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Linking wall shear stress with cardiac trabeculation in zebrafish (LB654)

Biomechanical forces are intimately linked with cardiac development. Defects in the genetic programming are associated with congenital heart disease such as noncompaction cardiomyopathy. However, the mechano‐transduction mechanism underlying this morphological event remains elusive. Trabeculation starts to develop at 2 days post fertilization (dpf), and it is visualized at 3 dpf in zebrafish embryos. We hypothesized that endocardial wall shear stress (WSS) is implicated in trabecular formation during development. Gata1a morpholino oligonucleotides (MO) micro‐injection reduced erythropoiesis, leading a reduction in viscosity by 70% and consequently, a reduction in wall WSS by 70% via 2D Computational Fluid Dynamics. Similarly, gata2a MO resulted in 90% reduction in viscosity. Using the selective plane illumination microscopy technique, we observed an absence in ventricular trabeculation at 3 dap after gata1a, and gata2a MO injections, in line with that of tnnt2a MO silent heart morphant. Unlike gata1a, gata2a MO injected fish developed reappearance of trabeculation at 4 dfp from a compensatory increase in blood velocity by 32% via particle image velocimetry. Neither gata1a nor tnnt2a MO‐injected fish were able to compensate ventricular WSS with an increase in blood velocity at 4 dpf. Our preliminary finding provides a basis to link shear stress and ventricular trabeculation. Further co‐injection with gata MO and epo mRNA to test gene expression signaling involved in trabeculation would strengthen the mechano‐transduction mechanism.