Evidence map›Paper›PMID 19666840›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2009

T-type calcium channels are regulated by hypoxia/reoxygenation in ventricular myocytes.

Florentina Pluteanu, Leanne L Cribbs

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Indirect evidence that anoxia exposure and cold acclimation alter transarcolemmal CaComparative biochemistry and physiology. Part A, Molecular & integrative physiology · 2021
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Transcriptional regulation of α1H T-type calcium channel under hypoxia.American journal of physiology. Cell physiology · 2014
    Article
  10. Role of T-type channels in vasomotor function: team player or chameleon?Pflugers Archiv : European journal of physiology · 2014
    Review
  11. T-type calcium channels blockers as new tools in cancer therapies.Pflugers Archiv : European journal of physiology · 2014
    Review
  12. Article
  13. Review
  14. Article
  15. 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

2 authors at 1 institution in 1 country.

Florentina PluteanuDepartments of Medicine and Physiology, Cardiovascular Institute, Loyola University Chicago, Maywood, Illinois 60153, USA.
Leanne L Cribbs
Loyola University Chicago · US

Funding

T-type Ca channels in development and cell proliferationR01HL075115 · NHLBI · LOYOLA UNIVERSITY CHICAGO · PI CRIBBS, LEANNE L · 2004 to 2006
$958k
NHLBI NIH HHS R01 HL075115
6 · The paper itself

Abstract

Low-voltage-activated calcium channels are reexpressed in ventricular myocytes in pathological conditions associated with hypoxic episodes, but a direct relation between oxidative stress and T-type channel function and regulation in cardiomyocytes has not been established. We aimed to investigate low-voltage-activated channel regulation under oxidative stress in neonatal rat ventricular myocytes. RT-PCR measurements of voltage-gated Ca(2+) (Ca(v))3.1 and Ca(v)3.2 mRNA levels in oxidative stress were compared with whole cell patch-clamp recordings of T-type calcium current. The results indicate that hypoxia reduces T-type current density at -30 mV (the hallmark of this channel) based on the shift of the voltage dependence of activation to more depolarized values and downregulation of Ca(v)3.1 at the mRNA level. Upon reoxygenation, both Ca(v)3.1 mRNA levels and the voltage dependence of total T-type current are restored, although differently for activation and inactivation. Using Ni(2+), we distinguished different effects of hypoxia/reoxygenation on the two current components. Long-term incubation in the presence of 100 microM CoCl(2) reproduced the effects of hypoxia on T-type current activation and inactivation, indicating that the chemically induced oxidative state is sufficient to alter T-type calcium current activity, and that hypoxia-inducible factor-1alpha is involved in Ca(v)3.1 downregulation. Our results demonstrate that Ca(v)3.1 and Ca(v)3.2 T-type calcium channels are differentially regulated by hypoxia/reoxygenation injury, and, therefore, they may serve different functions in the myocyte in response to hypoxic injury.

Indexed as

Calcium SignalingOxidative StressAnimalsAnimals, NewbornCalcium Channels, T-TypeCell HypoxiaCells, CulturedCobaltGene Expression RegulationHeart VentriclesMembrane PotentialsMyocytes, CardiacNickelOxidation-ReductionPatch-Clamp TechniquesRatsCacna1g protein, ratCacna1h protein, ratCalcium Channels, T-TypeCobaltcobaltous chlorideNickelnickel chlorideRNA, Messenger

Identifiers

PMID19666840
PMCPMC2770772
OpenAlexW2157371192

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.