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cow pulmonary artery endothelial  (ATCC)


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    Structured Review

    ATCC cow pulmonary artery endothelial
    Schematic illustration depicting the fabrication of the core/shell PCL-cECM (C/S PE) vascular graft and the cell seeding process. A novel bioreactor was constructed to culture rBMSCs under dynamic conditions to promote <t>endothelial</t> differentiation. Subsequently, the pre-endothelialized C/S PE (EC) was implanted into the rat abdominal aorta for biological assessment.
    Cow Pulmonary Artery Endothelial, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 327 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cow pulmonary artery endothelial/product/ATCC
    Average 94 stars, based on 327 article reviews
    cow pulmonary artery endothelial - by Bioz Stars, 2026-05
    94/100 stars

    Images

    1) Product Images from "Ex vivo endothelialized cECM-enriched core–shell fibrous vascular graft promotes rapid regenerative remodeling in vivo"

    Article Title: Ex vivo endothelialized cECM-enriched core–shell fibrous vascular graft promotes rapid regenerative remodeling in vivo

    Journal: Bioactive Materials

    doi: 10.1016/j.bioactmat.2026.03.040

    Schematic illustration depicting the fabrication of the core/shell PCL-cECM (C/S PE) vascular graft and the cell seeding process. A novel bioreactor was constructed to culture rBMSCs under dynamic conditions to promote endothelial differentiation. Subsequently, the pre-endothelialized C/S PE (EC) was implanted into the rat abdominal aorta for biological assessment.
    Figure Legend Snippet: Schematic illustration depicting the fabrication of the core/shell PCL-cECM (C/S PE) vascular graft and the cell seeding process. A novel bioreactor was constructed to culture rBMSCs under dynamic conditions to promote endothelial differentiation. Subsequently, the pre-endothelialized C/S PE (EC) was implanted into the rat abdominal aorta for biological assessment.

    Techniques Used: Construct

    in vitro biocompatibility evaluation . (A) MTT assay shows enhanced proliferation on C/S PE at day 7 (n = 5). (B) F-actin (green) and Hoechst (blue) staining reveal improved spreading and confluence compared with PCL and control. (C–D) Quantification of F-actin area (n = 3) and nuclei number (n = 3) confirm higher cytoskeletal organization and cell density. (E) Viability assay demonstrates increased survival on C/S PE at day 5. (F) Live/Dead staining shows predominantly viable cells with fewer dead cells (n = 5). (G) Schematic summary of C/S PE promoting endothelial proliferation, biocompatibility, and reduced cytotoxicity. Scale bars: 200 μm. Statistical significance was calculated by two-way ANOVA with Tukey's test. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. “N.S” means not significant.
    Figure Legend Snippet: in vitro biocompatibility evaluation . (A) MTT assay shows enhanced proliferation on C/S PE at day 7 (n = 5). (B) F-actin (green) and Hoechst (blue) staining reveal improved spreading and confluence compared with PCL and control. (C–D) Quantification of F-actin area (n = 3) and nuclei number (n = 3) confirm higher cytoskeletal organization and cell density. (E) Viability assay demonstrates increased survival on C/S PE at day 5. (F) Live/Dead staining shows predominantly viable cells with fewer dead cells (n = 5). (G) Schematic summary of C/S PE promoting endothelial proliferation, biocompatibility, and reduced cytotoxicity. Scale bars: 200 μm. Statistical significance was calculated by two-way ANOVA with Tukey's test. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. “N.S” means not significant.

    Techniques Used: In Vitro, MTT Assay, Staining, Control, Viability Assay

    rBMSCs to endothelial differentiation and activation of different pathways . (A) Schematic representation of rBMSCs differentiated into ECs. (B) Immunofluorescent detection of (i) CD31, (ii) ICAM1, (iii) Flk1, and (iv) eNOS (scale bars: 200 μm). Quantitative analysis of circumferential coverage for (C) CD31, (D) ICAM1, (E) Flk1, and (F) eNOS (n = 4 sections). (G) Venn diagram displaying differentially expressed genes (DEGs) between rBMSCs and differentiated endothelial-like cells in C/S PE grafts analyzed via RNA sequencing. (H) Scatter plot visualizing the distribution of upregulated and downregulated DEGs. (I) Gene ontology (GO) analysis indicating enrichment of terms linked to endothelial proliferation, angiogenesis, and blood vessel development. (J–M) Heatmaps presenting clustered DEGs associated with cell differentiation (J), endothelial cell proliferation (K), angiogenesis (L), and blood vessel development (M). (N–O) Gene set enrichment analysis (GSEA) highlighting significant gene enrichment in angiogenesis and vascular remodeling pathways. (P) Bubble plot showing pathway enrichment and signaling activation, including VEGF, MAPK, PI3K-Akt, mTOR, HIF-1, Notch, TGF-β, and JAK-STAT pathways. (Q–R) Heatmaps illustrating the activation of Notch (Q) and VEGF (R) signaling pathway genes, supporting robust pathway engagement. (S) Circular plot showing marked upregulation of major endothelial genes (Vegfa, Nos3, Flt1, Kdr) compared to MSC-specific markers.
    Figure Legend Snippet: rBMSCs to endothelial differentiation and activation of different pathways . (A) Schematic representation of rBMSCs differentiated into ECs. (B) Immunofluorescent detection of (i) CD31, (ii) ICAM1, (iii) Flk1, and (iv) eNOS (scale bars: 200 μm). Quantitative analysis of circumferential coverage for (C) CD31, (D) ICAM1, (E) Flk1, and (F) eNOS (n = 4 sections). (G) Venn diagram displaying differentially expressed genes (DEGs) between rBMSCs and differentiated endothelial-like cells in C/S PE grafts analyzed via RNA sequencing. (H) Scatter plot visualizing the distribution of upregulated and downregulated DEGs. (I) Gene ontology (GO) analysis indicating enrichment of terms linked to endothelial proliferation, angiogenesis, and blood vessel development. (J–M) Heatmaps presenting clustered DEGs associated with cell differentiation (J), endothelial cell proliferation (K), angiogenesis (L), and blood vessel development (M). (N–O) Gene set enrichment analysis (GSEA) highlighting significant gene enrichment in angiogenesis and vascular remodeling pathways. (P) Bubble plot showing pathway enrichment and signaling activation, including VEGF, MAPK, PI3K-Akt, mTOR, HIF-1, Notch, TGF-β, and JAK-STAT pathways. (Q–R) Heatmaps illustrating the activation of Notch (Q) and VEGF (R) signaling pathway genes, supporting robust pathway engagement. (S) Circular plot showing marked upregulation of major endothelial genes (Vegfa, Nos3, Flt1, Kdr) compared to MSC-specific markers.

    Techniques Used: Activation Assay, RNA Sequencing, Cell Differentiation



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    Image Search Results


    Schematic illustration depicting the fabrication of the core/shell PCL-cECM (C/S PE) vascular graft and the cell seeding process. A novel bioreactor was constructed to culture rBMSCs under dynamic conditions to promote endothelial differentiation. Subsequently, the pre-endothelialized C/S PE (EC) was implanted into the rat abdominal aorta for biological assessment.

    Journal: Bioactive Materials

    Article Title: Ex vivo endothelialized cECM-enriched core–shell fibrous vascular graft promotes rapid regenerative remodeling in vivo

    doi: 10.1016/j.bioactmat.2026.03.040

    Figure Lengend Snippet: Schematic illustration depicting the fabrication of the core/shell PCL-cECM (C/S PE) vascular graft and the cell seeding process. A novel bioreactor was constructed to culture rBMSCs under dynamic conditions to promote endothelial differentiation. Subsequently, the pre-endothelialized C/S PE (EC) was implanted into the rat abdominal aorta for biological assessment.

    Article Snippet: Cow pulmonary artery endothelial (CPAE, CCL-209, ATCC) endothelial cells were used for initial cytocompatibility screening to evaluate endothelial adhesion and material safety using a standardized mature endothelial model.

    Techniques: Construct

    in vitro biocompatibility evaluation . (A) MTT assay shows enhanced proliferation on C/S PE at day 7 (n = 5). (B) F-actin (green) and Hoechst (blue) staining reveal improved spreading and confluence compared with PCL and control. (C–D) Quantification of F-actin area (n = 3) and nuclei number (n = 3) confirm higher cytoskeletal organization and cell density. (E) Viability assay demonstrates increased survival on C/S PE at day 5. (F) Live/Dead staining shows predominantly viable cells with fewer dead cells (n = 5). (G) Schematic summary of C/S PE promoting endothelial proliferation, biocompatibility, and reduced cytotoxicity. Scale bars: 200 μm. Statistical significance was calculated by two-way ANOVA with Tukey's test. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. “N.S” means not significant.

    Journal: Bioactive Materials

    Article Title: Ex vivo endothelialized cECM-enriched core–shell fibrous vascular graft promotes rapid regenerative remodeling in vivo

    doi: 10.1016/j.bioactmat.2026.03.040

    Figure Lengend Snippet: in vitro biocompatibility evaluation . (A) MTT assay shows enhanced proliferation on C/S PE at day 7 (n = 5). (B) F-actin (green) and Hoechst (blue) staining reveal improved spreading and confluence compared with PCL and control. (C–D) Quantification of F-actin area (n = 3) and nuclei number (n = 3) confirm higher cytoskeletal organization and cell density. (E) Viability assay demonstrates increased survival on C/S PE at day 5. (F) Live/Dead staining shows predominantly viable cells with fewer dead cells (n = 5). (G) Schematic summary of C/S PE promoting endothelial proliferation, biocompatibility, and reduced cytotoxicity. Scale bars: 200 μm. Statistical significance was calculated by two-way ANOVA with Tukey's test. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. “N.S” means not significant.

    Article Snippet: Cow pulmonary artery endothelial (CPAE, CCL-209, ATCC) endothelial cells were used for initial cytocompatibility screening to evaluate endothelial adhesion and material safety using a standardized mature endothelial model.

    Techniques: In Vitro, MTT Assay, Staining, Control, Viability Assay

    rBMSCs to endothelial differentiation and activation of different pathways . (A) Schematic representation of rBMSCs differentiated into ECs. (B) Immunofluorescent detection of (i) CD31, (ii) ICAM1, (iii) Flk1, and (iv) eNOS (scale bars: 200 μm). Quantitative analysis of circumferential coverage for (C) CD31, (D) ICAM1, (E) Flk1, and (F) eNOS (n = 4 sections). (G) Venn diagram displaying differentially expressed genes (DEGs) between rBMSCs and differentiated endothelial-like cells in C/S PE grafts analyzed via RNA sequencing. (H) Scatter plot visualizing the distribution of upregulated and downregulated DEGs. (I) Gene ontology (GO) analysis indicating enrichment of terms linked to endothelial proliferation, angiogenesis, and blood vessel development. (J–M) Heatmaps presenting clustered DEGs associated with cell differentiation (J), endothelial cell proliferation (K), angiogenesis (L), and blood vessel development (M). (N–O) Gene set enrichment analysis (GSEA) highlighting significant gene enrichment in angiogenesis and vascular remodeling pathways. (P) Bubble plot showing pathway enrichment and signaling activation, including VEGF, MAPK, PI3K-Akt, mTOR, HIF-1, Notch, TGF-β, and JAK-STAT pathways. (Q–R) Heatmaps illustrating the activation of Notch (Q) and VEGF (R) signaling pathway genes, supporting robust pathway engagement. (S) Circular plot showing marked upregulation of major endothelial genes (Vegfa, Nos3, Flt1, Kdr) compared to MSC-specific markers.

    Journal: Bioactive Materials

    Article Title: Ex vivo endothelialized cECM-enriched core–shell fibrous vascular graft promotes rapid regenerative remodeling in vivo

    doi: 10.1016/j.bioactmat.2026.03.040

    Figure Lengend Snippet: rBMSCs to endothelial differentiation and activation of different pathways . (A) Schematic representation of rBMSCs differentiated into ECs. (B) Immunofluorescent detection of (i) CD31, (ii) ICAM1, (iii) Flk1, and (iv) eNOS (scale bars: 200 μm). Quantitative analysis of circumferential coverage for (C) CD31, (D) ICAM1, (E) Flk1, and (F) eNOS (n = 4 sections). (G) Venn diagram displaying differentially expressed genes (DEGs) between rBMSCs and differentiated endothelial-like cells in C/S PE grafts analyzed via RNA sequencing. (H) Scatter plot visualizing the distribution of upregulated and downregulated DEGs. (I) Gene ontology (GO) analysis indicating enrichment of terms linked to endothelial proliferation, angiogenesis, and blood vessel development. (J–M) Heatmaps presenting clustered DEGs associated with cell differentiation (J), endothelial cell proliferation (K), angiogenesis (L), and blood vessel development (M). (N–O) Gene set enrichment analysis (GSEA) highlighting significant gene enrichment in angiogenesis and vascular remodeling pathways. (P) Bubble plot showing pathway enrichment and signaling activation, including VEGF, MAPK, PI3K-Akt, mTOR, HIF-1, Notch, TGF-β, and JAK-STAT pathways. (Q–R) Heatmaps illustrating the activation of Notch (Q) and VEGF (R) signaling pathway genes, supporting robust pathway engagement. (S) Circular plot showing marked upregulation of major endothelial genes (Vegfa, Nos3, Flt1, Kdr) compared to MSC-specific markers.

    Article Snippet: Cow pulmonary artery endothelial (CPAE, CCL-209, ATCC) endothelial cells were used for initial cytocompatibility screening to evaluate endothelial adhesion and material safety using a standardized mature endothelial model.

    Techniques: Activation Assay, RNA Sequencing, Cell Differentiation

    Compatibility and permeability studies of CBD-loaded Pluronic® F127 polymeric micelles in the human nasal epithelium cell line RPMI 2650. (A) Cell viability upon exposure to micellar systems with different final CBD concentrations for 24 h at 37 °C, as estimated by the MTT assay (n = 3). The original 25% w/w CBD-loaded Pluronic® F127 polymeric micelles were diluted in culture medium to final concentrations of 0.005-0.25 % w/v. All data are presented as mean ± S.D. respectively (p < 0.0001). (B) Apparent permeability coefficient (Papp) of 0.01% and 0.05% w/v CBD-loaded Pluronic® F127 polymeric micelles under ALI conditions (n = 6). ∗∗ Statistically significant difference (p < 0.01) and ∗∗∗∗ statistically significant difference (p < 0.0001).

    Journal: Bioactive Materials

    Article Title: Nose-to-brain administration of cannabidiol-loaded polymeric micelles improves the core behavioral symptoms of autism spectrum disorder

    doi: 10.1016/j.bioactmat.2026.03.019

    Figure Lengend Snippet: Compatibility and permeability studies of CBD-loaded Pluronic® F127 polymeric micelles in the human nasal epithelium cell line RPMI 2650. (A) Cell viability upon exposure to micellar systems with different final CBD concentrations for 24 h at 37 °C, as estimated by the MTT assay (n = 3). The original 25% w/w CBD-loaded Pluronic® F127 polymeric micelles were diluted in culture medium to final concentrations of 0.005-0.25 % w/v. All data are presented as mean ± S.D. respectively (p < 0.0001). (B) Apparent permeability coefficient (Papp) of 0.01% and 0.05% w/v CBD-loaded Pluronic® F127 polymeric micelles under ALI conditions (n = 6). ∗∗ Statistically significant difference (p < 0.01) and ∗∗∗∗ statistically significant difference (p < 0.0001).

    Article Snippet: The compatibility of 25% w/w CBD-loaded Pluronic® F127 polymeric micelles was assessed in the human nasal septum epithelium cell line RPMI 2650 (ATCC CMCL-30, American Type Culture Collection, Manassas, VA, USA) [ ].

    Techniques: Permeability, MTT Assay

    Validation of CL16-RhoA binding by LC-MS/MS experiments (A) Workflow of LC-MS/MS experiments to detect RhoA-CL16 engagement in HCT116 cells. CL16-treated cells were harvested, digested and analyzed by LC-MS/MS. (B) Representative MS/MS showing CL16 modification on RhoA Cys16 in HCT116 cells. (C) Workflow of LC-MS/MS experiments using CL16-alkyne (a CL16-molecular probe) to study target profile of CL16. (D) Volcano plot revealing protein targets of CL16 identified by CL16-molecular probe. Statistical analyses were performed by two-tailed Student’s t-test by MS Excel. (E) Venn diagram summarizing the protein targets of CL16 identified in (A) and (C), highlighting RhoA as the primary target.

    Journal: STAR Protocols

    Article Title: Protocol to identify covalent inhibitors targeting RhoA Cys16

    doi: 10.1016/j.xpro.2026.104494

    Figure Lengend Snippet: Validation of CL16-RhoA binding by LC-MS/MS experiments (A) Workflow of LC-MS/MS experiments to detect RhoA-CL16 engagement in HCT116 cells. CL16-treated cells were harvested, digested and analyzed by LC-MS/MS. (B) Representative MS/MS showing CL16 modification on RhoA Cys16 in HCT116 cells. (C) Workflow of LC-MS/MS experiments using CL16-alkyne (a CL16-molecular probe) to study target profile of CL16. (D) Volcano plot revealing protein targets of CL16 identified by CL16-molecular probe. Statistical analyses were performed by two-tailed Student’s t-test by MS Excel. (E) Venn diagram summarizing the protein targets of CL16 identified in (A) and (C), highlighting RhoA as the primary target.

    Article Snippet: Human: HCT116 (Wildtype/48Y/Male) , ATCC , #CCL-247.

    Techniques: Biomarker Discovery, Binding Assay, Liquid Chromatography with Mass Spectroscopy, Tandem Mass Spectroscopy, Modification, Two Tailed Test

    Hypoxia increases expression of EZH2, H3K27me3 and survivin. (A) Immunoblots of WCEs from U2OS, HeLa and MRC5 lines cultured under normoxic or hypoxic environments (24 h). Blots were immunoprobed with anti-EZH2, anti-H3K27me3 and anti-survivin antibodies. Anti-Hif1a used to prove the hypoxic state had been induced, and anti-tubulin was used as a loading control. (B–D) Quantification of immunoblots represented in A from three independent experiments demonstrating that EZH2, H3K27me3 and survivin are all more abundant under hypoxia. Data presented are means±s.d. * P <0.05, ** P <0.01, *** P <0.001 (two-way ANOVA with Tukey's multiple comparisons post test).

    Journal: Journal of Cell Science

    Article Title: Interplay between nuclear survivin and the PRC2 complex and its impact on H3K27me3-directed transcriptional repression

    doi: 10.1242/jcs.264572

    Figure Lengend Snippet: Hypoxia increases expression of EZH2, H3K27me3 and survivin. (A) Immunoblots of WCEs from U2OS, HeLa and MRC5 lines cultured under normoxic or hypoxic environments (24 h). Blots were immunoprobed with anti-EZH2, anti-H3K27me3 and anti-survivin antibodies. Anti-Hif1a used to prove the hypoxic state had been induced, and anti-tubulin was used as a loading control. (B–D) Quantification of immunoblots represented in A from three independent experiments demonstrating that EZH2, H3K27me3 and survivin are all more abundant under hypoxia. Data presented are means±s.d. * P <0.05, ** P <0.01, *** P <0.001 (two-way ANOVA with Tukey's multiple comparisons post test).

    Article Snippet: Human cervical cancer cells (HeLa), human bone osteosarcoma cells (U2OS), retinal pigment epithelial cells (RPE) and human breast cancer cells (MCF7) were originally from ATCC.

    Techniques: Expressing, Western Blot, Cell Culture, Control