Evidence map›Paper›PMID 21285296›Full record

ArticleCardiovascular research2011

Two distinct phases of calcium signalling under flow.

Bo Liu, Shaoying Lu, Shuai Zheng, Zonglai Jiang, Yingxiao Wang

Open access · greenAbstract readVideo-Audio Media
In one paragraph

Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

21 citing papers in PubMed, 48 citations in OpenAlex.

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  6. Mitochondrial CaJournal of the Royal Society, Interface · 2017
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  20. Ca2+/calmodulin-dependent protein kinase kinase β phosphorylation of Sirtuin 1 in endothelium is atheroprotective.Proceedings of the National Academy of Sciences of the United States of America · 2013
    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 2 institutions in 2 countries.

Bo LiuDepartment of Bioengineering and Beckman Institute for Advanced Science and Technology, University of Illinois, Urbana-Champaign, Urbana, IL 61801, USA.
Shaoying Lu
Shuai Zheng
Zonglai Jiang
Yingxiao Wang
University of Illinois Urbana-Champaign · USShanghai Jiao Tong University · CN

Funding

FRET Imaging of Molecular Hierarchy at Subcellular Levels in MechanotransductionR01HL098472 · NHLBI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI WANG, YINGXIAO · 2010 to 2014
$1.9M
Mechanical Force and Neural RegenerationR01NS063405 · NINDS · UNIVERSITY OF MIAMI CORAL GABLES · PI CHIBA, AKIRA, JAKOBSSON, ERIC G · 2008 to 2011
$1.2M
The integration of FLIM with FRET biosensors for the sub-cellular visualization oR21CA139272 · NCI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI WANG, YINGXIAO · 2009 to 2010
$443k
NCI NIH HHS CA139272NHLBI NIH HHS HL098472NHLBI NIH HHS R01 HL098472NINDS NIH HHS NS063405
6 · The paper itself

Abstract

aimsHigh shear stress (HSS) can have significant impact on angiogenesis and atherosclerosis in collateral arteries near the bifurcation and curvature regions. Here, we investigate the spatiotemporal pattern of HSS-induced intracellular calcium alteration. METHODS AND

resultsGenetically encoded biosensors based on fluorescence resonance energy transfer were targeted in the cytoplasm and the endoplasmic reticulum (ER) to visualize the subcellular calcium dynamics in bovine aortic endothelial cells under HSS (65 dyn/cm(2)). Upon HSS application, the intracellular Ca(2+) concentration ([Ca(2+)](i)) increased immediately and maintained a sustained high level, while the ER-stored calcium had a significant decrease only after 300 s. The perturbation of calcium influx across the plasma membrane (PM) by the removal of extracellular calcium or the blockage of membrane channels inhibited the early phase of [Ca(2+)](i) increase upon HSS application, which was further shown to be sensitive to the magnitudes of shear stress and the integrity of cytoskeletal support. In contrast, Src, phospholipase C(PLC), and the inositol 1,4,5-trisphosphate receptor (IP(3)R) can regulate the late phase of HSS-induced [Ca(2+)](i) increase via the promotion of the ER calcium efflux.

conclusionThe HSS-induced [Ca(2+)](i) increase consists of two well-co-ordinated phases with different sources and mechanisms: (i) an early phase due to the calcium influx across the PM which is dependent on the mechanical impact and cytoskeletal support and (ii) a late phase originated from the ER-calcium efflux which is regulated by the Src, PLC, and IP(3)R signalling pathway. Therefore, our work presented new molecular-level insights into systematic understanding of mechanotransduction in cardiovascular systems.

Indexed as

Calcium SignalingMechanotransduction, CellularAnalysis of VarianceAnimalsBacterial ProteinsBiosensing TechniquesCalcium Channel BlockersCalcium ChannelsCattleCell MembraneCells, CulturedChelating AgentsCytoplasmCytoskeletonEndoplasmic ReticulumEndothelial CellsBacterial ProteinsCalcium Channel BlockersCalcium ChannelsChelating Agentscitrine protein, bacteriaenhanced cyan fluorescent proteinEnzyme InhibitorsGreen Fluorescent ProteinsInositol 1,4,5-Trisphosphate ReceptorsLuminescent Proteinssrc-Family KinasesType C Phospholipases

Identifiers

PMID21285296
PMCPMC3112016
OpenAlexW1972947365

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.