Evidence map›Paper›PMID 22984613›Full record

ArticlePloS one2012

β3 integrin in cardiac fibroblast is critical for extracellular matrix accumulation during pressure overload hypertrophy in mouse.

Sundaravadivel Balasubramanian, Lakeya Quinones, Harinath Kasiganesan, Yuhua Zhang, Dorea L Pleasant, Kamala P Sundararaj, Michael R Zile, Amy D Bradshaw, Dhandapani Kuppuswamy

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

42 citing papers in PubMed, 59 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Sundaravadivel BalasubramanianCardiology Division, Department of Medicine, Gazes Cardiac Research Institute, Medical University of South Carolina, Charleston, South Carolina, United States of America.
Lakeya Quinones
Harinath Kasiganesan
Yuhua Zhang
Dorea L Pleasant
Kamala P Sundararaj
Michael R Zile
Amy D Bradshaw
Dhandapani Kuppuswamy
Medical University of South Carolina · US

Funding

MUSC Minority Student Development ProgramR25GM072643 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI ERGUL, ADVIYE, RINKER, JENNIFER ANNE · 2005 to 2023
$5.8M
mTOR in Growth and Protection of Hypertrophying MyocardiumR01HL092124 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KUPPUSWAMY, DHANDAPANI · 2009 to 2012
$1.5M
NHLBI NIH HHS R01 HL092124NIGMS NIH HHS R25 GM072643PHS HHS R01 RHL092124A
6 · The paper itself

Abstract

The adhesion receptor β3 integrin regulates diverse cellular functions in various tissues. As β3 integrin has been implicated in extracellular matrix (ECM) remodeling, we sought to explore the role of β3 integrin in cardiac fibrosis by using wild type (WT) and β3 integrin null (β3-/-) mice for in vivo pressure overload (PO) and in vitro primary cardiac fibroblast phenotypic studies. Compared to WT mice, β3-/- mice upon pressure overload hypertrophy for 4 wk by transverse aortic constriction (TAC) showed a substantially reduced accumulation of interstitial fibronectin and collagen. Moreover, pressure overloaded LV from β3-/- mice exhibited reduced levels of both fibroblast proliferation and fibroblast-specific protein-1 (FSP1) expression in early time points of PO. To test if the observed impairment of ECM accumulation in β3-/- mice was due to compromised cardiac fibroblast function, we analyzed primary cardiac fibroblasts from WT and β3-/- mice for adhesion to ECM proteins, cell spreading, proliferation, and migration in response to platelet derived growth factor-BB (PDGF, a growth factor known to promote fibrosis) stimulation. Our results showed that β3-/- cardiac fibroblasts exhibited a significant reduction in cell-matrix adhesion, cell spreading, proliferation and migration. In addition, the activation of PDGF receptor associated tyrosine kinase and non-receptor tyrosine kinase Pyk2, upon PDGF stimulation were impaired in β3-/- cells. Adenoviral expression of a dominant negative form of Pyk2 (Y402F) resulted in reduced accumulation of fibronectin. These results indicate that β3 integrin-mediated Pyk2 signaling in cardiac fibroblasts plays a critical role in PO-induced cardiac fibrosis.

Indexed as

AnimalsAortaBecaplerminBlotting, WesternCardiomegalyCell AdhesionCell MovementCell ProliferationCells, CulturedCollagenConstriction, PathologicExtracellular MatrixFibroblastsFibronectinsFocal Adhesion Kinase 2HypertrophyBecaplerminCollagenFibronectinsFocal Adhesion Kinase 2Integrin beta3Proto-Oncogene Proteins c-sisPtk2b protein, mouseS100a4 protein, mouseS100 Calcium-Binding Protein A4S100 Proteins

Identifiers

PMID22984613
PMCPMC3440340
OpenAlexW2011011942

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.