Fig. 4: LncDACH1 promotes dedifferentiated VSMC proliferation, migration, and phenotypic switching by upregulating HSP90.

a, b Protein expression levels of HSP90, p-AKT and AKT after overexpression (n = 3) or silencing (n = 5) of LncDACH1 in VSMC were detected using Western Blot. VSMC is divided into the following four groups: si-NC, si-LncDACH1, si-HSP90, si-LncDACH1+si-HSP90. c p-AKT and AKT protein expression levels were detected by Western Blot (n = 3). d, e The proliferation capacity of VSMC was tested by EdU staining assay (n = 3). Scale bar, 25 μm. f The proliferation capacity of VSMC was examined by CCK8 assay (n = 3). g, h The ability of VSMC to migrate was tested by Wound Healing assays (n = 3). Scale bar, 100 μm. i The ability of VSMC to migrate was tested by Transwell assay (n = 3). Scale bar, 50 μm. j, k Protein expression levels of VSMC differentiation phenotype markers and dedifferentiation phenotype markers were measured by Western Blot assay (n = 3). l RIP was used to assess the binding capacity between LncDACH1 and HSP90 proteins. PDGF-BB (P), control (CTRL), negative control (NC), overexpression (OE), small interfering (SI). The n numbers represent biologically independent samples. Data are presented as mean values ± SD (a–c, e, f, h, i, k, l). P-values were determined by two-sided nonparametric tests (b, l) and two-sided one-way ANOVA (a, c, e, f, h, i, k) by Bonferroni’s multiple comparisons test. Source data are provided as a Source Data file.