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. 2021 Apr 22;6(8):e143285. doi: 10.1172/jci.insight.143285

Figure 4. Pericyte-driven angiogenesis is controlled by VEGFA165 signaling.

Figure 4

(A) The illustration shows selective blockage of VEGFA165 signaling with the drug BAW2881, which targets 2 VEGFA receptors, Flt1 and KDR/Flk1. (B) The number of new vessels is significantly reduced in a dose-dependent manner when VEGFA receptors are blocked with the specific VEGFA blocker, BAW2881 (n = 3 for control group, n = 4 for 1 nM, n = 3 for 4 nM, n = 3 for 40 nM, and ****P < 0.0001 by 1-way ANOVA). (C and D) Representative confocal projection images show branch formation in the VEGFA165 and VEGFA receptor blocked groups. (E) Illustration of construction of the AAV1-FLEX-VEGFA165-GFP viral vector, a Cre-dependent inversion gene switch (FLEX) vector, which specifically targets pericytes to produce VEGFA165. (F) Pericytes (red, genetically labeled by tdTomato) drive sprouting angiogenesis, as seen on day 5 in a Pdgfrb-CreER/tdTomato mouse cochlea. (G) The green AAV1-FLEX-VEGFA165-GFP signal is primarily targeted in tdTomato-labeled pericytes. (H) Merged image from F and G. (I and J) Sprouting growth in the AAV1-GFP control and AAV1-FLEX-VEGFA165 viral vector groups. (K) The number of branches is significantly higher in the AAV1-FLEX-VEGFA165 viral vector–transfected strial explant (n = 4 for AVV1-GFP group, n = 5 for AAV1-VEGFA165 group, and *P < 0.05 by Student’s t test). Data are presented as mean ± SEM. Scale bars: 100 μm (C, D, F–H), 150 μm (I, J).