Fig. 2: miR-322/-503 was dysregulated in myotonic dystrophy type 1. | Cell Death & Disease

Fig. 2: miR-322/-503 was dysregulated in myotonic dystrophy type 1.

From: miR-322/-503 rescues myoblast defects in myotonic dystrophy type 1 cell model by targeting CUG repeats

Fig. 2

A Schematic diagram of GFP-CUG5 and GFP-CUG200. GFP-CUG5 was used to produce the normal C2C12 cell model (C2C12-CUG5) and GFP-CUG200 was used to produce the DM1 C2C12 model (C2C12-CUG200). B, C Ribonuclear foci were detected in C2C12-CUG200 cells with CAG probe RNA FISH, but not detected in C2C12-CUG5 cells. D Myogenic markers (MyoD, MyoG, and Mef2C) were significantly repressed but Celf1 was upregulated during myoblast differentiation of C2C12-CUG200 compared to C2C12-CUG5. All expression levels were normalized to the CUG5 group at day 0. E C2C12-CUG200 differentiation displayed impaired myotube formation compared to C2C12-CUG5. Myotube formation was displayed by immunostaining of MF20 on day 6. F C2C12-CUG200 differentiation showed decreased myotube areas (left) and fusion index (right) compared to C2C12-CUG5. G miR-322 and miR-503 were significantly downregulated at day 2 in C2C12-CUG200 differentiation. All expression levels were normalized to the CUG5 group at day 0. CUG5, C2C12-CUG5 cells; CUG200, C2C12-CUG200 cells; * statistically significant (p < 0.05).

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