Figure 7. Reducing oxidative stress rescues cell fate commitment and regenerative deficiency of ATGL-deficient SCs.

(A and B) Representative ROS staining (A) and quantification of ROS level (B) in FACS-sorted SCs from WT and Pnpla2^PKO mice. SCs were cultured for 4 days with or without 5 mM NAC. Vehicle: n = 3 mice, NAC: n = 4 mice. Scale bar, 10 μm.

(C and D) Representative cell growth image (C) and quantification of SC number (D) after NAC treatment. FACS-sorted SCs from WT and Pnpla2^PKO mice were cultured for 4 days with or without 5 mM NAC. Vehicle: n = 4 mice, NAC: n = 5 mice.

(E and F) Immunostaining of PAX7 and MyoD (E) and quantification of SC population (F) in WT and Pnpla2^PKO cultured muscle cell mixtures treated with 5 mM NAC (n = 3 mice). Scale bar, 10 μm.

(G and H) Immunostaining of PAX7 and MyoD (G) and quantification of quiescent (PAX7⁺/MyoD⁻) SCs reserved in cultures (H) upon 2 days differentiation (n = 4 mice). Scale bar, 10 μm.

(I) Experimental scheme for NAC treatment and CTX injury in WT and Pnpla2^PKO mice.

(J–L) Immunostaining of eMyHC and dystrophin (J) and quantification of the number (K) and CSA (L) of dystrophin⁺ myofiber on TA muscle cross-sections at 5.5 dpi after NAC treatment (n = 4 mice). Scale bar, 50 μm.

Data are mean ± standard deviation; Student’s t test. *p < 0.05, **p < 0.01, ***p < 0.001. n.s., not significant. See also Figure S7.