Fig. 5

The abnormalities of vascular structures are associated with an absence of close contact with perivascular cells and with a functional perfusion defect post-FI in the KI mice. a–f Longitudinal blood vessel organization of the TA respectively before and 30 days post-FI in a, d WT (Flk1^GFP/+) and b, c, e, f KI (CXCL12^Gagtm/Gagtm:Flk1^GFP/+) mice. Scale bar represent 10 μm. n = 3 animals per condition and per time point. All the experiments were repeated independently two times. Representative Sirius Red staining 1 month post-FI of the TA from g WT (C57Bl6) and i KI (CXCL12^Gagtm/Gagtm) mice. Scale bar represent 200 μm. Immunostaining for ECs (CD31, red), pericytes (NG2, white), and smooth muscle cells (α-SMA, yellow) from the indicated zones of h injured TA from the WT, and j the regenerated or k the fibrotic TA from KI mice. Scale bar represent 20 μm. n = 3 animals per condition. All the experiments were repeated independently two times. l, m Direct contrast enhancement MRI assessment of vascular functionality: vascular tracer signal intensity per number of acquisitions comparing one WT (C57Bl6) to one KI (CXCL12^Gagtm/Gagtm) mouse l before and m after 1 month post-FI. n The mean area under curve (AUC) ± SEM of vascular tracer intensity 1 month post-FI is given (n = 6 WT mice and n = 7 KI mice). *p < 0.05