pcsk9 (Boster Bio)
Structured Review

Pcsk9, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/pcsk9/product/Boster Bio
Average 94 stars, based on 1 article reviews
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1) Product Images from "A composite hydrogel enables the spatiotemporal delivery of distinct cytokines to drive the native vascularized bone regeneration"
Article Title: A composite hydrogel enables the spatiotemporal delivery of distinct cytokines to drive the native vascularized bone regeneration
Journal: Bioactive Materials
doi: 10.1016/j.bioactmat.2026.02.048
Figure Legend Snippet: Full fabrication and application schematic diagram of GelMA-VEGF/ECM-PCSK9 composite hydrogel and the related signaling pathway of PCSK9 that promotes BMSC osteogenic differentiation.
Techniques Used:
Figure Legend Snippet: Construction and characterization of GelMA-VEGF/ECM-PCSK9 composite hydrogel. A Schematic diagram showing the process of composite hydrogel construction; B) Photographs of GelMA-VEGF hydrogel and GelMA-VEGF/ECM-PCSK9 hydrogel formation after UV light respectively; C i) Electron microscopic image of pure GelMA hydrogel, with a scale of 100 μm; ii) Enlarged electron microscopic image of GelMA hydrogel, with a scale of 50 μm; D) i The electron microscope image of the combination of GelMA hydrogel and ECM, with a scale of 100 μm; ii Electron microscope magnified image of GelMA hydrogel combined with ECM, with a scale of 50 μm; E) The infrared spectrum (FITR) diagram of the acellular ECM, GelMA hydrogel and GelMA/ECM composite hydrogel contains common basic energy groups; F) Load rate of PCSK9 in ECM; G) Release rate of VEGF loaded with GelMA hydrogel and GelMA/ECM composite hydrogel respectively; H) Release rate of PCSK9 loaded with ECM and GelMA/ECM composite hydrogel respectively; I) Release rate of VEGF and PCSK9 loaded in GelMA and GelMA/ECM on different time points respectively; J) Release rate of VEGF and PCSK9 respectively when loaded in GelMA/ECM; K) The swelling rate of GelMA gel and GelMA/ECM composite gel dissolved in PBS (n = 6); L) Degradation rate of GelMA hydrogel and GelMA/ECM composite gel in vitro (n = 6).∗means that compared with the control group, p < 0.05; ∗means that compared with the control group, p < 0.01; ∗∗∗means that compared with the control group, p < 0.001.
Techniques Used: Microscopy, In Vitro, Control
Figure Legend Snippet: Angiogenic capacity formulations of HUVECs in response to different composite biomaterial in vitro. A) Calcein/PI staining of HUVECs seeded on glass slides, showing the cell migration profiles of HUVECs treated with different material groups, scale bar = 200 μm; B) Quantitative analysis of the intercellular blank areas in each group, with the baseline group serving as the negative control; C) Angiogenic images of HUVECs co-cultured with different composite materials for 4 h and 8 h respectively, scale bar = 250 μm; D–G) Quantitative assessment of angiogenic capacity in each group via ImageJ software analysis of key angiogenic parameters. Abbreviations: NC = negative control group; V = exogenous VEGF protein-only group; GV=GelMA + exogenous VEGF protein group; GVE = GelMA + VEGF + ECM group; GVEP= GelMA/VEGF + ECM/PCSK9 group. Statistical notations: ∗∗means that compared with the control group, p < 0.01; ns = no significant difference between group.
Techniques Used: In Vitro, Staining, Migration, Negative Control, Cell Culture, Software, Control
Figure Legend Snippet: The effect of different composite hydrogel on the osteogenic differentiation of BMMSC in vitro. Cultivate BMMSC for osteogenic differentiation in osteogenic medium with GelMA, GelMA-VEGF, GelMA-VEGF/ECM, ECM-PCSK9, and GelMA-VEGF/ECM-PCSK9 for 7 days respectively. A,B) The cell nucleus was stained with DAPI (blue), RUNX2 was stained with RUNX2 antibody (green), and COL1A1 was stained with COL1A1 antibody (red), with a scale bar of 200 μm. C,D) The quantitative analysis results of COL1A1 and RUNX2 immunofluorescence images; E,F) Quantitative analysis of ALP staining and ARS staining for BMMSC co-culture with different kinds of hydrogels; G) ALP staining result for BMMSC co-culture with different kinds of hydrogels for 7days, scale bar = 200 μm; F) ARS staining result for BMMSC co-culture with different kinds of hydrogels for 14days, scale bar = 200 μm; I, J) After 7 and 14 days of co-culture with different combinations of composite hydrogels and BMMSC for osteogenesis and differentiation, the PCR experiment results of osteogenesis related indicators suggest that compared with the control group. G = simple GelMA hydrogel group, GV=GelMA hydrogels + VEGF protein group, GV/E = GelMA + VEGF/ECM group, EP = ECM + PCSK9 protein group, GVEP=GelMA + VEGF/ECM + PCSK9 protein group, the significant differences between the groups are expressed as ∗ p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, and ns means there is no significant difference between the groups.
Techniques Used: In Vitro, Staining, Immunofluorescence, Co-Culture Assay, Control
Figure Legend Snippet: After adding different concentrations of PCSK9 to BMMSC for osteogenic induction, western blotting (WB) experiment was performed to evaluate the expression of phosphorylated proteins and total proteins among different osteogenic differentiation relevant signaling pathways. A) WB images of different signaling pathways that related to osteogenic differentiation after adding different concentrations of PCSK9; B-D) Quantitative analysis results of phosphorylated protein and total protein. Compared with the control group, ∗ means p < 0.05, ∗∗ means p < 0.01.
Techniques Used: Western Blot, Expressing, Protein-Protein interactions, Control


![<t>Vectorized</t> <t>IFNβ</t> drives durable signaling and complete tumor regression in human glioblastoma models in vivo (A) Sustained hIFNβ secretion in human GBM6 cells treated with AAV9-hIFNβ (red, MOI = 4E5 vg/cell) or recombinant hIFNβ cytokine (r-hIFNβ, purple, 47 IU/mL, equivalent to 114 pg/mL), measured by ELISA at indicated time points. 50% media washouts every 5 h for the first 20 h in the r-hIFNβ condition mimic in vivo cytokine clearance (half-life = 4–5 h). Full media exchanges were performed at 24, 48, 72, and 96 h post-treatment. (B) Number of differentially expressed genes (DEGs, p -Adj<0.01) in GBM6 cells 24–96 h post-treatment with AAV9-hIFNβ or r-hIFNβ vs. media controls. (C) Enrichment scores for type I <t>IFN</t> and TNFα response pathways across treatments and time points. (D) Heatmap of the top 10 IFN and TNFα response genes (Log2FC vs. media controls) in GBM6 cells treated as in (A). (E) Schematic of orthotopic PDX (SF11411) and cell line-derived xenograft ([CDX], GBM6-FLuc) studies in athymic nu/nu mice treated intratumorally with saline, AAV9-GFP, or AAV9-hIFNβ via CED. (F) Kaplan-Meier survival curves for PDX mice treated as in (E). Saline = black, AAV9-GFP (2E11 vg/brain) = blue, AAV9-hIFNβ (2E11 vg/brain) = red. Vertical dashed line = day of treatment (day 9). p < 0.04 by log-rank (Mantel-Cox) test. n = 30 (10 per treatment arm). (G) Longitudinal BLI of GBM6-FLuc tumor growth in CDX mice treated as in (E). Saline = black, AAV9-GFP (2E11 vg/brain) = blue, AAV9-hIFNβ (2E11 vg/brain) = red. Thin lines = individual mice, thick lines = geometric mean. Vertical dashed line = day of treatment (day 9). ∗ p < 0.04 by Kruskal-Wallis test with Dunn’s multiple comparisons correction on day 22. n = 30 (10 per treatment arm). (G′) Representative BLI images from each treatment group 11 days post-treatment. (H) Kaplan-Meier survival curves for CDX mice. p < 0.001 by log-rank (Mantel-Cox) test. (I) Distribution of treatment responses in CDX by BLI flux (photons/second) at day 27. Tumor free = BLI flux <2.5 × 10 5 p/s, tumor reduction = ≥30% decrease from assignment on day 9, no change = between 30% decrease and 20% increase from assignment on day 9, tumor growth = ≥20% increase from assignment on day 9, death = mice that died before day 27. (J) Dose-response analysis of AAV9-hIFNβ efficacy in CDX mice. AAV9-GFP (2E11 vg/brain) = blue, AAV9-hIFNβ hi (2E11 vg/brain) = solid red, and AAV9-hIFNβ lo (1E11 vg/brain) = dashed red. Thin lines = individual mice, thick lines = geometric mean. Vertical dashed line = day of treatment (day 9). ∗∗ p < 0.02 by Kruskal-Wallis test with Dunn’s multiple comparisons correction on day 20. n = 45 (15 per treatment arm). For data interpretation, tumor burden threshold = 2.5 × 10 5 . (J′) Representative BLI images of tumors 11 days post-treatment. (K) Kaplan-Meier survival curves from (J). p < 0.002 (AAV9-hIFNβ hi), p < 0.005 (AAV9-hIFNβ lo) by log-rank (Mantel-Cox) test compared to AAV9-GFP. (I) Distribution of treatment responses in CDX mice at day 27 by BLI flux as in (I).](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_1051/pmc13091051/pmc13091051__gr2.jpg)

