Molecular and cellular aspects of renin during kidney ontogeny

Gomez, R. Ariel; Pupilli, Cinzia; Everett, Allen D.

doi:10.1007/bf00852854

Cited by 57 publications

(40 citation statements)

References 52 publications

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“…We anticipate that these mice will be useful to investigators interested in obtaining simultaneous in vivo information on the effects of physiological manipulations on renin gene transcription and its correlation with the steady state and distribution of renin mRNA and its protein. Because it is possible to view and count the cells actively transcribing the renin gene in vivo, these mice can also be used to distinguish the recruitment of renin gene-expressing cells versus the presence of renin due to uptake in the renal vasculature (21). In addition, since in these mice the renin cell lineage is marked with CFP, they can be used to assess the effect of deletion of specific genes on renin cell fate/differentiation.…”

Section: Discussionmentioning

confidence: 99%

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

Pentz¹,

López²,

Cordaillat³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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105

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Pentz ES, Sequeira Lopez ML, Cordaillat M, Gomez RA. Identity of the renin cell is mediated by cAMP and chromatin remodeling: an in vitro model for studying cell recruitment and plasticity. Am J Physiol Heart Circ Physiol 294: H699-H707, 2008. First published November 30, 2007 doi:10.1152/ajpheart.01152.2007.-The renin-angiotensin system (RAS) regulates blood pressure and fluid-electrolyte homeostasis. A key step in the RAS cascade is the regulation of renin synthesis and release by the kidney. We and others have shown that a major mechanism to control renin availability is the regulation of the number of cells capable of making renin. The kidney possesses a pool of cells, mainly in its vasculature but also in the glomeruli, capable of switching from smooth muscle to endocrine renin-producing cells when homeostasis is threatened. The molecular mechanisms governing the ability of these cells to turn the renin phenotype on and off have been very difficult to study in vivo. We, therefore, developed an in vitro model in which cells of the renin lineage are labeled with cyan fluorescent protein and cells actively making renin mRNA are labeled with yellow fluorescent protein. The model allowed us to determine that it is possible to culture cells of the renin lineage for numerous passages and that the memory to express the renin gene is maintained in culture and can be reenacted by cAMP and chromatin remodeling (histone H4 acetylation) at the cAMPresponsive element in the renin gene.

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Section: Discussionmentioning

confidence: 99%

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

Pentz¹,

López²,

Cordaillat³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

105

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“…1H and 2D). From ϳ5 dpf, increasingly intense mural renin expression appeared at the posterior mesenteric arteries (PMAs), which also supply the gastrointestinal tract ( To test if ren expression in larval zebrafish increases during development, as observed in mammals (19,49,63), mean ren-RFP intensity (a surrogate of ren expression) and RFP area over the AMA were quantified using image analysis in Tg(ren: RFP) fish (Fig. 3A) from 3 to 7 dpf.…”

Section: Larval Fish Renin Characterizationmentioning

confidence: 99%

Renin expression in developing zebrafish is associated with angiogenesis and requires the Notch pathway and endothelium

Rider

Mullins

Verdon

et al. 2015

American Journal of Physiology-Renal Physiology

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Rider SA, Mullins LJ, Verdon RF, MacRae CA, Mullins JJ. Renin expression in developing zebrafish is associated with angiogenesis and requires the Notch pathway and endothelium. Am J Physiol Renal Physiol 309: F531-F539, 2015. First published July 22, 2015 doi:10.1152/ajprenal.00247.2015.-Although renin is a critical regulatory enzyme of the cardiovascular system, its roles in organogenesis and the establishment of cardiovascular homeostasis remain unclear. Mammalian renin-expressing cells are widespread in embryonic kidneys but are highly restricted, specialized endocrine cells in adults. With a functional pronephros, embryonic zebrafish are ideal for delineating the developmental functions of renin-expressing cells and the mechanisms governing renin transcription. Larval zebrafish renin expression originates in the mural cells of the juxtaglomerular anterior mesenteric artery and subsequently at extrarenal sites. The role of renin was determined by assessing responses to renin-angiotensin system blockade, salinity variation, and renal perfusion ablation. Renin expression did not respond to renal flow ablation but was modulated by inhibition of angiotensin-converting enzyme and altered salinity. Our data in larval fish are consistent with conservation of renin's physiological functions. Using transgenic renin reporter fish, with mindbomb and cloche mutants, we show that Notch signaling and the endothelium are essential for developmental renin expression. After inhibition of angiogenesis, renin-expressing cells precede angiogenic sprouts. Arising from separate lineages, but relying on mutual interplay with endothelial cells, renin-expressing cells are among the earliest mural cells observed in larval fish, performing both endocrine and paracrine functions. renin; zebrafish; notch; endothelium; angiogenesis RENIN is the rate-limiting enzyme of the renin-angiotensin system (RAS). Mammalian ANG II, the effector of the RAS, is principally involved in blood pressure homeostasis by regulation of vasomotor tone and Na ϩ retention. ANG II also regulates cell proliferation and angiogenesis (12,22). Pathological activation of the RAS is associated with cardiovascular diseases, including hypertension and heart failure, and is consequently a major target of therapeutic agents (11).Renin and its cognate cells are required for normal renal development (2), including angiogenesis of the renal vascular tree (59). In mice, ablation of the renin gene or renin-expressing cells leads to renal developmental abnormalities (55,71,79). The vasculature of mammalian embryonic kidneys have a transient but extensive coverage of mural renin-expressing cells (17,31,32,47,63); however, their function is unclear. Adult renin-expressing cells are restricted to the juxtaglomerular apparatus and play a vital role in ion homeostasis by secreting activated renin enzyme via cytoplasmic granules (17,31,36,63). Upon physiological challenge by RAS inhibition or low Na ϩ , prearteriolar vascular smooth muscle cells (VSMC) reestablish their embryonic re...

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“…Indeed, studies in mammals (1)(2)(3)(4)(5) have demonstrated that genes for all the components of the renin-angiotensin system Moreover, pharmacological blockade of RAS in maturing young rats results in abnormal kidney morphology (6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Gene targeting in mice reveals a requirement for angiotensin in the development and maintenance of kidney morphology and growth factor regulation.

Niimura¹,

Labosky²,

Kakuchi³

et al. 1995

J. Clin. Invest.

319

219

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Elevated levels of endogenous angiotensin can cause hypertensive nephrosclerosis as a result of the potent vasopressor action of the peptide. We have produced by gene targeting mice homozygous for a null mutation in the angiotensinogen gene (Atg-'-). Postnatally, Atg-'-animals show a modest delay in glomerular maturation. Although Atg-'-animals are hypotensive by 7 wk of age, they develop, by 3 wk of age, pronounced lesions in the renal cortex, similar to those of hypertensive nephrosclerosis. In addition, the papillae of homozygous mutant kidneys are reduced in size. These lesions are accompanied by local up-regulation of PDGF-B and TGF-fi1 mRNA in the cortex and down-regulation of PDGF-A mRNA in the papilla. The study demonstrates an important requirement for angiotensin in achieving and maintaining the normal morphology of the kidney. The mechanism through which angiotensin maintains the volume homeostasis in mammals includes promotion of the maturational growth of the papilla. (J. Clin. Invest. 1995.

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Molecular and cellular aspects of renin during kidney ontogeny

Cited by 57 publications

References 52 publications

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

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

Renin expression in developing zebrafish is associated with angiogenesis and requires the Notch pathway and endothelium

Gene targeting in mice reveals a requirement for angiotensin in the development and maintenance of kidney morphology and growth factor regulation.

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