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- W2785020289 abstract "Endothelial cells respond to different levels of fluid shear stress through adaptations of their mechanosensitivity. Currently, we lack a good understanding of how this contributes to sculpting of the cardiovascular system. Cerebral cavernous malformation (CCM) is an inherited vascular disease that occurs when a second somatic mutation causes a loss of CCM1/KRIT1, CCM2, or CCM3 proteins. Here, we demonstrate that zebrafish Krit1 regulates the formation of cardiac valves. Expression of heg1, which encodes a binding partner of Krit1, is positively regulated by blood-flow. In turn, Heg1 stabilizes levels of Krit1 protein, and both Heg1 and Krit1 dampen expression levels of klf2a, a major mechanosensitive gene. Conversely, loss of Krit1 results in increased expression of klf2a and notch1b throughout the endocardium and prevents cardiac valve leaflet formation. Hence, the correct balance of blood-flow-dependent induction and Krit1 protein-mediated repression of klf2a and notch1b ultimately shapes cardiac valve leaflet morphology." @default.
- W2785020289 created "2018-02-02" @default.
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- W2785020289 date "2018-02-01" @default.
- W2785020289 modified "2023-10-13" @default.
- W2785020289 title "Heg1 and Ccm1/2 proteins control endocardial mechanosensitivity during zebrafish valvulogenesis" @default.
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- W2785020289 doi "https://doi.org/10.7554/elife.28939" @default.
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