The Juxtaglomerular Apparatus

Taugner, R.; Hackenthal, E.

doi:10.1007/978-3-642-88426-9

Cited by 80 publications

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“…Recently, a Ren-1 c -null mouse was generated (35), and similar changes in kidney morphology to the Ren-1 d knockout model were reported, consistent with our interpretation that expression of renin-1 is not causal in the differentiation of JG cells. During chronic hypotension the smooth muscle cells neighboring JG cells can be recruited and modified to a renin expressing phenotype by a process termed metaplastic differentiation (36). The genetic cues required for metaplastic differentiation remain unknown, but the BAC transgenics may prove useful in addressing the mechanisms behind metaplastic differentiation of smooth muscle cells and also the contribution of the macula densa to the tubuloglomerular feedback loop.…”

Section: Discussionmentioning

confidence: 99%

Granulation Rescue and Developmental Marking of Juxtaglomerular Cells Using “Piggy-BAC” Recombination of the Mouse RenLocus

Mullins¹,

Payne²,

Kotelevtseva³

et al. 2000

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Granulation Rescue and Developmental Marking of Juxtaglomerular Cells Using “Piggy-BAC” Recombination of the Mouse RenLocus

Mullins¹,

Payne²,

Kotelevtseva³

et al. 2000

Journal of Biological Chemistry

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“…IN THE ADULT MAMMALIAN KIDNEY renin is synthesized, stored, and released by juxtaglomerular (JG) cells, a specialized group of myoepithelioid granulated cells located in the afferent arteriole at the entrance to the glomerulus (6,34). We have shown that renin precursor cells originate from the metanephric mesenchyme and give rise to JG cells, arteriolar smooth muscle cells (SMCs), mesangial cells, and a subset of proximal tubular cells (30,31).…”

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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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“…1 This octapeptide acts to increase peripheral vascular resistance and promote salt and fluid retention in concert with the hormone aldosterone. Renin is synthesized principally in the kidney juxtaglomerular (JG) cells, a group of modified smooth muscle cells located at the distal end of the renal afferent arteriole of the glomerulus (1). JG cells are in close contact with the macula densa, a specialized plaque of epithelial cells of the kidney distal tubule, which signal to the renal arterioles to regulate glomerular filtration rate and the secretion of renin, in response to ionic concentration and flow rate in the distal tubule (2,3), the so-called tubuloglomerular feedback loop.…”

mentioning

confidence: 99%

Renin-1 Is Essential for Normal Renal Juxtaglomerular Cell Granulation and Macula Densa Morphology

Clark¹,

Sharp²,

Morley³

et al. 1997

Journal of Biological Chemistry

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The secretion of renin from granules stored in renal juxtaglomerular cells plays a key role in blood pressure homeostasis. The synthesis and release of renin and the extent of granulation is regulated by several mechanisms including signaling from the macula densa, neuronal input, and blood pressure. Through the use of a gene-targeting vector containing homology arms generated using the polymerase chain reaction, we have inactivated the Ren-1 d gene, one of two mouse genes encoding renin, and report that lack of renin-1 d results in altered morphology of the macula densa of the kidney distal tubule and complete absence of juxtaglomerular cell granulation. Furthermore, Ren-1 d؊/؊ mice exhibit sexually dimorphic hypotension. The altered growth morphology of the macula densa in Ren-1 d -null mice should provide a tool for the investigation of the JG cell-macula densa signaling. Furthermore, the current data indicate that expression of the Ren-1 d gene is a prerequisite for the formation of storage granules, even though the related protein renin-2 is present in these mice, suggesting that renin-1 d and renin-2 are secreted by distinct pathways in vivo.Renin (EC 3.4.23.15) is an aspartyl protease, which catalyzes the first step in the renin angiotensin system, the end product of which is the potent vasopressor peptide hormone, angiotensin II (AngII).1 This octapeptide acts to increase peripheral vascular resistance and promote salt and fluid retention in concert with the hormone aldosterone. Renin is synthesized principally in the kidney juxtaglomerular (JG) cells, a group of modified smooth muscle cells located at the distal end of the renal afferent arteriole of the glomerulus (1). JG cells are in close contact with the macula densa, a specialized plaque of epithelial cells of the kidney distal tubule, which signal to the renal arterioles to regulate glomerular filtration rate and the secretion of renin, in response to ionic concentration and flow rate in the distal tubule (2, 3), the so-called tubuloglomerular feedback loop. Except for the submandibular gland (SMG) of the mouse, the JG cells are the only site where prorenin, the inactive zymogen, is known to be converted to the active form of renin. SMG renin does not, however, make its way into the plasma in large quantities and is thought not to play a significant role in blood pressure regulation under normal circumstances (reviewed in Bing et al. (4)). The release of renin from JG cells is mediated by two pathways: regulated release of the mature, active renin from modified lysosomal storage granules and constitutive release of the inactive zymogen. While the regulated pathway of renin secretion is responsive to baroreceptor, neurogenic, and macula densa signals (5), the physiological significance of the constitutive secretion of prorenin is not understood, nor are the molecular pathways that link secretory signals to renin maturation and release. Clarification of the mechanisms underlying these processes will be crucial to our understanding of the control of ...

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The Juxtaglomerular Apparatus

Cited by 80 publications

References 0 publications

Granulation Rescue and Developmental Marking of Juxtaglomerular Cells Using “Piggy-BAC” Recombination of the Mouse RenLocus

Granulation Rescue and Developmental Marking of Juxtaglomerular Cells Using “Piggy-BAC” Recombination of the Mouse RenLocus

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

Renin-1 Is Essential for Normal Renal Juxtaglomerular Cell Granulation and Macula Densa Morphology

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