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March 19, 2011Journal of Biological ChemistryOpen Access

Deficiency of Biglycan Causes Cardiac Fibroblasts to Differentiate into a Myofibroblast Phenotype

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Key result

Biglycan deficiency promotes myofibroblast differentiation and proliferation in vitro and in vivo, likely due to increased responses to TGF-β and SMAD2 signaling.

Why the study?

Does biglycan deficiency promote myofibroblast differentiation and proliferation in cardiac fibroblasts?

Population

Cardiac fibroblasts isolated from hearts of wild-type versus bgn mice, and in vivo post-myocardial…

Comparison

Biglycan deficiency (bgn), reconstitution of… vs Wild-type (WT) mice and fibroblasts

Design

Preclinical

Authors

AMAriane Melchior‐BeckerGDGuang DaiZDZhaoping Ding

Discussion

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Overview

May inform post-MI fibrosis research; leaves open translation to human cardiac remodeling.

Structured PICO

Does biglycan deficiency promote myofibroblast differentiation and proliferation in cardiac fibroblasts?

P
Population
Cardiac fibroblasts isolated from hearts of wild-type (WT) versus bgn(-/0) mice, and in vivo post-myocardial infarction mouse models
E
Exposure
Biglycan deficiency (bgn(-/0)), reconstitution of biglycan in the extracellular matrix, and administration of neutralizing antibodies to TGF-β
C
Comparator
Wild-type (WT) mice and fibroblasts
O
Outcome
Phenotypic characterization of cardiac fibroblasts including proliferation, myofibroblast differentiation, TGF-β receptor II expression, and SMAD2 phosphorylationsurrogate

Biglycan deficiency promotes cardiac fibroblast differentiation into myofibroblasts and proliferation via enhanced TGF-β and SMAD2 signaling, highlighting its role in post-infarct extracellular matrix remodeling.

Cite This Study

Melchior‐Becker et al. (2011) studied Myocardial infarction and cardiac fibrosis. Biglycan deficiency (bgn(-/0)) vs. Wild-type (WT) was evaluated on Myofibroblast differentiation and proliferation. Biglycan deficiency promotes myofibroblast differentiation and proliferation in vitro and in vivo, likely due to increased responses to TGF-β and SMAD2 signaling.

synapsesocial.com/papers/6a97a5e2883af1d6c8a67710https://doi.org/10.1074/jbc.m110.192682
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Transforming growth factor-beta1-mediated collagen gel contraction by cardiac fibroblasts2004 · 12 citations
  2. 2Biglycan Is Required for Adaptive Remodeling After Myocardial Infarction2008 · 125 citations
  3. 3Temporal relationships of F-actin bundle formation, collagen and fibronectin matrix assembly, and fibronectin receptor expression to wound contraction.1990 · 364 citations
  4. 4Transforming Growth Factor-β1 (TGF-β)–induced Apoptosis of Prostate Cancer Cells Involves Smad7-dependent Activation of p38 by TGF-β-activated Kinase 1 and Mitogen-activated Protein Kinase Kinase 32003 · 229 citations
  5. 5Phenotypic Effects of Biglycan Deficiency Are Linked to Collagen Fibril Abnormalities, Are Synergized by Decorin Deficiency, and Mimic Ehlers-Danlos-Like Changes in Bone and Other Connective Tissues2002 · 466 citations