Notch signaling regulates venous arterialization during zebrafish fin regeneration.

To protect against blood pressure, a mature artery is supported by mural cells which include vascular smooth muscle cells and pericytes. To regenerate a functional vascular system, arteries should be properly reconstructed with mural cells although the mechanisms underlying artery reconstruction remain unclear. In this study, we examined the process of artery reconstruction during regeneration of the zebrafish caudal fin as a model to study arterial formation in an adult setting. During fin regeneration, the arteries and veins form a net-like vasculature called the vascular plexus, and this plexus undergoes remodeling to form a new artery and two flanking veins. We found that the new vascular plexus originates mainly from venous cells in the stump but very rarely from the arterial cells. Interestingly, these vein-derived cells contributed to the reconstructed arteries. This arterialization was dependent on Notch signaling, and further analysis showed that Notch signaling was required for the initiation of arterial gene expression. In contrast, venous remodeling did not require Notch signaling. These results provide new insights toward understanding mechanisms of vascular regeneration and illustrate the utility of the adult zebrafish fin to study this process.

Basal-to-apical cadherin flow at cell junctions.

Stable cell-cell adhesion is essential for maintaining tissue integrity, but cells are also able to relocate, implying the existence of mechanisms for coordinating cell adhesion and movement. Here, we show that, in some transformed lines, cadherin adhesion molecules exhibit a flow-like movement in a basal-apical direction at the cell junction and that this flow is associated with reorganizing actin filaments. Such flow also occurs in normal epithelial sheets, but solely at the junctions formed by moving cells. We propose that cadherin flow may provide a mechanism for facilitating the sliding of the two contacting cell membranes in morphogenetically active cell sheets.