Evidence map›Paper›PMID 25208915›Full record

ArticlePflugers Archiv : European journal of physiology2015

Kv1.3 channels modulate human vascular smooth muscle cells proliferation independently of mTOR signaling pathway.

Pilar Cidad, Eduardo Miguel-Velado, Christian Ruiz-McDavitt, Esperanza Alonso, Laura Jiménez-Pérez, Agustín Asuaje, Yamila Carmona, Daniel García-Arribas, Javier López, Yngrid Marroquín and 4 more

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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.8field-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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  3. Article
  4. Article
  5. Review
  6. Article
  7. The Kv1.3 KBiologia futura · 2021
    Review
  8. Article
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  14. KMicrocirculation (New York, N.Y. : 1994) · 2018
    Review
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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

14 authors at 4 institutions in 1 country.

Pilar CidadDepartamento de Bioquímica y Biología Molecular y Fisiología e Instituto de Biología y Genética Molecular (IBGM), Universidad de Valladolid y CSIC, Edificio IBGM, c/ Sanz y Forés s/n, 47003, Valladolid, Spain.
Eduardo Miguel-Velado
Christian Ruiz-McDavitt
Esperanza Alonso
Laura Jiménez-Pérez
Agustín Asuaje
Yamila Carmona
Daniel García-Arribas
Javier López
Yngrid Marroquín
Mirella Fernández
Mercè Roqué
M Teresa Pérez-García
José Ramón López-López
Universidad de Valladolid · ESInstituto de Biomedicina y Genética Molecular de Valladolid · ESHospital Clínico Universitario de Valladolid · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phenotypic modulation (PM) of vascular smooth muscle cells (VSMCs) is central to the process of intimal hyperplasia which constitutes a common pathological lesion in occlusive vascular diseases. Changes in the functional expression of Kv1.5 and Kv1.3 currents upon PM in mice VSMCs have been found to contribute to cell migration and proliferation. Using human VSMCs from vessels in which unwanted remodeling is a relevant clinical complication, we explored the contribution of the Kv1.5 to Kv1.3 switch to PM. Changes in the expression and the functional contribution of Kv1.3 and Kv1.5 channels were studied in contractile and proliferating VSMCs obtained from human donors. Both a Kv1.5 to Kv1.3 switch upon PM and an anti-proliferative effect of Kv1.3 blockers on PDGF-induced proliferation were observed in all vascular beds studied. When investigating the signaling pathways modulated by the blockade of Kv1.3 channels, we found that anti-proliferative effects of Kv1.3 blockers on human coronary artery VSMCs were occluded by selective inhibition of MEK/ERK and PLCγ signaling pathways, but were unaffected upon blockade of PI3K/mTOR pathway. The temporal course of the anti-proliferative effects of Kv1.3 blockers indicates that they have a role in the late signaling events essential for the mitogenic response to growth factors. These findings establish the involvement of Kv1.3 channels in the PM of human VSMCs. Moreover, as current therapies to prevent restenosis rely on mTOR blockers, our results provide the basis for the development of novel, more specific therapies.

Indexed as

Cell ProliferationSignal TransductionCells, CulturedHumansKv1.3 Potassium ChannelKv1.5 Potassium ChannelMembrane PotentialsMuscle, Smooth, VascularMyocytes, Smooth MusclePhenotypePhosphodiesterase InhibitorsPlatelet-Derived Growth FactorPotassium Channel BlockersProtein Kinase InhibitorsRNA, MessengerTime FactorsKCNA3 protein, humanKCNA5 protein, humanKv1.3 Potassium ChannelKv1.5 Potassium ChannelMTOR protein, humanPhosphodiesterase InhibitorsPlatelet-Derived Growth FactorPotassium Channel BlockersProtein Kinase InhibitorsRNA, MessengerTOR Serine-Threonine Kinases

Identifiers

PMID25208915
OpenAlexW2151344601

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.