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November 25, 2010Circulation Research

A Dynamic Notch Injury Response Activates Epicardium and Contributes to Fibrosis Repair

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Population

Transgenic Notch reporter mice (CBF1-RE₄-EGFP) and NOD-SCID mice

Design

Preclinical

Authors

JRJamie L. RussellUnited States Department of DefenseSGSean C. GoetschJohns Hopkins UniversityNGNicholas GaianoJohns Hopkins University

Discussion

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Implication

Supports Notch investigation in cardiac fibrosis models; leaves open clinical relevance pending human validation.

Structured PICO

P
Population
Transgenic Notch reporter mice (CBF1-RE(x)₄-EGFP) and NOD-SCID (nonobese diabetic-severe combined immunodeficiency) mice
I
Intervention
Myocardial infarction, thoracic aortic banding, serum growth factors, immobilized Notch ligand Delta-like 1, cardiomyocyte coculture, and engraftment
O
Outcome
Identification, isolation, and functional characterization of Notch-activated epicardial-derived cells (NECs) and their response to cardiac injurysurrogate

A dynamic Notch injury response activates adult epicardium to produce a multipotent cell population that contributes to fibrosis repair following cardiac injury.

Cite This Study

Russell et al. (2010) studied this question.

synapsesocial.com/papers/6a6f5c3226770c2b8ddff3a1https://doi.org/10.1161/circresaha.110.233262
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Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Inhibition of Notch1-Dependent Cardiomyogenesis Leads to a Dilated Myopathy in the Neonatal Heart2010 · 89 citations
  2. 2Identification of Myocardial and Vascular Precursor Cells in Human and Mouse Epicardium2007 · 223 citations
  3. 3Cardiac renewing: interstitial Cajal‐like cells nurse cardiomyocyte progenitors in epicardial stem cell niches2009 · 135 citations
  4. 4The origin of fibroblasts and mechanism of cardiac fibrosis2010 · 599 citations