Abstract
Blood flow is critical for normal cardiac development. Hemodynamic stimuli outside of normal ranges can lead to overt cardiac defects, but how early heart tissue remodels in response to altered hemodynamics is poorly understood. This study investigated changes in tissue collagen in response to hemodynamic overload in the chicken embryonic heart outflow tract (OFT) during tubular heart stages (HH18 to HH24, ~24 h). A suture tied around the OFT at HH18 was tightened to constrict the lumen for ~24 h (constriction range at HH24: 15–60%). Expression of fibril collagens I and III and fibril organizing collagens VI and XIV were quantified at the gene and protein levels via qPCR and quantitative immunofluorescence. Collagen I was slightly elevated upstream of the band and in the cushions in banded versus control OFTs. Changes in collagen III were not observed. Collagen VI deposition was elevated downstream of the band, but not overall. Collagen XIV deposition increased throughout the OFT, and strongly correlated to lumen constriction. Interestingly, organization of collagen I fibrils was observed for the tighter banded embryos in regions that also showed increase in collagen XIV deposition, suggesting a potentially key role for collagens I and XIV in the structural adaptation of embryonic heart tissue to hemodynamic overload.
Highlights
Blood flow is needed for normal heart development, and in its absence cardiac formation is severely impaired [1]
Blood flow velocity through the banded outflow tract (OFT) at HH24 was dependent on the degree of band constriction (20–60% band tightness, relative to average OFT diameter at an equivalent location in shams); a strong linear relationship was observed between peak velocity and OFT maximum diameter at the band site (Pearson’s correlation coefficient = −0.88, Figure 3E)
Hemodynamic overload during early heart development alters OFT collagen distribution, which may lead to a detrimental tissue remodeling and the formation of cardiac defects
Summary
Blood flow is needed for normal heart development, and in its absence cardiac formation is severely impaired [1]. Perturbations in hemodynamic stresses (blood pressure, wall shear stress) outside the normal range during early embryonic heart development lead to overt cardiac structural changes, e.g., [3,4,5,6,7], that are similar to human congenital heart defects. Human congenital heart defects such as transposition of the great arteries, truncus arteriosus, tetralogy of Fallot (TOF), double-outlet right ventricle (DORV), and ventricular septal defects (VSD) are known to arise from abnormalities of the OFT [8,9] These defects are found in animal models after interventions that alter normal blood flow conditions [3,4,5,6,7]. About the cardiac tissue remodeling (change in composition) that occurs in response to altered hemodynamic conditions
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