Evidence map›Paper›PMID 19675303›Full record

ArticleAmerican journal of physiology. Cell physiology2009

Orai1, a critical component of store-operated Ca2+ entry, is functionally associated with Na+/Ca2+ exchanger and plasma membrane Ca2+ pump in proliferating human arterial myocytes.

Sergey G Baryshnikov, Maria V Pulina, Alessandra Zulian, Cristina I Linde, Vera A Golovina

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
5.3field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
  2. Article
  3. Alterations of the CaFrontiers in physiology · 2023
    Article
  4. Article
  5. Article
  6. Article
  7. Proteins Interacting with STIM1 and Store-Operated CaProgress in molecular and subcellular biology · 2021
    Review
  8. ORAI1 CaFrontiers in cell and developmental biology · 2021
    Review
  9. Differential regulation of CaScience signaling · 2019
    Article
  10. NaAmerican journal of physiology. Heart and circulatory physiology · 2019
    Article
  11. AMP-Activated Protein Kinase (AMPK)-Dependent Regulation of Renal Transport.International journal of molecular sciences · 2018
    Review
  12. Article
  13. Review
  14. Article
  15. Orai channel-mediated Ca2+ signals in vascular and airway smooth muscle.American journal of physiology. Cell physiology · 2016
    Review
  16. Article
  17. Article
  18. Signaling in muscle contraction.Cold Spring Harbor perspectives in biology · 2015
    Review
  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

5 authors at 1 institution in 1 country.

Sergey G BaryshnikovDepartment of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
Maria V Pulina
Alessandra Zulian
Cristina I Linde
Vera A Golovina
University of Maryland, Baltimore · US

Funding

Sympathetic Neurotransmitters and Ouabain HypertensionP01HL078870 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BLAUSTEIN, MORDECAI P · 2005 to 2009
$9.9M
Altered Glial Calcium Signaling in NeurodegenerationR01NS048263 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI GOLOVINA, VERA · 2004 to 2008
$1.4M
NHLBI NIH HHS HL-PO1-078870NINDS NIH HHS NS-048263
6 · The paper itself

Abstract

Ca(2+) entry through store-operated channels (SOCs) in the plasma membrane plays an important role in regulation of vascular smooth muscle contraction, tone, and cell proliferation. The C-type transient receptor potential (TRPC) channels have been proposed as major candidates for SOCs in vascular smooth muscle. Recently, two families of transmembrane proteins, Orai [also known as Ca(2+) release-activated Ca(2+) channel modulator (CRACM)] and stromal interacting molecule 1 (STIM1), were shown to be essential for the activation of SOCs mainly in nonexcitable cells. Here, using small interfering RNA, we show that Orai1 plays an essential role in activating store-operated Ca(2+) entry (SOCE) in primary cultured proliferating human aortic smooth muscle cells (hASMCs), whereas Orai2 and Orai3 do not contribute to SOCE. Knockdown of Orai1 protein expression significantly attenuated SOCE. Moreover, inhibition of Orai1 downregulated expression of Na(+)/Ca(2+) exchanger type 1 (NCX1) and plasma membrane Ca(2+) pump isoform 1 (PMCA1). The rate of cytosolic free Ca(2+) concentration decay after Ca(2+) transients in Ca(2+)-free medium was also greatly decreased under these conditions. This reduction of Ca(2+) extrusion, presumably via NCX1 and PMCA1, may be a compensation for the reduced SOCE. Immunocytochemical observations indicate that Orai1 and NCX1 are clustered in plasma membrane microdomains. Cell proliferation was attenuated in hASMCs with disrupted Orai1 expression and reduced SOCE. Thus Orai1 appears to be a critical component of SOCE in proliferating vascular smooth muscle cells, and may therefore be a key player during vascular growth and remodeling.

Indexed as

AortaBlotting, WesternCalciumCalcium ChannelsCalcium SignalingCell ProliferationCells, CulturedDown-RegulationFluorescent Antibody TechniqueGene ExpressionGene Expression RegulationHumansImmunohistochemistryMuscle, Smooth, VascularMyocytes, Smooth MuscleORAI1 ProteinATP2B1 protein, humanCalciumCalcium ChannelsORAI1 ProteinORAI1 protein, humanPlasma Membrane Calcium-Transporting ATPasesRNA, Small InterferingSodium-Calcium Exchangersodium-calcium exchanger 1

Identifiers

PMID19675303
PMCPMC2777402
OpenAlexW2053907473

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.