Fig. 9: Notch activation enhances endothelial sprouting after calvarial bone injury.

a Longitudinal intravital multiphoton microscopy showing hypersprouting of Flk1-GFP⁺ (green) microvessels in Fbxw7 ^iΔEC Flk1-GFP transgenic mice after calvarial bone lesions at PLD12, PLD18, PLD27 and PLD36. Control Flk1-GFP⁺ transgenic mice are shown at PLD18 and PLD36. SHG⁺ calvarial bone (cb) and new bone (nb) are shown in blue. b Zoom-in view of control and Fbxw7 ^iΔEC microvasculature of controls at PLD12. Arrowheads point to luminized vessels in control. Note that mutant microvessels are aluminal. c Histograms showing complete and perfused vascular areas in calvarial lesions (as 100%) in control (left) and Fbxw7 ^iΔEC mice (right) over a period of 6 weeks. Data are presented as mean values ± SD. n = 6 independent vascular areas were examined over 3 biologically independent control animals and 3 biologically independent Fbxw7 ^iΔEC animals. d Histograms showing the number of sprouts in the lesion area in control and Fbxw7 ^iΔEC mice over a period of 6 weeks. Data are presented as mean values ± SD. n = 6 independent vessel areas were examined over 3 biologically independent control animals and 3 biologically independent Fbxw7 ^iΔEC animals. e Intravital multiphoton microscopy showing newly formed SHG⁺ bone (nb) with Flk1-GFP⁺ microvessels in close proximity to the growing bone edge in control and Fbxw7 ^iΔEC mice. Maximum intensity projections (top) and single planes (bottom) are shown. Arrowheads point to microvessels in proximity to the growing bone edge in control and Fbxw7 ^iΔEC mice. f Histogram showing the area of newly formed bone in calvarial lesions (as 100%) in control and Fbxw7 ^iΔEC mice over a period of 4 weeks. Data are presented as mean values ± SD with n = 4 biologically independent control animals and n = 3 biologically independent Fbxw7 ^iΔEC animals. Source data are provided as a Source Data file.