glomerulus-the bonafide adult JG cell-is different from the set of genes expressed by other renin cells, we developed a single cell isolation and amplification procedure that allowed us to uncover the expression profile of the classical JG cell.…”

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confidence: 99%

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Genes that Confer the Identity of the Renin Cell

Brunskill

Sequeira-Lόpez

Pentz

et al. 2011

Journal of the American Society of Nephrology

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Renin-expressing cells modulate BP, fluid-electrolyte homeostasis, and kidney development, but remarkably little is known regarding the genetic regulatory network that governs the identity of these cells.Here we compared the gene expression profiles of renin cells with most cells in the kidney at various stages of development as well as after a physiologic challenge known to induce the transformation of arteriolar smooth muscle cells into renin-expressing cells. At all stages, renin cells expressed a distinct set of genes characteristic of the renin phenotype, which was vastly different from other cell types in the kidney. For example, cells programmed to exhibit the renin phenotype expressed Akr1b7, and maturing cells expressed angiogenic factors necessary for the development of the kidney vasculature and RGS (regulator of G-protein signaling) genes, suggesting a potential relationship between renin cells and pericytes. Contrary to the plasticity of arteriolar smooth muscle cells upstream from the glomerulus, which can transiently acquire the embryonic phenotype in the adult under physiologic stress, the adult juxtaglomerular cell always possessed characteristics of both smooth muscle and renin cells. Taken together, these results identify the gene expression profile of renin-expressing cells at various stages of maturity, and suggest that juxtaglomerular cells maintain properties of both smooth muscle and renin-expressing cells, likely to allow the rapid control of body fluids and BP through both contractile and endocrine functions.

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Section: Transcriptional Control Of the Renin Phenotypementioning

confidence: 84%

mentioning

confidence: 99%

Genes that Confer the Identity of the Renin Cell

Brunskill

Sequeira-Lόpez

Pentz

et al. 2011

Journal of the American Society of Nephrology

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111

162

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“…Recently, in vitro and in vivo studies demonstrate the crucial role of the cAMP pathway on the acquisition and maintenance of the renin cell identity. 51,52 Activation of the cAMP pathway was proven to be of importance not only for the well known stimulation of renin release but also for vascular development early in fetal life. Conditional deletion of G␣ s in cells from the renin lineage such as arteriolar SMCs and mesangial cells results in almost complete absence of renin-expressing cells in the fetal kidney accompanied by blunted development of the preglomerular arterial tree.…”

Section: Role Of the Camp Pathwaymentioning

confidence: 99%

Development of the Renal Arterioles

López

Gómez

2011

Journal of the American Society of Nephrology

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128

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“…Different mechanisms seem to control the phenotype of renin-expressing cells (3,14,15,17,26,29,32). Interactions of renin cells with other cell types are likely to be crucial to promote, maintain, and regulate the expression of renin.…”

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confidence: 99%

Transcriptional regulator RBP-J regulates the number and plasticity of renin cells

Rivera

Monteagudo²,

Pentz³

et al. 2011

Physiological Genomics

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scriptional regulator RBP-J regulates the number and plasticity of renin cells. Physiol Genomics 43: 1021-1028, 2011. First published July 12, 2011 doi:10.1152 doi:10. /physiolgenomics.00061.2011 cells are crucial in the control of blood pressure and fluidelectrolyte homeostasis. Notch receptors convey cell-cell signals that may regulate the renin cell phenotype. Because the common downstream effector for all Notch receptors is the transcription factor RBP-J, we used a conditional knockout approach to delete RBP-J in cells of the renin lineage. The resultant RBP-J conditional knockout (cKO) mice displayed a severe reduction in the number of reninpositive juxtaglomerular apparatuses (JGA) and a reduction in the total number of renin positive cells per JGA and along the afferent arterioles. This reduction in renin protein was accompanied by a decrease in renin mRNA expression, decreased circulating renin, and low blood pressure. To investigate whether deletion of RBP-J altered the ability of mice to increase the number of renin cells normally elicited by a physiological threat, we treated RBP-J cKO mice with captopril and sodium depletion for 10 days. The resultant treated RBP-J cKO mice had a 65% reduction in renin mRNA levels (compared with treated controls) and were unable to increase circulating renin. Although these mice attempted to increase the number of renin cells, the cells were unusually thin and had few granules and barely detectable amounts of immunoreactive renin. As a consequence, the cells were incapable of fully adopting the endocrine phenotype of a renin cell. We conclude that RBP-J is required to maintain basal renin expression and the ability of smooth muscle cells along the kidney vasculature to regain the renin phenotype, a fundamental mechanism to preserve homeostasis. juxtaglomerular cells; cell identity; homeostasis; recruitment; conditional knockout; recombination signal binding protein for immunoglobulin kappa J region

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Identity of the renin cell is mediated by cAMP and chromatin remodeling: an in vitro model for studying cell recruitment and plasticity

Cited by 69 publications

References 47 publications

Genes that Confer the Identity of the Renin Cell

Genes that Confer the Identity of the Renin Cell

Development of the Renal Arterioles

Transcriptional regulator RBP-J regulates the number and plasticity of renin cells

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