ArticlePhysiological genomics2011
Transcriptional regulator RBP-J regulates the number and plasticity of renin cells.
Article in Physiological genomics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 75 citations in OpenAlex.
- Krüppel-like factor 2 regulates renin expression in mature juxtaglomerular cells.American journal of physiology. Renal physiology · 2026Article
- Four-week inhibition of the renin-angiotensin system in spontaneously hypertensive rats results in persistently lower blood pressure with reduced kidney renin and changes in expression of relevant gene networks.Cardiovascular research · 2024Article
- Kidney Renin Release under Hypoxia and Its Potential Link with Nitric Oxide: A Narrative Review.Biomedicines · 2023Review
- Targetable NOTCH1 rearrangements in reninoma.Nature communications · 2023Article
- Polycystic kidneys: interaction of notch and renin.Clinical science (London, England : 1979) · 2023Article
- Renin Cells, From Vascular Development to Blood Pressure Sensing.Hypertension (Dallas, Tex. : 1979) · 2023Review
- The role of Gata3 in renin cell identity.American journal of physiology. Renal physiology · 2023Article
- Overexpression of notch signaling in renin cells leads to a polycystic kidney phenotype.Clinical science (London, England : 1979) · 2023Article
- Survey of the binding preferences of RNA-binding proteins to RNA editing events.Genome biology · 2022Article
- Flexible and multifaceted: the plasticity of renin-expressing cells.Pflugers Archiv : European journal of physiology · 2022Review
- Kidney Angiotensin in Cardiovascular Disease: Formation and Drug Targeting.Pharmacological reviews · 2022Review
- A novel renal perivascular mesenchymal cell subset gives rise to fibroblasts distinct from classic myofibroblasts.Scientific reports · 2022Article
- Renin Cells, the Kidney, and Hypertension.Circulation research · 2021Review
- A primitive type of renin-expressing lymphocyte protects the organism against infections.Scientific reports · 2021Article
- Deciphering the Identity of Renin Cells in Health and Disease.Trends in molecular medicine · 2021Review
- Macrophage secretion of miR-106b-5p causes renin-dependent hypertension.Nature communications · 2020Article
- Renin-Expressing Cells Require β1-Integrin for Survival and for Development and Maintenance of the Renal Vasculature.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Sox6 as a new modulator of renin expression in the kidney.American journal of physiology. Renal physiology · 2020Article
- Single-Cell RNA Sequencing Reveals Renal Endothelium Heterogeneity and Metabolic Adaptation to Water Deprivation.Journal of the American Society of Nephrology : JASN · 2020Article
- Development of the renal vasculature.Seminars in cell & developmental biology · 2019Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Renin-expressing cells are crucial in the control of blood pressure and fluid-electrolyte 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 renin-positive 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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.