Resident fibroblast expansion during cardiac growth and remodeling

• Published in: Journal of molecular and cellular cardiology Vol. 114; pp. 161 - 174
• Main Authors: Ivey, Malina J., Kuwabara, Jill T., Pai, Jonathan T., Moore, Richard E., Sun, Zuyue, Tallquist, Michelle D.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-01-2018
• Subjects: Cardiac fibroblast; Endothelial cell; Fibrosis; Proliferation; Endothelial cell; Col1a1; mCrem; IVS; Cardiac fibroblast; Proliferation; ECM; LAD; GFP; EdU; TAC; Fibrosis; αSMA; IB4; MI
• ISSN: 0022-2828; 1095-8584
• DOI: 10.1016/j.yjmcc.2017.11.012

Cardiac fibrosis, denoted by the deposition of extracellular matrix, manifests with a variety of diseases such as hypertension, diabetes, and myocardial infarction. Underlying this pathological extracellular matrix secretion is an expansion of fibroblasts. The mouse is now a common experimental model system for the study of cardiovascular remodeling and elucidation of fibroblast responses to cardiac growth and stress is vital for understanding disease processes. Here, using diverse but fibroblast specific markers, we report murine fibroblast distribution and proliferation in early postnatal, adult, and injured hearts. We find that perinatal fibroblasts and endothelial cells proliferate at similar rates. Furthermore, regardless of the injury model, fibroblast proliferation peaks within the first week after injury, a time window similar to the period of the inflammatory phase. In addition, fibroblast densities remain high weeks after the initial insult. These results provide detailed information regarding fibroblast distribution and proliferation in experimental methods of heart injury.
•Perinatal cardiac fibroblast proliferation parallels cardiomyocyte proliferation•Resident cardiac fibroblasts expand in distinct patterns after cardiac injury.•Fibroblast proliferation peaks in the first week after injury, then returns to basal levels.•The fibroblast proliferative phase is similar to the reported inflammatory phase.