Evidence map›Paper›PMID 10449440›Full record

ArticleThe Journal of clinical investigation1999

Rapid downregulation of rat renal Na/P(i) cotransporter in response to parathyroid hormone involves microtubule rearrangement.

M Lötscher, Y Scarpetta, M Levi, N Halaihel, H Wang, H K Zajicek, J Biber, H Murer, B Kaissling

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 120 citations in OpenAlex.

  1. The Intricacies of Renal Phosphate Reabsorption-An Overview.International journal of molecular sciences · 2024
    Review
  2. Review
  3. Mechanisms of phosphate transport.Nature reviews. Nephrology · 2019
    Review
  4. Visualizing the regulation of SLC34 proteins at the apical membrane.Pflugers Archiv : European journal of physiology · 2019
    Review
  5. NaPi-IIa interacting partners and their (un)known functional roles.Pflugers Archiv : European journal of physiology · 2019
    Review
  6. Review
  7. Renal phosphate wasting in the absence of adenylyl cyclase 6.Journal of the American Society of Nephrology : JASN · 2014
    Article
  8. Article
  9. Article
  10. Article
  11. Vitamin D and the kidney.Archives of biochemistry and biophysics · 2012
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Kidney and phosphate metabolism.Electrolyte & blood pressure : E & BP · 2008
    Review
  18. Article
  19. Article
  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

9 authors at 3 institutions in 2 countries.

M LötscherInstitute of Anatomy, University of Zürich, CH-8057 Zürich, Switzerland.
Y Scarpetta
M Levi
N Halaihel
H Wang
H K Zajicek
J Biber
H Murer
B Kaissling
The University of Texas Southwestern Medical Center · USZürcher Fachhochschule · CHUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal proximal tubule cells express in their apical brush border membrane (BBM) a Na/P(i) cotransporter type IIa that is rapidly downregulated in response to parathyroid hormone (PTH). We used the rat renal Na/P(i) cotransporter type IIa (NaPi-2) as an in vivo model to assess early cellular events in the rapid downregulation of this transporter. When rats were treated with PTH for 15 minutes, NaPi-2 abundance in the BBM was decreased. In parallel, transporter accumulated in intracellular vesicles. Concomitantly, microtubules (MTs) were found to form dense bundles of apical-to-basal orientation. After 60 minutes of PTH action, the cells were vastly depleted of NaPi-2, whereas their microtubular cytoskeleton had returned to its normal appearance. Prevention of MT rearrangement by taxol resulted in accumulation of NaPi-2 in the subapical cell portion after 15 minutes and a strong delay in depletion of intracellular transporter after 60 minutes of PTH action. Furthermore, the subapical accumulation of NaPi-2 was associated with the expansion of dense apical tubules of the subapical endocytic apparatus (SEA). Depolymerization of MTs by colchicine likewise caused a retardation of intracellular NaPi-2 depletion. These results suggest that NaPi-2 is downregulated in response to PTH through a rapid endocytic process in 2 separate steps: (a) internalization of the transporter into the SEA, and (b) its delivery to degradative organelles by a trafficking mechanism whose efficiency depends on a taxol-sensitive rearrangement of MTs.

Indexed as

SymportersAnimalsCarrier ProteinsColchicineEndocytosisImmunohistochemistryKidney Tubules, ProximalMaleMicroscopy, ElectronMicrotubulesMicrovilliPaclitaxelParathyroid HormonePeptide FragmentsPhosphatesRatsCarrier ProteinsColchicinePaclitaxelParathyroid HormonePeptide FragmentsPhosphatesSlc34a1 protein, ratSodiumSodium-Phosphate Cotransporter ProteinsSodium-Phosphate Cotransporter Proteins, Type IIaSymporters

Identifiers

PMID10449440
PMCPMC408517
OpenAlexW2079687125

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.