[Retracted] NORAD Promotes the Viability, Migration, and Phenotypic Switch of Human Vascular Smooth Muscle Cells during Aortic Dissection via LIN28B-Mediated TGF-β Promotion and Subsequent Enhanced Glycolysis

Figure 4

NORAD facilitates VSMC growth and migration via NORAD/LIN28B/TGF-β axis. (a) TGF-β high expression partially corrected the antagonistic impact of NORAD silencing upon the CCK-8 assay of VSMCs. (b) TGF-β overexpression partly reversed the effects of NORAD knockdown on migration of VSMCs. (c, d) The impact of NORAD silencing on the suppression of glucose intake and lactate generation in VSMCs could be rescued by TGF-β overexpression. (e, f) TGF-β overexpression could rescue the antagonistic impact of NORAD silencing on the glycolytic process in VSMCs, as reflected by ECAR and OCR analysis. Data were represented as the . was shown in comparison to the negative control. ^# was shown in comparison to the sh-NORAD with the negative control.

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