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Characterization of cardiac fibroblast-extracellular matrix crosstalk across developmental ages provides insight into age-related changes in cardiac repair.
Perreault, Luke R; Daley, Mark C; Watson, Matthew C; Rastogi, Sagar; Jaiganesh, Ajith; Porter, Elizabeth C; Duffy, Breanna M; Black, Lauren D.
Afiliación
  • Perreault LR; Department of Biomedical Engineering, Tufts University, Medford, MA, United States.
  • Daley MC; Department of Biomedical Engineering, Tufts University, Medford, MA, United States.
  • Watson MC; Department of Biomedical Engineering, Tufts University, Medford, MA, United States.
  • Rastogi S; Department of Biomedical Engineering, Tufts University, Medford, MA, United States.
  • Jaiganesh A; Department of Biomedical Engineering, Tufts University, Medford, MA, United States.
  • Porter EC; Cellular, Molecular and Developmental Biology Program, Graduate School for Biomedical Sciences, Tufts University School of Medicine, Boston, MA, United States.
  • Duffy BM; Department of Biomedical Engineering, Tufts University, Medford, MA, United States.
  • Black LD; Department of Biomedical Engineering, Tufts University, Medford, MA, United States.
Front Cell Dev Biol ; 12: 1279932, 2024.
Article en En | MEDLINE | ID: mdl-38434619
ABSTRACT
Heart failure afflicts an estimated 6.5 million people in the United States, driven largely by incidents of coronary heart disease (CHD). CHD leads to heart failure due to the inability of adult myocardial tissue to regenerate after myocardial infarction (MI). Instead, immune cells and resident cardiac fibroblasts (CFs), the cells responsible for the maintenance of the cardiac extracellular matrix (cECM), drive an inflammatory wound healing response, which leads to fibrotic scar tissue. However, fibrosis is reduced in fetal and early (<1-week-old) neonatal mammals, which exhibit a transient capability for regenerative tissue remodeling. Recent work by our laboratory and others suggests this is in part due to compositional differences in the cECM and functional differences in CFs with respect to developmental age. Specifically, fetal cECM and CFs appear to mitigate functional loss in MI models and engineered cardiac tissues, compared to adult CFs and cECM. We conducted 2D studies of CFs on solubilized fetal and adult cECM to investigate whether these age-specific functional differences are synergistic with respect to their impact on CF phenotype and, therefore, cardiac wound healing. We found that the CF migration rate and stiffness vary with respect to cell and cECM developmental age and that CF transition to a fibrotic phenotype can be partially attenuated in the fetal cECM. However, this effect was not observed when cells were treated with cytokine TGF-ß1, suggesting that inflammatory signaling factors are the dominant driver of the fibroblast phenotype. This information may be valuable for targeted therapies aimed at modifying the CF wound healing response and is broadly applicable to age-related studies of cardiac remodeling.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Front Cell Dev Biol Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Front Cell Dev Biol Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Suiza