creb1 shrna  (Genechem)

Journal: Nature Communications

Article Title: Catecholaminergic neurons boost fibroblast osteogenic activity in keloid

doi: 10.1038/s41467-026-72823-9

Figure Lengend Snippet: a cAMP quantitation of keloid fibroblasts treated or not with epinephrine in the presence or absence of metoprolol for 30 min ( n = 2 biologically independent samples for fibroblasts treated with epinephrine in the presence of metoprolol, and n = 3 biologically independent samples for other groups). b qPCR analysis of TSN expression in keloid fibroblasts treated or not with epinephrine in the presence or absence of PKA inhibitor or CREB inhibitor for 6 h ( n = 4 biologically independent samples for fibroblasts treated with epinephrine in the presence of CREB inhibitor, and n = 5 biologically independent samples for other groups). c Immunoblotting and quantitative analysis of IBSP and TSN expression in keloid fibroblasts treated or not with epinephrine in the presence or absence of PKA inhibitor or CREB inhibitor for 24 h ( n = 3 biologically independent samples). d qPCR analysis of the abundance of the TSN promoter that immunoprecipitated with αCREB1 or IgG control in keloid fibroblasts treated or not with epinephrine in the presence or absence of metoprolol for 30 min ( n = 6 biologically independent samples for Epinephrine-CREB1 and Epinephrine & Metoprolol-CREB1, and n = 5 biologically independent samples for other groups). Data are presented as the percentages of αCREB1- or IgG-pulled TSN promoter relative to that in the input. Data represent the mean ± SD; p -values were determined by one-way ANOVA. Data are representative of at least 2 independent experiments.

Article Snippet: For the assays involving PKA or CREB antagonism, keloid fibroblasts were treated with 1 μM PKA Inhibitor Fragment (6-22) amide TFA (MCE cat. HY-P1290A) or the CREB inhibitor 666-15 (MCE cat. HY-101120) for 1 h before the addition of epinephrine.

Techniques: Quantitation Assay, Expressing, Western Blot, Immunoprecipitation, Control

Journal: Bioactive Materials

Article Title: Integrated cryopreservation-thawing-transplantation platform for neural stem cell-based spinal cord injury repair

doi: 10.1016/j.bioactmat.2026.01.024

Figure Lengend Snippet: Mechanisms of NSC Differentiation into Neurons Promoted by Composite In Vitro. A) Schematic of the interactive system with NSCs and the composites. B) Representative confocal images of NSCs treated with distinct groups for 72 h. NSCs were stained with Tuj-1 (red), GFAP (green), and DAPI (blue). Scale bar: 50 μm. C-D) Quantitative analysis of Tuj-1 (C) and GFAP (D) fluorescence intensity in each group (n = 4). E) Western blot bands of Tuj-1 and GFAP protein expression in NSCs treated with separate groups. F-G) Quantitative analysis of Tuj-1/GAPDH (F) and GFAP/GAPDH (G) ratios in each group (n = 3). H) Volcano plots of DEGs in the hUCMSC-Exo + PM vs. control. DEGs are defined as |log2FC| ≥ 1 with q < 0.05. I-J) GO and KEGG pathway enrichment analysis of DEGs in NSCs after intervention with hUCMSC-Exo + PM. K) Heatmap showing the expression levels of significantly altered genes in the hUCMSC-Exo + PM and Control. L) GSEA showing pathways significantly positively correlated with DEGs in the hUCMSC-Exo + PM group. Enrichment scores (ES), P values, and false discovery rates (FDR) values are indicated for each pathway. M) Western blot bands of p-CaMK II, CaMK II, p-CREB, CREB, p-PI3K, PI3K, p-AKT, and AKT protein expression in NSCs treated with distinct groups. N) Quantitative analysis of p-CaMK II/CaMK II, p-CREB/CREB, p-PI3K/PI3K, and p-AKT/AKT ratios (n = 3). All data are presented as the mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: The primary antibodies used in this research are listed below: CD68 (Abcam, Cambridge, UK), CD206 (Abcam, Cambridge, UK), GFAP (Bioss, Beijing, China), iNOS (Abcam, Cambridge, UK), Tuj-1 (Abcam, Cambridge, UK), NF-200 (Invitrogen, CA, USA), MBP (Abcam, Cambridge, UK), HIF-1α (Abcam, Cambridge, UK), VEGFA (Abcam, Cambridge, UK), P-CaMKII (Abcam, Cambridge, UK), CaMKII (Abcam, Cambridge, UK), P-CREB (Cell Signaling Technology, USA), CREB (Cell Signaling Technology, USA), P-PI3K (Cell Signaling Technology, USA), PI3K (Cell Signaling Technology, USA), P-AKT (Cell Signaling Technology, USA), AKT (Cell Signaling Technology, USA), Cleaved-Caspase3 (Cell Signaling Technology, USA), Bcl-2 (Cell Signaling Technology, USA), Bax (Cell Signaling Technology, USA), GAPDH (Proteintech, IL, USA).

Techniques: In Vitro, Staining, Fluorescence, Western Blot, Expressing, Control

Journal: Bioactive Materials

Article Title: Integrated cryopreservation-thawing-transplantation platform for neural stem cell-based spinal cord injury repair

doi: 10.1016/j.bioactmat.2026.01.024

Figure Lengend Snippet: Mechanisms of NSC Differentiation into Neurons Promoted by Composite In Vitro. A) Schematic of the interactive system with NSCs and the composites. B) Representative confocal images of NSCs treated with distinct groups for 72 h. NSCs were stained with Tuj-1 (red), GFAP (green), and DAPI (blue). Scale bar: 50 μm. C-D) Quantitative analysis of Tuj-1 (C) and GFAP (D) fluorescence intensity in each group (n = 4). E) Western blot bands of Tuj-1 and GFAP protein expression in NSCs treated with separate groups. F-G) Quantitative analysis of Tuj-1/GAPDH (F) and GFAP/GAPDH (G) ratios in each group (n = 3). H) Volcano plots of DEGs in the hUCMSC-Exo + PM vs. control. DEGs are defined as |log2FC| ≥ 1 with q < 0.05. I-J) GO and KEGG pathway enrichment analysis of DEGs in NSCs after intervention with hUCMSC-Exo + PM. K) Heatmap showing the expression levels of significantly altered genes in the hUCMSC-Exo + PM and Control. L) GSEA showing pathways significantly positively correlated with DEGs in the hUCMSC-Exo + PM group. Enrichment scores (ES), P values, and false discovery rates (FDR) values are indicated for each pathway. M) Western blot bands of p-CaMK II, CaMK II, p-CREB, CREB, p-PI3K, PI3K, p-AKT, and AKT protein expression in NSCs treated with distinct groups. N) Quantitative analysis of p-CaMK II/CaMK II, p-CREB/CREB, p-PI3K/PI3K, and p-AKT/AKT ratios (n = 3). All data are presented as the mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: The primary antibodies used in this research are listed below: CD68 (Abcam, Cambridge, UK), CD206 (Abcam, Cambridge, UK), GFAP (Bioss, Beijing, China), iNOS (Abcam, Cambridge, UK), Tuj-1 (Abcam, Cambridge, UK), NF-200 (Invitrogen, CA, USA), MBP (Abcam, Cambridge, UK), HIF-1α (Abcam, Cambridge, UK), VEGFA (Abcam, Cambridge, UK), P-CaMKII (Abcam, Cambridge, UK), CaMKII (Abcam, Cambridge, UK), P-CREB (Cell Signaling Technology, USA), CREB (Cell Signaling Technology, USA), P-PI3K (Cell Signaling Technology, USA), PI3K (Cell Signaling Technology, USA), P-AKT (Cell Signaling Technology, USA), AKT (Cell Signaling Technology, USA), Cleaved-Caspase3 (Cell Signaling Technology, USA), Bcl-2 (Cell Signaling Technology, USA), Bax (Cell Signaling Technology, USA), GAPDH (Proteintech, IL, USA).

Techniques: In Vitro, Staining, Fluorescence, Western Blot, Expressing, Control