Fig. 5: Anti-insulin-like growth factor 1 receptor (IGF1R) antibody administration inhibits specific signaling molecules involved in the regulation of the neuromuscular junction (NMJ). | Cell Death & Disease

Fig. 5: Anti-insulin-like growth factor 1 receptor (IGF1R) antibody administration inhibits specific signaling molecules involved in the regulation of the neuromuscular junction (NMJ).

From: Blocking insulin-like growth factor 1 receptor signaling pathway inhibits neuromuscular junction regeneration after botulinum toxin-A treatment

Fig. 5

A Representative images of western blot analysis of downstream signaling molecules of IGF1R in mouse gastrocnemius (GC) muscles at 2 weeks after saline or botulinum toxin-A (BTX) injection with antibody administration. Control IgG antibody treatment is represented as cont IgG and anti-IGF1R antibody treatment as IGF1R. B Quantification of the p-mTOR (S2448)/mTOR, p-mTOR (S2481)/mTOR, p-S6K/S6K, p-Akt/Akt, p-FoxO1/FoxO1, and light chain 3BII/light chain 3BI(LC3BII/LC3BI) ratios. Values are presented as the mean ± standard error of the mean (SEM), ns, not significant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, analyzed with one-way ANOVA followed by post-hoc Tukey’s test (N = 4 per group). C Transcript levels of Hdac4, Myog, Fbxo32, Chrna1, Chrnd, Musk, Lrp4, and Ache in the GC muscle 2 weeks following saline or BTX injection with an antibody treatment. Values are presented as mean ± SEM, ns, not significant, *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, analyzed with one-way ANOVA followed by post-hoc Tukey’s test (N = 3 per group). D Scheme illustrating the role of IGF signaling pathway in the muscle response to denervation by BTX and signaling pathway affected by anti-IGF1R antibody administration.

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