Fig. 2: LYPLAL1-AS1 depletion inhibits adipogenic differentiation of hAMSCs, whereas its overexpression promotes this process. | Cell Death Discovery

Fig. 2: LYPLAL1-AS1 depletion inhibits adipogenic differentiation of hAMSCs, whereas its overexpression promotes this process.

From: Long noncoding RNA LYPLAL1-AS1 regulates adipogenic differentiation of human mesenchymal stem cells by targeting desmoplakin and inhibiting the Wnt/β-catenin pathway

Fig. 2

a LYPLAL1-AS1 was silenced in hAMSCs using two independent siRNAs (siRNA-1 and siRNA-2). The knockdown efficiency was verified by qRT-PCR as compared with the negative control (si-NC). b. qRT-PCR analysis of adipogenic markers (PPARγ, AP2, LPL, and CEBPα) in hAMSCs with LYPLAL1-AS1 knockdown and in control hAMSCs on day 3 after adipogenic induction. c Western blot analysis of adipogenic markers (PPARγ, AP2, LPL, and CEBPα) in LYPLAL1-AS1 knockdown hAMSCs or control hAMSCs on days 3 and 6 after adipogenic induction. d, e Oil red O staining of adipose lipids in hAMSCs treated with LYPLAL1-AS1 siRNAs and in control hAMSCs on day 10 after adipogenic induction (d) and quantification of the oil red O staining (e). f, g hAMSCs were transduced with lentivirus overexpressing LYPLAL1-AS1 (Lenti-LYPLAL1-AS1) or control lentivirus (Lenti-NC), and ectopic overexpression efficiency was detected by fluorescence observation (f) and qRT-PCR (g). h, i qRT-PCR (h) and western blot (i) analysis of adipogenic markers (PPARγ, AP2, and LPL) in hAMSCs that overexpressed LYPLAL1-AS1 and in control hAMSCs on day 3 after adipogenic induction. j, k Oil red O staining of adipose lipids in hAMSCs that overexpressed LYPLAL1-AS1 and in control hAMSCs on day 10 after adipogenic induction (j) and quantification of the oil red O staining (k). GAPDH was used as internal controls for western blotting. The quantitative data were normalized to GAPDH, n = 3; data are shown as the mean ± SD; **P < 0.01, ***P < 0.001; scale bars: 200 µm.

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