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. 2019 Jan 30;10(2):391–410. doi: 10.1002/jcsm.12374

Figure 7.

Figure 7

LncIRS1 promotes myoblast differentiation via IGF‐1 signalling pathway. (A) mRNA expression of lncIRS1 and IRS1 after lncIRS1 knockdown in myoblasts. (B) mRNA expression of lncIRS1 and IRS1 after IRS1 knockdown in myoblasts. (C) Co‐expression of miR‐15a, miR‐15b‐5p, or miR‐15c‐5p with lncIRS1 up‐regulated the expression level of IRS1. (D) Overexpression of lncIRS1 or IRS1 increased the protein expression level of IRS1, p‐AKT, MyoG, and MyHC. (E) Knockdown of lncIRS1 or IRS1 reduced the protein expression level of IRS1, p‐AKT, MyoG, and MyHC. (F) Effect of lncIRS1 overexpression, lncIRS1 knockdown, and miR‐15 family on Atrogin‐1 protein expression. (G) Effect of lncIRS1 overexpression on Atrogin‐1 RNA expression. (H) Effect of lncIRS1 overexpression on MuRF1 RNA expression. (I) Effect of lncIRS1 knockdown on Atrogin‐1 RNA expression. (J) Effect of lncIRS1 knockdown on MuRF1 RNA expression in all panels, Myoblast cells transfected with above‐indicated chemicals (plasmid DNA, siRNAs, or miRNAs) were induced to differentiate for 48 hr then detected with qRT‐PCR or Western blot analysis. Results are shown as the mean ± SEM of three independent experiments. Independent sample t‐test was used to analysis the statistical differences between groups. * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.