Microscopy, image analysis and computational data underlying the publication "A non-canonical role for Jagged1 in endothelial mechanotransduction"

The Notch signaling pathway plays a crucial role in regulating endothelial biology. Notch signaling is sensitive to hemodynamic forces and governs mechanically-driven cardiovascular development, physiology, and remodeling. However, mechanisms integrating mechanical forces with the Notch pathway remain largely unknown. Here, we uncover a non-canonical role for the Notch ligand Jagged1 as a mechanotransducer in endothelial cells. Jagged1 undergoes polarization in response to laminar shear stress and exhibits an unimodal expression pattern, peaking at a shear stress magnitude of 0.8-1 Pa. Jagged1 regulates endothelial mechanotransduction via the VEGFR2/ERK pathway. Deletion of Jagged1 results in reduced shear stress-induced kinase activity in vitro and diminished kinase activity in zebrafish embryos, without affecting canonical Notch signaling. Furthermore, direct physical activation of Jagged1 using antibody-conjugated beads triggers VEGFR2/ERK2 signaling, mediated by Jagged1-Src interaction and Src activation. These findings highlight a novel, non-canonical function of Jagged1 as a mechanotransducer in endothelial cells.<br>This dataset contains microscopy and image analysis data from in vivo and in vitro experiments related to Jagged1 in the endothelial response to hemodynamic stress. It also includes computer fluid dynamics simulations of an orbital shaker system to induce controlled shear stress magnitude and flow pattern.