Evidence map›Paper›PMID 18259612›Full record

ArticleThe Journal of clinical investigation2008

A single nucleotide mutation in the mouse renin promoter disrupts blood pressure regulation.

Keiji Tanimoto, Akiko Sugiura, Sumiyo Kanafusa, Tomoko Saito, Naoto Masui, Kazuyuki Yanai, Akiyoshi Fukamizu

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Homeostatic Response of MouseMolecular and cellular biology · 2018
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Control of renin [corrected] gene expression.Pflugers Archiv : European journal of physiology · 2013
    Review
  10. Adipocyte-specific deficiency of angiotensinogen decreases plasma angiotensinogen concentration and systolic blood pressure in mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2012
    Article
  11. Article
  12. The renin phenotype: roles and regulation in the kidney.Current opinion in nephrology and hypertension · 2010
    Review
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Keiji TanimotoGraduate School of Life and Environmental Sciences, University of Tsukuba, Tsukuba, Ibaraki, Japan. keiji@tara.tsukuba.ac.jp
Akiko Sugiura
Sumiyo Kanafusa
Tomoko Saito
Naoto Masui
Kazuyuki Yanai
Akiyoshi Fukamizu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renin, a major regulatory component of the renin-angiotensin system, plays a pivotal role in regulating blood pressure and electrolyte homeostasis and is predominantly expressed in the kidney. Several cAMP-responsive elements have been identified within renin gene promoters. Here, we study how 2 such elements, renin proximal promoter element-2 (RP-2) and overlapping cAMP and negative regulatory elements (CNRE), affect the transcriptional regulation of renin. We generated Tg mice (TgM) bearing BACs containing either WT or mutant RP-2 or CNRE, integrated at single chromosomal loci. Analysis of the TgM revealed that RP-2 was essential to basal promoter activity in the kidney, while renin mRNA levels did not significantly change in any tissues tested in the CNRE mutant TgM. To evaluate the physiological significance of these mutations, we used the BAC Tg to rescue hypotensive Renin-null mutant mice. As predicted, no renin expression was observed in the kidneys of RP-2 mutant/Renin-null compound mice, whereas renin expression in CNRE mutant compound mice was indistinguishable from that in control mice. Consistent with this, RP-2 mutant animals were hypotensive, while CNRE mutants had normal blood pressure. Thus, transcriptional regulation of renin expression via RP-2 but not CNRE is critical for blood pressure regulation by this gene.

Indexed as

Blood PressurePromoter Regions, GeneticAnimalsCyclic AMPFemaleGene Expression RegulationMaleMiceMice, Inbred C57BLMice, Inbred ICRMice, TransgenicMutationReninResponse ElementsCyclic AMPRenin

Identifiers

PMID18259612
PMCPMC2230662

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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.