Recruitment of renin gene-expressing cells in adult rat kidneys

Gómez, R. Ariel; Chevalier, Robert L.; Everett, Allen D.; Elwood, John; Peach, Michael J.; Lynch, Kevin R.; Carey, Robert M.

doi:10.1152/ajprenal.1990.259.4.f660

Cited by 106 publications

(114 citation statements)

References 0 publications

Supporting

Mentioning

103

Contrasting

Order By: Relevance

“…In response to sodium depletion and captopril treatment RBP-J cKO mice were unable to increase circulating renin. The lack of increase in circulating renin was due to the combination of several factors: first, in response to the homeostatic threat, RBP-J cKO mice were unable to increase the number of cells expressing renin, which normally occurs by retransforming vascular SMCs along the afferent arterioles into renin-expressing cells (5,30,35,36). Thus, RBP-J may play a role in the reacquisition of the endocrine phenotype of arteriolar SMCs.…”

Section: Role Of Rbp-j In Renin-expressing Cellsmentioning

confidence: 99%

“…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). In adult animals, when homeostasis is threatened (such as by dehydration or hypotension) there is an increase in the number of renin-expressing cells along the renal arterioles and in the glomeruli and interstitium, resembling the fetal pattern, a phenomenon called recruitment (5,7). The process does not involve cell replication and/or migration (2), but it occurs by retransformation of arteriolar SMCs and mesangial cells into renin-expressing cells (30).…”

mentioning

confidence: 99%

See 1 more Smart Citation

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

Rivera

Monteagudo²,

Pentz³

et al. 2011

Physiological Genomics

View full text Add to dashboard Cite

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

show abstract

Section: Role Of Rbp-j In Renin-expressing Cellsmentioning

confidence: 99%

mentioning

confidence: 99%

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

Rivera

Monteagudo²,

Pentz³

et al. 2011

Physiological Genomics

View full text Add to dashboard Cite

show abstract

“…Increases in circulating renin levels (14,17) and hypertrophy and hyperplasia of renin-producing cells of the JGA (3,27) (8,16,21), although effects on renin mRNA ex-pression are dependent on the duration of treatment with ACE inhibitors (6,8,18,19).…”

Section: Introductionmentioning

confidence: 99%

The Effects of ZENECA ZD8731, an Angiotensin II Antagonist, on Renin Expression by Juxtaglomerular Cells in the Rat: Comparison of Protein and mRNA Expression as Detected by Immunohistochemistry and In Situ Hybridization

et al. 1995

View full text Add to dashboard Cite

Changes in the mRNA and protein expression of renin-secreting cells in the juxtaglomerular apparatus (JGA) were examined in the rat following administration of ZENECA ZD8731, an angiotensin II receptor antagonist. Doses RESULTS Histopathological FindingsFollowing treatment with ZD8731, nephropathy, characterized by basement membrane thickening, tubular epithelial hyperplasia and basophilia, and interstitial mononuclear cell infiltration, was evident in the cortex. Hypertrophy of afferent vessels in the juxtaglomerular region was also seen. The incidence and severity of both nephropathy and JGA changes were greater in males than in females. ImmunohistochemistryRenin immunoreactivity was localized to the outer media of the afferent arterioles and was predominant in the superficial cortex. In control kidney, immunohistochemistry revealed renin-containing cells to be confined to the proximal afferent arteriole (Fig. l a) (Fig. 2a).In Situ HybridizationIn situ hybridization signals colocalized precisely with renin immunoreactivity and were limited to the vasculature of the cortex in both groups of animals ; there was no evidence of renin mRNA in either the medulla or papilla. In control kidney, renin mRNA was mainly localized to the vascular pole of the glomerulus ( Fig. 1 b); renin mRNA was not detected in the proximal tubules. A dramatic increase in renin mRNA signals was observed in kidneys from all animals treated with ZD8731; the increase was apparently greater in males than females. Intense staining was evident in the usual juxtaglomerular position and in the afferent arteriole upstream from the glomerulus (Fig. 2b). DISCUSSIONThe results of the present study demonstrated a marked change in the distribution and expression of renin and renin mRNA during All receptor antagonism. Colocalization of renin and renin mRNA confirmed that the renin detected by immunohistochemistry was localized to the site of its mRNA synthesis and did not, therefore, result from reabsorption of filtered renin from the tubular fluid and/ or uptake from interstitial fluid (22,23). Administration of ZD8731 for 26 wk increased the number of renin-secreting and renin gene-expressing cells in both the JGA and the afferent arteriole. These find-

show abstract

“…Thereby, an increase in renal renin mRNA may be due to an increase in the number of renin-producing cells rather than in renin synthesis per cell as shown in isolated renal microvessels (40). Stimulation of renal renin mRNA content with recruitment of renin producing cells is induced by treatment with CEI (39,41,42). CEI enhance renal renin expression probably by the interruption of the negative feedback inhibition of renin synthesis exerted by ANG II (43).…”

Section: Kidneymentioning

confidence: 99%

The Role of the Renin-Angiotensin System in Cardiovascular Disease.

et al. 1994

View full text Add to dashboard Cite

Recent findings have increased our understanding of the role of the renin-angiotensin system in cardiovascular diseases. This was possible by the progress made in molecular biology and the import of this methodology into cardiovascular research by several groups in the past few years. Studies by these groups accumulated evidence especially for the existence and physiological importance of organ-based renin-angiotensin systems and their involvement in the pathogenesis of hypertension and the accompanying disorders of the heart, the kidney, and the vessels. This Review will focus mainly on the relevance of the local renin-angiotensin systems for cardiovascular diseases and the value of transgenic animals as models to analyse these systems (Hypertens Res 1994; 17: 1-16).

show abstract

Recruitment of renin gene-expressing cells in adult rat kidneys

Cited by 106 publications

References 0 publications

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

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

The Effects of ZENECA ZD8731, an Angiotensin II Antagonist, on Renin Expression by Juxtaglomerular Cells in the Rat: Comparison of Protein and mRNA Expression as Detected by Immunohistochemistry and In Situ Hybridization

The Role of the Renin-Angiotensin System in Cardiovascular Disease.

Contact Info

Product

Resources

About