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Fig. 8 | Journal of Nanobiotechnology

Fig. 8

From: Congenital microtia patients: the genetically engineered exosomes released from porous gelatin methacryloyl hydrogel for downstream small RNA profiling, functional modulation of microtia chondrocytes and tissue-engineered ear cartilage regeneration

Fig. 8

The hsa-miR-23a-3p overexpressing or silencing promoted or attenuated the effect of 3D-Exo on microtia chondrocytes. (A) Microtia chondrocytes were treated with hsa-miR-23a-3p mimics/inhibitor or their negative control (nc) for 24 h, and the expression of miR-23a-3p was measured by qPCR. (B) Cell proliferation assessed by the Cell Counting Kit-8 after exposure to hsa-miR-23a-3p mimics/inhibitor or their negative control (nc). (C) Representative images of cell apoptosis analysis and a quantified comparison of cell early/late apoptosis between the treatment of mimics and nc, or between the treatment of inhibitor and nc. (D) Quantitative RT-PCR analysis showed regulation of genes at 48h post-treatment associated with anti-apoptosis (Survivin, Bcl-2), proliferation (PCNA, FGF-2), as well as chondrogenic differentiation and ear cartilage matrix proteins synthesis (TGF-β1, COL2A1, ACAN, ELN, SOX9 and COMP). The genes (COL1A1 and MMP 9) unfavorable for the synthesis of hyaline cartilage and elastic cartilage were also assessed. After exposure to hsa-miR-23a-3p mimics/nc (E), or inhibitor/nc (F), western blotting analysis was used for quantifying the protein levels of PTEN, P-PI3K/PI3K, P-AKT/ AKT, mTOR and cartilage matrix (i.e. elastin, collagen II, SOX9 and collagen I) in microtia chondrocytes. Data was presented as the mean ±SD of three number of replicates. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, ns: no significance

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