Embryo exposure to elevated cortisol level leads to cardiac performance dysfunction in zebrafish.

In zebrafish (Danio rerio), de novo cortisol synthesis commences only after hatching, providing an interesting model to study the effects of maternal stress and abnormal cortisol deposition on embryo development and performance. We hypothesized that elevated cortisol levels during pre-hatch embryogenesis compromise cardiac performance in developing zebrafish. Cortisol was microinjected into one-cell embryos to elevate basal cortisol levels during embryogenesis. Elevated embryo cortisol content increased heart deformities, including pericardial edema and malformed chambers, and lowered resting heartbeat post-hatch. This phenotype coincided with suppression of key cardiac genes, including nkx2.5, cardiac myosin light chain 1, cardiac troponin type T2A, and calcium transporting ATPase, underpinning a mechanistic link to heart malformation. The attenuation of the heartbeat response to a secondary stressor post-hatch also confirms a functional reduction in cardiac performance. Altogether, high cortisol content during embryogenesis, mimicking increased deposition due to maternal stress, decreases cardiac performance and may reduce zebrafish offspring survival.