Zis: a developmentally regulated gene expressed in juxtaglomerular cells

Karginova, Elena A.; Pentz, Ellen S.; Kazakova, Irina; Norwood, Victoria F.; Carey, Robert M.; Gómez, R. Ariel

doi:10.1152/ajprenal.1997.273.5.f731

Cited by 33 publications

(31 citation statements)

References 27 publications

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“…Currently, little information is available regarding the role of ZRANB2 in mammalian embryonic development, although it has been shown to be a developmentally regulated factor expressed in juxtaglomerular cells (37). Given the high conservation rate of ZRANB2 from fish to mammals, we thus speculate that mammalian ZRANB2 may also play a similar role in early development.…”

Section: Discussionmentioning

confidence: 92%

Identification of the Zinc Finger Protein ZRANB2 as a Novel Maternal Lipopolysaccharide-binding Protein That Protects Embryos of Zebrafish against Gram-negative Bacterial Infections

Wang

et al. 2016

Journal of Biological Chemistry

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Zinc finger ZRANB2 proteins are widespread in animals, but their functions and mechanisms remain poorly defined. Here we clearly demonstrate that ZRANB2 is a newly identified LPSbinding protein present abundantly in the eggs/embryos of zebrafish. We also show that recombinant ZRANB2 (rZRANB2) acts as a pattern recognition receptor capable of identifying the bacterial signature molecule LPS as well as binding the Gramnegative bacteria Escherichia coli, Vibrio anguilarum, and Aeromonas hydrophila and functions as an antibacterial effector molecule capable of directly killing the bacteria. Furthermore, we reveal that N-terminal residues 11-37 consisting of the first ZnF_RBZ domain are indispensable for ZRANB2 antimicrobial activity. Importantly, microinjection of rZRANB2 into early embryos significantly enhanced the resistance of the embryos against pathogenic A. hydrophila challenge, and this enhanced bacterial resistance was markedly reduced by co-injection of anti-ZRANB2 antibody. Moreover, precipitation of ZRANB2 in the embryo extracts by preincubation with anti-ZRANB2 antibody caused a marked decrease in the antibacterial activity of the extracts against the bacteria tested. In addition, the N-terminal peptide Z 1/37 or Z 11/37 with in vitro antibacterial activity also promoted the resistance of embryos against A. hydrophila, but the peptide Z 38/198 without in vitro antibacterial activity did not. Collectively, these results indicate that ZRANB2 is a maternal LPS-binding protein that can protect the early embryos of zebrafish against pathogenic attacks, a novel role ever assigned to ZRANB2 proteins. This work also provides new insights into the immunological function of the zinc finger proteins that are widely distributed in various animals.

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Section: Discussionmentioning

confidence: 92%

Identification of the Zinc Finger Protein ZRANB2 as a Novel Maternal Lipopolysaccharide-binding Protein That Protects Embryos of Zebrafish against Gram-negative Bacterial Infections

Wang

et al. 2016

Journal of Biological Chemistry

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“…As a consequence, the mutant cells are incapable of fully adopting the renin phenotype and are limited to the phenotype of a smooth muscle cell. Interestingly, when renin cells are placed in culture and are deprived of their normal intercellular interactions with other cell types, they stop synthesizing renin and adopt the phenotypic characteristics of smooth muscle and/or fibroblast cells (11). Thus, lack of the transducing mechanism conveying cell-cell interactions normally provided by RBP-J impairs the plasticity of cells to switch phenotype when confronted with a homeostatic challenge.…”

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

confidence: 99%

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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“…Most investigators use acute preparations of JG cells with variable degrees of purity. Enriched populations of renin-expressing cells can be isolated, but after only a few days in culture, these cells usually stop making renin and differentiate into other cell types or die (6,8,24). JG cells propagated on Matrigel were reported to retain the ability to express renin for numerous passages (39); however, no subsequent use of this culture method has been reported.…”

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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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Zis: a developmentally regulated gene expressed in juxtaglomerular cells

Cited by 33 publications

References 27 publications

Identification of the Zinc Finger Protein ZRANB2 as a Novel Maternal Lipopolysaccharide-binding Protein That Protects Embryos of Zebrafish against Gram-negative Bacterial Infections

Identification of the Zinc Finger Protein ZRANB2 as a Novel Maternal Lipopolysaccharide-binding Protein That Protects Embryos of Zebrafish against Gram-negative Bacterial Infections

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

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

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