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MOESM5 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 5: Figure S4. (Related to Figure 3). Quantitative histological and cytometric parameters of the muscle one month post NTX injury in the WT and the CXCL12Gagtm/Gagtm mice. (A) Quantification of calcium deposits number by Von Kossa staining in 12 days and one month post NTX injured TA from WT (C57Bl6) and CXCL12Gagtm/Gagtm mice. Three animals (n=3) were used per condition and were repeated independently two times. (B) Representative Von Kossa stained TA section 12 post NTX injury in KI (CXCL12Gagtm/Gagtm) mice. Scale bar represent 100μm. Quantification of (C) fibers number and (D) fibers diameter by Hematoxylin-eosin staining in uninjured and post NTX injured TA from WT (C57Bl6) and CXCL12Gagtm/Gagtm mice. Three animals (n=3) were used per condition and were repeated independently two times. (E) Quantification of vessels number by CD31 immunostaining in the uninjured and the post NTX injured TA from WT (C57Bl6) and CXCL12Gagtm/Gagtm mice. Three animals (n=3) were used per condition and were repeated independently two times. (F) Quantification of GFP-positive cells by FACS analysis per TA of the uninjured and the post NTX 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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