Evidence map›Paper›PMID 19454490›Full record

ArticleCardiovascular research2009

Silencing TRPM7 promotes growth/proliferation and nitric oxide production of vascular endothelial cells via the ERK pathway.

Koichi Inoue, Zhi-Gang Xiong

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
6.2field-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

59 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
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  9. Arbitrary CaFrontiers in pharmacology · 2022
    Article
  10. Cytoskeletal Remodeling Mimics Endothelial Response to Microgravity.Frontiers in cell and developmental biology · 2021
    Article
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  12. Review
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  15. Article
  16. Article
  17. Article
  18. Endothelial CaInternational journal of molecular sciences · 2019
    Review
  19. Article
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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

2 authors at 1 institution in 1 country.

Koichi InoueRobert S. Dow Neurobiology Laboratories, Legacy Research, 1225 NE 2nd Ave. Portland, OR 97232, USA.
Zhi-Gang Xiong
Legacy Health · US

Funding

Ion channel role-glutamate-independent neuronal injuryR01NS042926 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI XIONG, ZHIGANG · 2002 to 2006
$1.4M
A novel cation channel in excitatory neuronal injuryR01NS049470 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI XIONG, ZHIGANG · 2005 to 2008
$1.2M
NINDS NIH HHS R01 NS042926NINDS NIH HHS R01 NS049470NINDS NIH HHS R01NS42926NINDS NIH HHS R01NS49470
6 · The paper itself

Abstract

aimsThe presence and potential function of transient receptor potential melastatin 7 (TRPM7), a Ca2+-permeable non-selective cation channel of the TRP channel superfamily in human vascular endothelial cells, were examined. METHODS AND

resultsWhole-cell patch-clamp recordings showed outward-rectifying currents in human umbilical vein endothelial cells (HUVECs), which was potentiated by removing the extracellular Ca2+ and Mg2+, but inhibited by non-specific TRPM7 blocker Gd3+ or 2-aminoethoxydiphenyl borate (2-APB). TRPM7 mRNA was detected in HUVECs by RT-PCR, but TRPM6, its closest homologue, was not. Silencing TRPM7 by small interfering RNA (siRNA) decreased the level of TRPM7 mRNA and the TRPM7-like current. Interestingly, knockdown of TRPM7 with siRNA or inhibition of TRPM7 function with 2-APB increased the phosphorylation of extracellular signal-regulated kinase (ERK) and enhanced growth/proliferation of HUVECs. This enhanced cell growth/proliferation was abolished by an inhibitor of the ERK signalling pathway. In addition to cell growth/proliferation, silencing TRPM7 also increased expression of nitric oxide synthase and nitric oxide production in an ERK pathway-dependent manner.

conclusionThese observations suggest that TRPM7 channels may play an important role in the function of vascular endothelial cells.

Indexed as

Cell ProliferationMAP Kinase Signaling SystemRNA InterferenceBoron CompoundsButadienesCalciumCells, CulturedEndothelial CellsExtracellular Signal-Regulated MAP KinasesHumansMagnesiumMembrane PotentialsMembrane Transport ModulatorsNitric OxideNitric Oxide Synthase Type IIINitriles2-aminoethoxydiphenyl borateBoron CompoundsButadienesCalciumExtracellular Signal-Regulated MAP KinasesMagnesiumMembrane Transport ModulatorsNitric OxideNitric Oxide Synthase Type IIINitrilesNOS3 protein, humanProtein Kinase InhibitorsProtein Serine-Threonine KinasesRNA, MessengerTRPM7 protein, humanTRPM Cation ChannelsU 0126

Identifiers

PMID19454490
PMCPMC2709465
OpenAlexW2145712678

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.