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MOESM6 of Defective angiogenesis in CXCL12 mutant mice impairs skeletal muscle regeneration

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posted on 2019-09-19, 04:10 authored by David Hardy, Mylène Fefeu, Aurore Besnard, David Briand, Paméla Gasse, Fernando Arenzana-Seisdedos, Pierre Rocheteau, Fabrice Chrétien
Additional file 6: Figure S5. (Related to Figure 4). Quantitative histological and cytometric parameters of the muscle one month post FI in WT and CXCL12Gagtm/Gagtm mice. RTqPCR gene expression in FACS-sorted MPs, FAPs, SCs, ECs from TA muscle without injury and TA 12 days post FI from WT-Pax7 and KI-Pax7 with relative expression, represented as a log2, of total CXCL12 gene (A), alpha CXCL12 isoform gene (B), beta CXCL12 isoform gene (C) and gamma CXCL12 isoform gene (D). The data are represented in Log2 and n=3 animals per condition for uninjured mice, n=5 animals for injured WT-Pax7 mice and n=6 animals for injured KI-Pax7 mice. Quantification of (E) the number of fibers and (F) the fiber’s diameter by Hematoxylin-eosin staining in the uninjured and post FI TA from WT (C57Bl6) and CXCL12Gagtm/Gagtm mice. Three animals (n=3) were used per condition and were repeated independently two times. (G) Quantification of the number of vessels by CD31 immunostaining in the uninjured and the post FI injured TA from WT (C57Bl6) and CXCL12Gagtm/Gagtm mice. Three animals (n=3) were used per condition and were repeated independently two times. (H) Quantification of GFP-positive cells by FACS analysis per the TA of uninjured and post FI injured WT (Flk1GFP/+) vs. KI (CXCL12Gagtm/Gagtm :: Flk1GFP/+) mice. (n=5 mice per condition). Data are given as the mean ± SEM. * p < 0.05; ** p < 0.01, *** p < 0.001.

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