Evidence map›Paper›PMID 22621787›Full record

ArticleAmerican journal of physiology. Cell physiology2012

Modulation of endothelial SK3 channel activity by Ca²+dependent caveolar trafficking.

Mike T Lin, John P Adelman, James Maylie

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Redox Regulation of KAntioxidants & redox signaling · 2024
    Review
  2. Article
  3. Vasodilators mobilize SK3 channels in endothelial cells to produce arterial relaxation.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. Caveolae facilitate TRPV4-mediated CaAmerican journal of physiology. Renal physiology · 2018
    Article
  5. Article
  6. Article
  7. Endothelial SK3 channel-associated Ca2+ microdomains modulate blood pressure.American journal of physiology. Heart and circulatory physiology · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. New advances in the genetic basis of atrial fibrillation.Journal of cardiovascular electrophysiology · 2012
    Review
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

3 authors at 2 institutions in 1 country.

Mike T LinVollum Institute, Oregon Health and Science University, Portland, Oregon, USA. mlin@usouthal.edu.
John P Adelman
James Maylie
Oregon Health & Science University · USVollum Institute · US

Funding

Molecular Physiology of the SK2 Channels in CA1 NeuronsR01NS038880 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI MAYLIE, JAMES G · 2000 to 2017
$6.0M
Coupled LTP-dependent trafficking of synaptic SK channels and NMDARsR01MH093599 · NIMH · OREGON HEALTH & SCIENCE UNIVERSITY · PI ADELMAN, JOHN P, MAYLIE, JAMES G · 2012 to 2015
$1.2M
Endothelial SK3 Channel Modulation of EDHF is Estrogen RegulatedR00HL102056 · NHLBI · UNIVERSITY OF SOUTH ALABAMA · PI LIN, MIKE T · 2012 to 2014
$686k
Endothelial SK3 Channel Modulation of EDHF is Estrogen RegulatedK99HL102056 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI LIN, MIKE T · 2010 to 2011
$194k
NHLBI NIH HHS K99 HL102056NHLBI NIH HHS K99-HL-102056NHLBI NIH HHS R00 HL102056NIMH NIH HHS R01 MH093599NINDS NIH HHS R01 NS038880
6 · The paper itself

Abstract

Small- and intermediate-conductance Ca(2+)-activated K(+) channels (SK3/Kcnn3 and IK1/Kcnn4) are expressed in vascular endothelium. Their activities play important roles in regulating vascular tone through their modulation of intracellular concentration ([Ca(2+)](i)) required for the production of endothelium-derived vasoactive agents. Activation of endothelial IK1 or SK3 channels hyperpolarizes endothelial cell membrane potential, increases Ca(2+) influx, and leads to the release of vasoactive factors, thereby impacting blood pressure. To examine the distinct roles of IK1 and SK3 channels, we used electrophysiological recordings to investigate IK1 and SK3 channel trafficking in acutely dissociated endothelial cells from mouse aorta. The results show that SK3 channels undergo Ca(2+)-dependent cycling between the plasma membrane and intracellular organelles; disrupting Ca(2+)-dependent endothelial caveolae cycling abolishes SK3 channel trafficking. Moreover, transmitter-induced changes in SK3 channel activity and surface expression modulate endothelial membrane potential. In contrast, IK1 channels do not undergo rapid trafficking and their activity remains unchanged when either exo- or endocytosis is block. Thus modulation of SK3 surface expression may play an important role in regulating endothelial membrane potential in a Ca(2+)-dependent manner.

Indexed as

AnimalsAortaCalciumCaveolaeEndothelial CellsEndothelium, VascularIntermediate-Conductance Calcium-Activated Potassium ChannelsMembrane PotentialsMiceMice, Inbred C57BLProtein TransportSmall-Conductance Calcium-Activated Potassium ChannelsCalciumIntermediate-Conductance Calcium-Activated Potassium ChannelsKcnn3 protein, mouseKcnn4 protein, mouseSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID22621787
PMCPMC3423019
OpenAlexW2046699837

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.