Evidence map›Paper›PMID 18422703›Full record

ArticleCell proliferation2008

Novel role for polycystin-1 in modulating cell proliferation through calcium oscillations in kidney cells.

G Aguiari, V Trimi, M Bogo, A Mangolini, G Szabadkai, P Pinton, R Witzgall, P C Harris, P A Borea, R Rizzuto and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cell proliferation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Computational study of biomechanical drivers of renal cystogenesis.Biomechanics and modeling in mechanobiology · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. A TRPM4-dependent current in murine renal primary cilia.American journal of physiology. Renal physiology · 2015
    Article
  10. Article
  11. Polycystins and cellular Ca2+ signaling.Cellular and molecular life sciences : CMLS · 2013
    Review
  12. Article
  13. Article
  14. Review
  15. Erk in kidney diseases.Journal of signal transduction · 2011
    Article
  16. Treatment strategies and clinical trial design in ADPKD.Advances in chronic kidney disease · 2010
    Review
  17. Article
  18. Review
  19. Article
  20. Novel roles of Pkd2 in male reproductive system development.Differentiation; research in biological diversity
    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

11 authors at 3 institutions in 3 countries.

G AguiariDepartment of Biochemistry and Molecular Biology, University of Ferrara, Ferrara, Italy.
V Trimi
M Bogo
A Mangolini
G Szabadkai
P Pinton
R Witzgall
P C Harris
P A Borea
R Rizzuto
L del Senno
University of Ferrara · ITMayo Clinic · USUniversity of Regensburg · DE

Funding

Telethon GTF01011
6 · The paper itself

Abstract

objectivesPolycystin-1 (PC1), a signalling receptor regulating Ca(2+)-permeable cation channels, is mutated in autosomal dominant polycystic kidney disease, which is typically characterized by increased cell proliferation. However, the precise mechanisms by which PC1 functions on Ca(2+) homeostasis, signalling and cell proliferation remain unclear. Here, we investigated the possible role of PC1 as a modulator of non-capacitative Ca(2+) entry (NCCE) and Ca(2+) oscillations, with downstream effects on cell proliferation. RESULTS AND DISCUSSION: By employing RNA interference, we show that depletion of endogenous PC1 in HEK293 cells leads to an increase in serum-induced Ca(2+) oscillations, triggering nuclear factor of activated T cell activation and leading to cell cycle progression. Consistently, Ca(2+) oscillations and cell proliferation are increased in PC1-mutated kidney cystic cell lines, but both abnormal features are reduced in cells that exogenously express PC1. Notably, blockers of the NCCE pathway, but not of the CCE, blunt abnormal oscillation and cell proliferation. Our study therefore provides the first demonstration that PC1 modulates Ca(2+) oscillations and a molecular mechanism to explain the association between abnormal Ca(2+) homeostasis and cell proliferation in autosomal dominant polycystic kidney disease.

Indexed as

Calcium SignalingCell LineCell Line, TransformedCell ProliferationCodon, NonsenseCytoplasmEnzyme ActivationHumansKidneyModels, BiologicalNFATC Transcription FactorsPolycystic Kidney, Autosomal DominantProtein Kinase C-alphaRNA InterferenceTRPP Cation ChannelsCodon, NonsenseNFATC Transcription FactorsProtein Kinase C-alphaTRPP Cation Channels

Identifiers

PMID18422703
PMCPMC2440503
OpenAlexW2156913879

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.