Evidence map›Paper›PMID 17283064›Full record

ArticleMolecular and cellular biology2007

Phenotypes developed in secretin receptor-null mice indicated a role for secretin in regulating renal water reabsorption.

Jessica Y S Chu, Samuel C K Chung, Amy K M Lam, Sidney Tam, Sookja K Chung, Billy K C Chow

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

52 citing papers in PubMed, 95 citations in OpenAlex.

  1. Novel effects of the gastrointestinal hormone secretin on cardiac metabolism and renal function.American journal of physiology. Endocrinology and metabolism · 2022
    Trial
  2. Article
  3. Article
  4. Article
  5. Secretin: a hormone for HCOPflugers Archiv : European journal of physiology · 2024
    Review
  6. Article
  7. Thirst: neuroendocrine regulation in mammals.Veterinary research communications · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Landscape of GPCR expression along the mouse nephron.American journal of physiology. Renal physiology · 2021
    Article
  14. Review
  15. Article
  16. Impaired Renal HCOJournal of the American Society of Nephrology : JASN · 2020
    Article
  17. Review
  18. Review
  19. Targeting the Trafficking of Kidney Water Channels for Therapeutic Benefit.Annual review of pharmacology and toxicology · 2020
    Review
  20. 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

6 authors at 1 institution in 1 country.

Jessica Y S ChuDepartment of Zoology, The University of Hong Kong, Pokfulam, Hong Kong SAR, China. bkcc@hkusua.hku.hk
Samuel C K Chung
Amy K M Lam
Sidney Tam
Sookja K Chung
Billy K C Chow
University of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aquaporin 2 (AQP2) is responsible for regulating the concentration of urine in the collecting tubules of the kidney under the control of vasopressin (Vp). Studies using Vp-deficient Brattleboro rats, however, indicated the existence of substantial Vp-independent mechanisms for membrane insertion, as well as transcriptional regulation, of this water channel. The Vp-independent mechanism(s) is clinically relevant to patients with X-linked nephrogenic diabetes insipidus (NDI) by therapeutically bypassing the dysfunctional Vp receptor. On the basis of studies with secretin receptor-null (SCTR(-/-)) mice, we report here for the first time that mutation of the SCTR gene could lead to mild polydipsia and polyuria. Additionally, SCTR(-/-) mice were shown to have reduced renal expression of AQP2 and AQP4, as well as altered glomerular and tubular morphology, suggesting possible disturbances in the filtration and/or water reabsorption process in these animals. By using SCTR(-/-) mice as controls and comparing them with wild-type animals, we performed both in vivo and in vitro studies that demonstrated a role for secretin in stimulating (i) AQP2 translocation from intracellular vesicles to the plasma membrane in renal medullary tubules and (ii) expression of this water channel under hyperosmotic conditions. The present study therefore provides information for at least one of the Vp-independent mechanisms that modulate the process of renal water reabsorption. Future investigations in this direction should be important in developing therapeutic means for treating NDI patients.

Indexed as

Amino Acid SequenceAnimalsAquaporin 2Aquaporin 4Biological Transport, ActiveCell MembraneCytoplasmic VesiclesKidney GlomerulusKidney TubulesMiceMice, KnockoutMolecular Sequence DataMutationPhenotypePolyuriaProtein TransportAqp2 protein, mouseAqp4 protein, mouseAquaporin 2Aquaporin 4Receptors, Gastrointestinal HormoneReceptors, G-Protein-CoupledSecretinsecretin receptorWater

Identifiers

PMID17283064
PMCPMC1899889
OpenAlexW2027844392

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.