Fig. 3: miR-322/-503 rescued myoblast differentiation defects and repressed ribonuclear foci in DM1. | Cell Death & Disease

Fig. 3: miR-322/-503 rescued myoblast differentiation defects and repressed ribonuclear foci in DM1.

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

Fig. 3

A Overexpression of miR-322/-503 in C2C12-CUG200 cells was verified by RT-qPCR. The expression levels of miR-322 and miR-503 were normalized to the control group. B miR-322/-503 overexpression significantly upregulated the expressions of myogenic markers (MyoD, MyoG, and Mef2C) and downregulated Celf1 during C2C12-CUG200 differentiation. All expression levels were normalized to the control group at day 0. C miR-322/-503 overexpression promoted myotube formation of C2C12-CUG200 differentiation. Myotube formation was displayed by immunostaining of MF20 on day 6. D miR-322/-503 overexpression increased myotube areas (left) and fusion index (right) of C2C12-CUG200 differentiation. E, F miR-322/-503 overexpression repressed ribonuclear foci formation in C212-CUG200 cell. The ribonuclear foci were detected with CAG probe RNA FISH. Control, C2C12-CUG200/control cells; miR-322/-503, C2C12-CUG200/miR-322/-503 cells; * statistically significant (p < 0.05).

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