Evidence map›Paper›PMID 16205939›Full record

ArticleHistochemistry and cell biology2006

Essential role of obscurin in cardiac myofibrillogenesis and hypertrophic response: evidence from small interfering RNA-mediated gene silencing.

Andrei B Borisov, Sarah B Sutter, Aikaterini Kontrogianni-Konstantopoulos, Robert J Bloch, Margaret V Westfall, Mark W Russell

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Histochemistry and cell biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Obscurin Maintains Myofiber Identity in Extraocular Muscles.Investigative ophthalmology & visual science · 2024
    Article
  5. Obscurin: A multitasking giant in the fight against cancer.Biochimica et biophysica acta. Reviews on cancer · 2021
    Review
  6. Article
  7. Unraveling obscurins in heart disease.Pflugers Archiv : European journal of physiology · 2019
    Review
  8. Article
  9. Article
  10. Deregulated CaScience advances · 2017
    Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  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 2 institutions in 1 country.

Andrei B BorisovDivision of Pediatric Cardiology, Department of Pediatrics and Communicable Diseases, University of Michigan Medical School, Ann Arbor, MI 48109, USA. aborisov@umich.edu
Sarah B Sutter
Aikaterini Kontrogianni-Konstantopoulos
Robert J Bloch
Margaret V Westfall
Mark W Russell
University of Michigan–Ann Arbor · USUniversity of Maryland, Baltimore · US

Funding

SMALL ANKYRINS IN EXCITABLE CELLSR01HL064304 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI BLOCH, ROBERT J · 1999 to 2009
$2.3M
Role of Obscurin and Obscurin-MLCK in myofibrillogenesisR01HL075093 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUSSELL, MARK W · 2005 to 2008
$1.2M
NHLBI NIH HHS R01 HL 075093-01NHLBI NIH HHS R01 HL 64304
6 · The paper itself

Abstract

Obscurin is a recently identified giant multidomain muscle protein (approximately 800 kDa) whose structural and regulatory functions remain to be defined. The goal of this study was to examine the effect of obscurin gene silencing induced by RNA interference on the dynamics of myofibrillogenesis and hypertrophic response to phenylephrine in cultured rat cardiomyocytes. We found that that the adenoviral transfection of short interfering RNA (siRNA) constructs targeting the first coding exon of obscurin sequence resulted in progressive depletion of cellular obscurin. Confocal microscopy demonstrated that downregulation of obscurin expression led to the impaired assembly of new myofibrillar clusters and considerable aberrations of the normal structure of the contractile apparatus. While the establishment of the initial periodic pattern of alpha-actinin localization remained mainly unaffected in siRNA-transfected cells, obscurin depletion did cause the defective lateral alignment of myofibrillar bundles, leading to their abnormal bifurcation, dispersal and multiple branching. Bending of immature myofibrils, apparently associated with the loss of their rigidity, a modified titin pattern, the absence of well-formed A-bands in newly formed contractile structures as documented by a diffuse localization of sarcomeric myosin labeling, and an occasional irregular periodicity of sarcomere spacing were typical of obscurin siRNA-treated cells. These results suggest that obscurin is indispensable for spatial positioning of contractile proteins and for the structural integration and stabilization of myofibrils, especially at the stage of myosin filament incorporation and A-band assembly. This demonstrates a vital role for obscurin in myofibrillogenesis and hypertrophic growth.

Indexed as

ActininAnimalsBase SequenceCardiomyopathy, HypertrophicCell EnlargementCells, CulturedGuanine Nucleotide Exchange FactorsImmunohistochemistryMuscle DevelopmentMuscle ProteinsMyocardial ContractionMyocytes, CardiacRatsRNA InterferenceRNA, Small InterferingTransfectionActininGuanine Nucleotide Exchange FactorsMuscle ProteinsObscn protein, ratRNA, Small Interfering

Identifiers

PMID16205939
OpenAlexW2096617205

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.