Fig. 7: Wnt/β-catenin pathway is involved in LYPLAL1-AS1/DSP-regulated adipogenic differentiation of hAMSCs.

a Western blot analysis of β-catenin and DSP in DSP knockdown hAMSCs (si-DSP-2, si-DSP-3) and control hAMSCs (si-NC) and western blot analysis of β-catenin in hAMSCs that overexpress LYPLAL1-AS1 (Lenti-LYPLAL1-AS1) and control hAMSCs (Lenti-NC). b Western blot analysis of β-catenin, DSP, and adipogenic markers (PPARγ, AP2, and LPL) in hAMSCs that overexpress LYPLAL1-AS1 (Lenti-LYPLAL1-AS1; Lenti-lnc+) and control hAMSCs (Lenti-NC; Lenti-lnc−) after treatment without or with chir99021. c qRT-PCR analysis of LYPLAL1-AS1 and adipogenic markers (PPARγ, AP2, and LPL) in hAMSCs that overexpress LYPLAL1-AS1 and control hAMSCs after treatment without or with chir99021. d qRT-PCR analysis of LYPLAL1-AS1 and DSP in DSP knockdown (si-DSP-2, si-DSP-3) and control hAMSCs after treatment without or with chir99021. e qRT-PCR analysis of adipogenic markers (PPARγ, AP2, and CEBPα) in DSP knockdown and control hAMSCs after treatment without or with chir99021. f Western blot analysis of β-catenin and adipogenic markers (PPARγ, AP2, and CEBPα) in DSP knockdown and control hAMSCs after treatment without or with chir99021.GAPDH was used as the internal control for the western blot assays. The quantitative data were normalized to GAPDH, n = 3; data are shown as the mean ± SD; *P < 0.05, **P < 0.01, ***P < 0.001; n.s., not significant.