Journal: Bioactive Materials

Article Title: Modeling human hypertrophic scars with 3D preformed cellular aggregates bioprinting

doi: 10.1016/j.bioactmat.2021.09.004

Figure Lengend Snippet: Performance of predicted drugs in the bioprinted scar model. (A) The enrichment of gene sets from the GO database. (B) Schematic illustration of mechanism of drug screen. (C, D) The expression of pro-fibrotic molecule and anti-fibrotic molecule at gene (C) (Data are mean ± SEM, n = 3, * p < 0.05) and protein (D) level (α-SMA, TGFβ1, TGFβ3: green, DAPI: blue, scale bar = 25 μm). 3ASS: 3A5G+SFb+scar ECM, 3A–D: 3ASS+DMSO, 3A–A: 3ASS+ Abemaciclib, 3A–C: 3ASS+ Cobimetinib, 3A–T: 3ASS+ Triamcinolone acetonide. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: 3D-bioprinted scar model was treated with Abemaciclib (CDK4/6 inhibitor, MCE), Cobimetinib (MEK1/2 inhibitor, MCE) and Triamcinolone acetonide (glucocorticoid for clinical application, KUNMIN JIDA).

Techniques: Expressing

Journal: Bioactive Materials

Article Title: Modeling human hypertrophic scars with 3D preformed cellular aggregates bioprinting

doi: 10.1016/j.bioactmat.2021.09.004

Figure Lengend Snippet: Transplantation of scar model into adult immunodeficient mice displays characteristics of early stage of scar and confirmed the effect of screened drugs. (A) Schematic illustration of the whole process of animal test. (B) The macroscophic images of scar formation in different groups. (C) HE (Scale bar = 200 μm) and Masson images (Scale bar = 200 μm) of scar tissue in different groups. (D) The expression of myofibroblasts markers in different groups (α-SMA, Col I: red, DAPI: blue, scale bar = 100 μm). 3A5G: 3A5G+SFb+scar ECM, 3A–C: 3ASS+ Cobimetinib, 3A–T: 3ASS+ Triamcinolone acetonide. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: 3D-bioprinted scar model was treated with Abemaciclib (CDK4/6 inhibitor, MCE), Cobimetinib (MEK1/2 inhibitor, MCE) and Triamcinolone acetonide (glucocorticoid for clinical application, KUNMIN JIDA).

Techniques: Transplantation Assay, Expressing

Journal: Arthritis research & therapy

Article Title: Semaphorin 5A promotes Th17 differentiation via PI3K-Akt-mTOR in systemic lupus erythematosus.

doi: 10.1186/s13075-024-03437-z

Figure Lengend Snippet: Fig. 6 Sema5A promotes the activation of AKT-mTOR pathway in CD4 + T cells through PlexinA1. A. Activated CD4+ T cells were cultured for 24 h in medium containing Sema5A or PBS solution, followed by stimulating for 1 h with the Th17 cocktail; the phosphorylation of AKT and mTOR was detected by Western-blotting. B. Activated CD4+ T cells were transfected with siRNA-Plexin A1- or universal control siRNA (NC) for 24 h, and resuspended in fresh medium containing Sema5A or PBS solution for another 24 h, followed by stimulating for 1 h with the Th17 cocktail; the phosphorylation of AKT and mTOR was detected by Western-blotting. * : P < 0.05, ** : P < 0.01. C. Activated CD4+ T cells were cultured for 4 h in medium containing pictilisib (PI3K in hibitor), MK-2206 (AKT inhibitor), and temsirolimus (mTOR inhibitor), then cells were resuspended in medium with Sema5A or PBS solution for 24 h under Th17-inducing conditions, and the IL-17 A level in the culture supernatant was detected by ELISA. Tukey test *: P < 0.05

Article Snippet: They are PI3K inhibitor, pictilisib (GDC-0941, HY-50094; MCE) 10 μM, AKT inhibitor, MK-2206 (HY-108232; MCE) 5 μM, and mTOR inhibitor, temsirolimus (CCI779, HY-50910; MCE) 100 nM.

Techniques: Activation Assay, Cell Culture, Phospho-proteomics, Western Blot, Transfection, Control, Enzyme-linked Immunosorbent Assay