ArticleJournal of the American Society of Nephrology : JASN2015
Recombination signal binding protein for Ig-κJ region regulates juxtaglomerular cell phenotype by activating the myo-endocrine program and suppressing ectopic gene expression.
Article in Journal of the American Society of Nephrology : JASN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 36 citations in OpenAlex.
- Krüppel-like factor 2 regulates renin expression in mature juxtaglomerular cells.American journal of physiology. Renal physiology · 2026Article
- Inhibition of Renin Expression Is Regulated by an Epigenetic Switch From an Active to a Poised State.Hypertension (Dallas, Tex. : 1979) · 2024Article
- An evolutionarily conserved olfactory receptor is required for sex differences in blood pressure.Science advances · 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
- Overexpression of notch signaling in renin cells leads to a polycystic kidney phenotype.Clinical science (London, England : 1979) · 2023Article
- 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
- Recent knowledge of NFATc4 in oncogenesis and cancer prognosis.Cancer cell international · 2022Review
- Renin Cells, the Kidney, and Hypertension.Circulation research · 2021Review
- A primitive type of renin-expressing lymphocyte protects the organism against infections.Scientific reports · 2021Article
- Renin-Expressing Cells Require β1-Integrin for Survival and for Development and Maintenance of the Renal Vasculature.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Development of the renal vasculature.Seminars in cell & developmental biology · 2019Review
- Super-enhancers maintain renin-expressing cell identity and memory to preserve multi-system homeostasis.The Journal of clinical investigation · 2018Article
- Renin cells in homeostasis, regeneration and immune defence mechanisms.Nature reviews. Nephrology · 2018Review
- Homeostatic Response of MouseMolecular and cellular biology · 2018Article
- Transcriptome-Wide Analysis Identifies Novel Associations With Blood Pressure.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Juxtaglomerular Cell Phenotypic Plasticity.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2017Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Recombination signal binding protein for Ig-κJ region (RBP-J), the major downstream effector of Notch signaling, is necessary to maintain the number of renin-positive juxtaglomerular cells and the plasticity of arteriolar smooth muscle cells to re-express renin when homeostasis is threatened. We hypothesized that RBP-J controls a repertoire of genes that defines the phenotype of the renin cell. Mice bearing a bacterial artificial chromosome reporter with a mutated RBP-J binding site in the renin promoter had markedly reduced reporter expression at the basal state and in response to a homeostatic challenge. Mice with conditional deletion of RBP-J in renin cells had decreased expression of endocrine (renin and Akr1b7) and smooth muscle (Acta2, Myh11, Cnn1, and Smtn) genes and regulators of smooth muscle expression (miR-145, SRF, Nfatc4, and Crip1). To determine whether RBP-J deletion decreased the endowment of renin cells, we traced the fate of these cells in RBP-J conditional deletion mice. Notably, the lineage staining patterns in mutant and control kidneys were identical, although mutant kidneys had fewer or no renin-expressing cells in the juxtaglomerular apparatus. Microarray analysis of mutant arterioles revealed upregulation of genes usually expressed in hematopoietic cells. Thus, these results suggest that RBP-J maintains the identity of the renin cell by not only activating genes characteristic of the myo-endocrine phenotype but also, preventing ectopic gene expression and adoption of an aberrant phenotype, which could have severe consequences for the control of 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.