Evidence map›Paper›PMID 28529049›Full record

ArticleJournal of molecular and cellular cardiology2017

Heterogeneity of transverse-axial tubule system in mouse atria: Remodeling in atrial-specific Na

Xin Yue, Rui Zhang, Brian Kim, Aiqun Ma, Kenneth D Philipson, Joshua I Goldhaber

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2017. 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
2.9field-weighted citation impact, top 8% 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. Article
  2. Review
  3. Review
  4. Article
  5. Enhanced CaJACC. Clinical electrophysiology · 2024
    Article
  6. Mechanisms of spontaneous CaThe Journal of physiology · 2023
    Article
  7. Mechanisms of spontaneous CaThe Journal of physiology · 2023
    Article
  8. Differences in Effects of Length-Dependent Regulation of Force and CaInternational journal of molecular sciences · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Calcium Signaling in Cardiomyocyte Function.Cold Spring Harbor perspectives in biology · 2020
    Review
  16. A compartmentalized mathematical model of mouse atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  17. Studying signal compartmentation in adult cardiomyocytes.Biochemical Society transactions · 2020
    Review
  18. Article
  19. Review
  20. 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

6 authors at 3 institutions in 2 countries.

Xin YueDepartment of Cardiovascular Medicine, First Affiliated Hospital of Xi'an Jiaotong University, No. 277 West Yanta Road, Xi'an, Shaanxi 710061, China; Cedars-Sinai Heart Institute, Division of Applied Cell Biology and Physiology, 8700 Beverly Blvd., Los Angeles, CA 90048, USA.
Rui ZhangCedars-Sinai Heart Institute, Division of Applied Cell Biology and Physiology, 8700 Beverly Blvd., Los Angeles, CA 90048, USA.
Brian KimCedars-Sinai Heart Institute, Division of Applied Cell Biology and Physiology, 8700 Beverly Blvd., Los Angeles, CA 90048, USA.
Aiqun MaDepartment of Cardiovascular Medicine, First Affiliated Hospital of Xi'an Jiaotong University, No. 277 West Yanta Road, Xi'an, Shaanxi 710061, China; Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education and Key Laboratory of Molecular Cardiology of Shaanxi Province, 277 Yanta West Road, Xi'an, Shaanxi 710061, China. Electronic address: maaiqun@medmail.com.cn.
Kenneth D PhilipsonDepartment of Physiology, David Geffen School of Medicine at UCLA, 650 Charles Young Drive South, Los Angeles, CA 90095, USA.
Joshua I GoldhaberCedars-Sinai Heart Institute, Division of Applied Cell Biology and Physiology, 8700 Beverly Blvd., Los Angeles, CA 90048, USA. Electronic address: Joshua.Goldhaber@cshs.org.
Cedars-Sinai Smidt Heart Institute · USFirst Affiliated Hospital of Xi'an Jiaotong University · CNUniversity of California, Los Angeles · US

Funding

Molecular Biology of Cardiac Sodium-Calcium ExchangeR01HL048509 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GOLDHABER, JOSHUA I, PHILIPSON, KENNETH · 2002 to 2016
$4.7M
NHLBI NIH HHS R01 HL048509
6 · The paper itself

Abstract

Transverse-axial tubules (TATs) are commonly assumed to be sparse or absent in atrial myocytes from small animals. Atrial myocytes from rats, cats and rabbits lack TATs, which results in a characteristic "V"-shaped Ca release pattern in confocal line-scan recordings due to the delayed rise of Ca in the center of the cell. To examine TAT expression in isolated mouse atrial myocytes, we loaded them with the membrane dye Di-4-ANEPPS to label TATs. We found that >80% of atrial myocytes had identifiable TATs. Atria from male mice had a higher TAT density than female mice, and TAT density correlated with cell width. Using the fluorescent Ca indicator Fluo-4-AM and confocal imaging, we found that wild type (WT) mouse atrial myocytes generate near-synchronous Ca transients, in contrast to the "V"-shaped pattern typically reported in other small animals such as rat. In atrial-specific Na-Ca exchanger (NCX) knockout (KO) mice, which develop sinus node dysfunction and atrial hypertrophy with dilation, we found a substantial loss of atrial TATs in isolated atrial myocytes. There was a greater loss of transverse tubules compared to axial tubules, resulting in a dominance of axial tubules. Consistent with the overall loss of TATs, NCX KO atrial myocytes displayed a "V"-shaped Ca transient with slower and reduced central (CT) Ca release and uptake in comparison to subsarcolemmal (SS) Ca release. We compared chemically detubulated (DT) WT cells to KO, and found similar slowing of CT Ca release and uptake. However, SS Ca transients in the WT DT cells had faster uptake kinetics than KO cells, consistent with the presence of NCX and normal sarcolemmal Ca efflux in the WT DT cells. We conclude that the remodeling of NCX KO atrial myocytes is accompanied by a loss of TATs leading to abnormal Ca release and uptake that could impact atrial contractility and rhythm.

Indexed as

AnimalsAtrial RemodelingCalciumCalcium SignalingDisease Models, AnimalExcitation Contraction CouplingFemaleHeart AtriaMaleMiceMice, KnockoutMolecular ImagingMyocardial ContractionMyocytes, CardiacSarcoplasmic ReticulumSodium-Calcium ExchangerCalciumSodium-Calcium ExchangerAtrial cardiomyocytesAtrial remodelingExcitation-contraction couplingSodium-calcium exchangeTransverse-axial tubules

Identifiers

PMID28529049
PMCPMC5791526
OpenAlexW2615079397

What OpenQuestion holds

Textmetadata
LicenceTDM
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.