Evidence map›Paper›PMID 24105430›Full record

ArticleJournal of cellular physiology2014

RGS2 regulates urotensin II-induced intracellular Ca2+ elevation and contraction in glomerular mesangial cells.

Adebowale Adebiyi

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Urotensin II system in chronic kidney disease.Current research in physiology · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Interleukin 1 beta-induced calcium signaling via TRPA1 channels promotes mitogen-activated protein kinase-dependent mesangial cell proliferation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  9. Renal vascular TRP channels.Current research in physiology · 2021
    Article
  10. The Glomerulus According to the Mesangium.Frontiers in medicine · 2021
    Review
  11. InsPBMC biology · 2018
    Article
  12. Urotensin II-induced store-operated CaScientific reports · 2017
    Article
  13. Article
  14. Adenosine AAmerican journal of physiology. Renal physiology · 2017
    Article
  15. Article
  16. Resveratrol inhibits the intracellular calcium increase and angiotensin/endothelin system activation induced by soluble uric acid in mesangial cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2015
    Article
  17. Review
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

1 author at 1 institution in 1 country.

Adebowale AdebiyiDepartment of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee.
University of Tennessee Health Science Center · US

Funding

Vasoregulation by IP3 receptor coupling to TRPC channelsK01HL096411 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI ADEBIYI, ADEBOWALE · 2009 to 2013
$576k
NHLBI NIH HHS HL096411NHLBI NIH HHS K01 HL096411
6 · The paper itself

Abstract

Urotensin II (UII), a vasoactive peptide modulates renal hemodynamics. However, the physiological functions of UII in glomerular cells are unclear. In particular, whether UII alters mesangial tone remains largely unknown. The present study investigates the physiological effects of UII on glomerular mesangial cells (GMCs). This study also tested the hypothesis that the regulator of G-protein signaling (RGS) controls UII receptor (UTR) activity in GMCs. RT-PCR, Western immunoblotting, and immunofluorescence revealed UTR expression in cultured murine GMCs. Mouse UII (mUII) stimulated Ca(2+) release from intracellular stores and activated store-operated Ca(2+) entry (SOCE) in the cells. mUII also caused a reduction in planar GMC surface area. mUII-induced [Ca(2+)]i elevation and contraction were attenuated by SB 657510, a UTR antagonist, araguspongin B, an inositol 1,4,5-trisphosphate receptor antagonist, thapsigargin, a sarco/endoplasmic reticulum Ca(2+)-ATPase inhibitor, and La(3+), a store-operated Ca(2+) channel blocker, but not nimodipine, an L-type Ca(2+) channel blocker. In situ proximity ligation assay indicated molecular proximity between endogenous RGS2 and UTR in the cells. Treatment of GMCs with mUII elevated plasma membrane expression of RGS2 by ∼2-fold. mUII also increased the interaction between RGS2 and UTR in the cells. siRNA-mediated knockdown of RGS2 in murine GMCs increased mUII-induced [Ca(2+)]i elevation and contraction by ∼35 and 31%, respectively. These findings indicate that mUII-induced SOCE results in murine GMC contraction. These data also suggest that UTR activation stimulates RGS2 recruitment to GMC plasma membrane as a negative feedback mechanism to regulate UTR signaling.

Indexed as

AnimalsCalciumCell LineCell MembraneCell ShapeGene Expression RegulationMesangial CellsMiceMice, Inbred C57BLProtein TransportReceptors, G-Protein-CoupledRGS ProteinsRNA, Small InterferingUrotensinsCalciumReceptors, G-Protein-CoupledRgs2 protein, mouseRGS ProteinsRNA, Small Interferingurotensin IIurotensin II receptor, mouseUrotensins

Identifiers

PMID24105430
PMCPMC11250777
OpenAlexW1948191990

What OpenQuestion holds

Textmetadata
LicenceTDM
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.