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mouse bone marrow stromal cell line op9  (ATCC)


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    ATCC mouse bone marrow stromal cell line op9
    A , B The MCP-1 levels in OP9A-CM/BMA-CM were overtly higher than those in <t>OP9-CM/BMSCs-CM,</t> with further increases observed in HG-OP9A-CM/HG-BMA-CM compared to OP9A-CM/BMA-CM ( n = 16 and 12). C , D Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly inhibited the proliferation of Min6 cells at 24 h and 48 h of co-culture, and HG-OP9A-CM/HG-BMA-CM further inhibited Min6 cells proliferation ( n = 12). E , F Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly aggravated the apoptosis of Min6 cells, and HG-OP9A-CM/HG-BMA-CM exacerbated the apoptosis of Min6 cells ( n = 6). G GSIS in Min6 cells increased by 2-fold under Ctrl condition, 1.6-fold with OP9-CM intervention, and 1.3, 0.4 and 0.2-fold with HG-OP9-CM, OP9A-CM and HG-OP9A-CM interventions, respectively ( n = 12). H GSIS in Min6 cells increased by 2.2-fold after BMSCs-CM intervention, while HG-BMSCs-CM, BMA-CM and HG-BMA-CM interventions resulted in increases of 0.7, 0.4 and 0.09-fold, respectively ( n = 8). I The expression levels of t-Akt in Min6 cells in different intervention groups did not change dramatically compared to each other. Whereas the protein levels of p-Akt in Min6 cells were obviously decreased in the OP9A-CM/HG-OP9A-CM intervention group compared to the OP9-CM intervention group ( n = 5). J Treatment with 10, 50 and 100 ng/mL of MCP-1 resulted in a gradual decrease in p-Akt protein levels of in Min6 cells compared to the Ctrl group ( n = 5). K Compared to the Ctrl + PBS group, OP9-CM/HG-OP9-CM + 100 ng/mL Mcp-1 significantly decreased the proliferation of Min6 cells. Conversely, pretreatment of Min6 cells with the MCP-1 receptor CCR2 antagonist RS (100 µM), followed by co-culture with OP9A-CM/HG-OP9A-CM for 24 or 48 h, did not significantly alter cell viability ( n = 12). L The protein level of p-Akt in Min6 cells after OP9-CM/HG-OP9-CM + 100 ng/mL MCP-1 intervention was obviously decreased compared to the Ctrl group, while the p-Akt protein level of Min6 cells regained to a level comparable to that of the Ctrl group when RS was added to block MCP-1 pathway ( n = 5). * p < 0.05, ** p < 0.01, ns means no statistical difference.
    Mouse Bone Marrow Stromal Cell Line Op9, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 413 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+bone+marrow+stromal+cell+line+op9/pmc10643445-319-1-11?v=ATCC
    Average 96 stars, based on 413 article reviews
    mouse bone marrow stromal cell line op9 - by Bioz Stars, 2026-08
    96/100 stars

    Images

    1) Product Images from "Pathological roles of bone marrow adipocyte-derived monocyte chemotactic protein-1 in type 2 diabetic mice"

    Article Title: Pathological roles of bone marrow adipocyte-derived monocyte chemotactic protein-1 in type 2 diabetic mice

    Journal: Cell Death Discovery

    doi: 10.1038/s41420-023-01708-3

    A , B The MCP-1 levels in OP9A-CM/BMA-CM were overtly higher than those in OP9-CM/BMSCs-CM, with further increases observed in HG-OP9A-CM/HG-BMA-CM compared to OP9A-CM/BMA-CM ( n = 16 and 12). C , D Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly inhibited the proliferation of Min6 cells at 24 h and 48 h of co-culture, and HG-OP9A-CM/HG-BMA-CM further inhibited Min6 cells proliferation ( n = 12). E , F Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly aggravated the apoptosis of Min6 cells, and HG-OP9A-CM/HG-BMA-CM exacerbated the apoptosis of Min6 cells ( n = 6). G GSIS in Min6 cells increased by 2-fold under Ctrl condition, 1.6-fold with OP9-CM intervention, and 1.3, 0.4 and 0.2-fold with HG-OP9-CM, OP9A-CM and HG-OP9A-CM interventions, respectively ( n = 12). H GSIS in Min6 cells increased by 2.2-fold after BMSCs-CM intervention, while HG-BMSCs-CM, BMA-CM and HG-BMA-CM interventions resulted in increases of 0.7, 0.4 and 0.09-fold, respectively ( n = 8). I The expression levels of t-Akt in Min6 cells in different intervention groups did not change dramatically compared to each other. Whereas the protein levels of p-Akt in Min6 cells were obviously decreased in the OP9A-CM/HG-OP9A-CM intervention group compared to the OP9-CM intervention group ( n = 5). J Treatment with 10, 50 and 100 ng/mL of MCP-1 resulted in a gradual decrease in p-Akt protein levels of in Min6 cells compared to the Ctrl group ( n = 5). K Compared to the Ctrl + PBS group, OP9-CM/HG-OP9-CM + 100 ng/mL Mcp-1 significantly decreased the proliferation of Min6 cells. Conversely, pretreatment of Min6 cells with the MCP-1 receptor CCR2 antagonist RS (100 µM), followed by co-culture with OP9A-CM/HG-OP9A-CM for 24 or 48 h, did not significantly alter cell viability ( n = 12). L The protein level of p-Akt in Min6 cells after OP9-CM/HG-OP9-CM + 100 ng/mL MCP-1 intervention was obviously decreased compared to the Ctrl group, while the p-Akt protein level of Min6 cells regained to a level comparable to that of the Ctrl group when RS was added to block MCP-1 pathway ( n = 5). * p < 0.05, ** p < 0.01, ns means no statistical difference.
    Figure Legend Snippet: A , B The MCP-1 levels in OP9A-CM/BMA-CM were overtly higher than those in OP9-CM/BMSCs-CM, with further increases observed in HG-OP9A-CM/HG-BMA-CM compared to OP9A-CM/BMA-CM ( n = 16 and 12). C , D Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly inhibited the proliferation of Min6 cells at 24 h and 48 h of co-culture, and HG-OP9A-CM/HG-BMA-CM further inhibited Min6 cells proliferation ( n = 12). E , F Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly aggravated the apoptosis of Min6 cells, and HG-OP9A-CM/HG-BMA-CM exacerbated the apoptosis of Min6 cells ( n = 6). G GSIS in Min6 cells increased by 2-fold under Ctrl condition, 1.6-fold with OP9-CM intervention, and 1.3, 0.4 and 0.2-fold with HG-OP9-CM, OP9A-CM and HG-OP9A-CM interventions, respectively ( n = 12). H GSIS in Min6 cells increased by 2.2-fold after BMSCs-CM intervention, while HG-BMSCs-CM, BMA-CM and HG-BMA-CM interventions resulted in increases of 0.7, 0.4 and 0.09-fold, respectively ( n = 8). I The expression levels of t-Akt in Min6 cells in different intervention groups did not change dramatically compared to each other. Whereas the protein levels of p-Akt in Min6 cells were obviously decreased in the OP9A-CM/HG-OP9A-CM intervention group compared to the OP9-CM intervention group ( n = 5). J Treatment with 10, 50 and 100 ng/mL of MCP-1 resulted in a gradual decrease in p-Akt protein levels of in Min6 cells compared to the Ctrl group ( n = 5). K Compared to the Ctrl + PBS group, OP9-CM/HG-OP9-CM + 100 ng/mL Mcp-1 significantly decreased the proliferation of Min6 cells. Conversely, pretreatment of Min6 cells with the MCP-1 receptor CCR2 antagonist RS (100 µM), followed by co-culture with OP9A-CM/HG-OP9A-CM for 24 or 48 h, did not significantly alter cell viability ( n = 12). L The protein level of p-Akt in Min6 cells after OP9-CM/HG-OP9-CM + 100 ng/mL MCP-1 intervention was obviously decreased compared to the Ctrl group, while the p-Akt protein level of Min6 cells regained to a level comparable to that of the Ctrl group when RS was added to block MCP-1 pathway ( n = 5). * p < 0.05, ** p < 0.01, ns means no statistical difference.

    Techniques Used: Co-Culture Assay, Expressing, Blocking Assay



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    mouse bone marrow stromal cell line op9  (ATCC)
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    ATCC mouse bone marrow stromal cell line op9
    A , B The MCP-1 levels in OP9A-CM/BMA-CM were overtly higher than those in <t>OP9-CM/BMSCs-CM,</t> with further increases observed in HG-OP9A-CM/HG-BMA-CM compared to OP9A-CM/BMA-CM ( n = 16 and 12). C , D Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly inhibited the proliferation of Min6 cells at 24 h and 48 h of co-culture, and HG-OP9A-CM/HG-BMA-CM further inhibited Min6 cells proliferation ( n = 12). E , F Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly aggravated the apoptosis of Min6 cells, and HG-OP9A-CM/HG-BMA-CM exacerbated the apoptosis of Min6 cells ( n = 6). G GSIS in Min6 cells increased by 2-fold under Ctrl condition, 1.6-fold with OP9-CM intervention, and 1.3, 0.4 and 0.2-fold with HG-OP9-CM, OP9A-CM and HG-OP9A-CM interventions, respectively ( n = 12). H GSIS in Min6 cells increased by 2.2-fold after BMSCs-CM intervention, while HG-BMSCs-CM, BMA-CM and HG-BMA-CM interventions resulted in increases of 0.7, 0.4 and 0.09-fold, respectively ( n = 8). I The expression levels of t-Akt in Min6 cells in different intervention groups did not change dramatically compared to each other. Whereas the protein levels of p-Akt in Min6 cells were obviously decreased in the OP9A-CM/HG-OP9A-CM intervention group compared to the OP9-CM intervention group ( n = 5). J Treatment with 10, 50 and 100 ng/mL of MCP-1 resulted in a gradual decrease in p-Akt protein levels of in Min6 cells compared to the Ctrl group ( n = 5). K Compared to the Ctrl + PBS group, OP9-CM/HG-OP9-CM + 100 ng/mL Mcp-1 significantly decreased the proliferation of Min6 cells. Conversely, pretreatment of Min6 cells with the MCP-1 receptor CCR2 antagonist RS (100 µM), followed by co-culture with OP9A-CM/HG-OP9A-CM for 24 or 48 h, did not significantly alter cell viability ( n = 12). L The protein level of p-Akt in Min6 cells after OP9-CM/HG-OP9-CM + 100 ng/mL MCP-1 intervention was obviously decreased compared to the Ctrl group, while the p-Akt protein level of Min6 cells regained to a level comparable to that of the Ctrl group when RS was added to block MCP-1 pathway ( n = 5). * p < 0.05, ** p < 0.01, ns means no statistical difference.
    Mouse Bone Marrow Stromal Cell Line Op9, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    A , B The MCP-1 levels in OP9A-CM/BMA-CM were overtly higher than those in <t>OP9-CM/BMSCs-CM,</t> with further increases observed in HG-OP9A-CM/HG-BMA-CM compared to OP9A-CM/BMA-CM ( n = 16 and 12). C , D Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly inhibited the proliferation of Min6 cells at 24 h and 48 h of co-culture, and HG-OP9A-CM/HG-BMA-CM further inhibited Min6 cells proliferation ( n = 12). E , F Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly aggravated the apoptosis of Min6 cells, and HG-OP9A-CM/HG-BMA-CM exacerbated the apoptosis of Min6 cells ( n = 6). G GSIS in Min6 cells increased by 2-fold under Ctrl condition, 1.6-fold with OP9-CM intervention, and 1.3, 0.4 and 0.2-fold with HG-OP9-CM, OP9A-CM and HG-OP9A-CM interventions, respectively ( n = 12). H GSIS in Min6 cells increased by 2.2-fold after BMSCs-CM intervention, while HG-BMSCs-CM, BMA-CM and HG-BMA-CM interventions resulted in increases of 0.7, 0.4 and 0.09-fold, respectively ( n = 8). I The expression levels of t-Akt in Min6 cells in different intervention groups did not change dramatically compared to each other. Whereas the protein levels of p-Akt in Min6 cells were obviously decreased in the OP9A-CM/HG-OP9A-CM intervention group compared to the OP9-CM intervention group ( n = 5). J Treatment with 10, 50 and 100 ng/mL of MCP-1 resulted in a gradual decrease in p-Akt protein levels of in Min6 cells compared to the Ctrl group ( n = 5). K Compared to the Ctrl + PBS group, OP9-CM/HG-OP9-CM + 100 ng/mL Mcp-1 significantly decreased the proliferation of Min6 cells. Conversely, pretreatment of Min6 cells with the MCP-1 receptor CCR2 antagonist RS (100 µM), followed by co-culture with OP9A-CM/HG-OP9A-CM for 24 or 48 h, did not significantly alter cell viability ( n = 12). L The protein level of p-Akt in Min6 cells after OP9-CM/HG-OP9-CM + 100 ng/mL MCP-1 intervention was obviously decreased compared to the Ctrl group, while the p-Akt protein level of Min6 cells regained to a level comparable to that of the Ctrl group when RS was added to block MCP-1 pathway ( n = 5). * p < 0.05, ** p < 0.01, ns means no statistical difference.
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    A , B The MCP-1 levels in OP9A-CM/BMA-CM were overtly higher than those in <t>OP9-CM/BMSCs-CM,</t> with further increases observed in HG-OP9A-CM/HG-BMA-CM compared to OP9A-CM/BMA-CM ( n = 16 and 12). C , D Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly inhibited the proliferation of Min6 cells at 24 h and 48 h of co-culture, and HG-OP9A-CM/HG-BMA-CM further inhibited Min6 cells proliferation ( n = 12). E , F Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly aggravated the apoptosis of Min6 cells, and HG-OP9A-CM/HG-BMA-CM exacerbated the apoptosis of Min6 cells ( n = 6). G GSIS in Min6 cells increased by 2-fold under Ctrl condition, 1.6-fold with OP9-CM intervention, and 1.3, 0.4 and 0.2-fold with HG-OP9-CM, OP9A-CM and HG-OP9A-CM interventions, respectively ( n = 12). H GSIS in Min6 cells increased by 2.2-fold after BMSCs-CM intervention, while HG-BMSCs-CM, BMA-CM and HG-BMA-CM interventions resulted in increases of 0.7, 0.4 and 0.09-fold, respectively ( n = 8). I The expression levels of t-Akt in Min6 cells in different intervention groups did not change dramatically compared to each other. Whereas the protein levels of p-Akt in Min6 cells were obviously decreased in the OP9A-CM/HG-OP9A-CM intervention group compared to the OP9-CM intervention group ( n = 5). J Treatment with 10, 50 and 100 ng/mL of MCP-1 resulted in a gradual decrease in p-Akt protein levels of in Min6 cells compared to the Ctrl group ( n = 5). K Compared to the Ctrl + PBS group, OP9-CM/HG-OP9-CM + 100 ng/mL Mcp-1 significantly decreased the proliferation of Min6 cells. Conversely, pretreatment of Min6 cells with the MCP-1 receptor CCR2 antagonist RS (100 µM), followed by co-culture with OP9A-CM/HG-OP9A-CM for 24 or 48 h, did not significantly alter cell viability ( n = 12). L The protein level of p-Akt in Min6 cells after OP9-CM/HG-OP9-CM + 100 ng/mL MCP-1 intervention was obviously decreased compared to the Ctrl group, while the p-Akt protein level of Min6 cells regained to a level comparable to that of the Ctrl group when RS was added to block MCP-1 pathway ( n = 5). * p < 0.05, ** p < 0.01, ns means no statistical difference.
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    A , B The MCP-1 levels in OP9A-CM/BMA-CM were overtly higher than those in <t>OP9-CM/BMSCs-CM,</t> with further increases observed in HG-OP9A-CM/HG-BMA-CM compared to OP9A-CM/BMA-CM ( n = 16 and 12). C , D Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly inhibited the proliferation of Min6 cells at 24 h and 48 h of co-culture, and HG-OP9A-CM/HG-BMA-CM further inhibited Min6 cells proliferation ( n = 12). E , F Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly aggravated the apoptosis of Min6 cells, and HG-OP9A-CM/HG-BMA-CM exacerbated the apoptosis of Min6 cells ( n = 6). G GSIS in Min6 cells increased by 2-fold under Ctrl condition, 1.6-fold with OP9-CM intervention, and 1.3, 0.4 and 0.2-fold with HG-OP9-CM, OP9A-CM and HG-OP9A-CM interventions, respectively ( n = 12). H GSIS in Min6 cells increased by 2.2-fold after BMSCs-CM intervention, while HG-BMSCs-CM, BMA-CM and HG-BMA-CM interventions resulted in increases of 0.7, 0.4 and 0.09-fold, respectively ( n = 8). I The expression levels of t-Akt in Min6 cells in different intervention groups did not change dramatically compared to each other. Whereas the protein levels of p-Akt in Min6 cells were obviously decreased in the OP9A-CM/HG-OP9A-CM intervention group compared to the OP9-CM intervention group ( n = 5). J Treatment with 10, 50 and 100 ng/mL of MCP-1 resulted in a gradual decrease in p-Akt protein levels of in Min6 cells compared to the Ctrl group ( n = 5). K Compared to the Ctrl + PBS group, OP9-CM/HG-OP9-CM + 100 ng/mL Mcp-1 significantly decreased the proliferation of Min6 cells. Conversely, pretreatment of Min6 cells with the MCP-1 receptor CCR2 antagonist RS (100 µM), followed by co-culture with OP9A-CM/HG-OP9A-CM for 24 or 48 h, did not significantly alter cell viability ( n = 12). L The protein level of p-Akt in Min6 cells after OP9-CM/HG-OP9-CM + 100 ng/mL MCP-1 intervention was obviously decreased compared to the Ctrl group, while the p-Akt protein level of Min6 cells regained to a level comparable to that of the Ctrl group when RS was added to block MCP-1 pathway ( n = 5). * p < 0.05, ** p < 0.01, ns means no statistical difference.
    Mouse Op9 Bone Marrow Stromal Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+bone+marrow+stromal+cell+line+op9/pmc06138936-355-11-17?v=ATCC
    Average 96 stars, based on 1 article reviews
    mouse op9 bone marrow stromal cell line - by Bioz Stars, 2026-08
    96/100 stars
    		  Buy from Supplier

    Image Search Results


    A , B The MCP-1 levels in OP9A-CM/BMA-CM were overtly higher than those in OP9-CM/BMSCs-CM, with further increases observed in HG-OP9A-CM/HG-BMA-CM compared to OP9A-CM/BMA-CM ( n = 16 and 12). C , D Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly inhibited the proliferation of Min6 cells at 24 h and 48 h of co-culture, and HG-OP9A-CM/HG-BMA-CM further inhibited Min6 cells proliferation ( n = 12). E , F Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly aggravated the apoptosis of Min6 cells, and HG-OP9A-CM/HG-BMA-CM exacerbated the apoptosis of Min6 cells ( n = 6). G GSIS in Min6 cells increased by 2-fold under Ctrl condition, 1.6-fold with OP9-CM intervention, and 1.3, 0.4 and 0.2-fold with HG-OP9-CM, OP9A-CM and HG-OP9A-CM interventions, respectively ( n = 12). H GSIS in Min6 cells increased by 2.2-fold after BMSCs-CM intervention, while HG-BMSCs-CM, BMA-CM and HG-BMA-CM interventions resulted in increases of 0.7, 0.4 and 0.09-fold, respectively ( n = 8). I The expression levels of t-Akt in Min6 cells in different intervention groups did not change dramatically compared to each other. Whereas the protein levels of p-Akt in Min6 cells were obviously decreased in the OP9A-CM/HG-OP9A-CM intervention group compared to the OP9-CM intervention group ( n = 5). J Treatment with 10, 50 and 100 ng/mL of MCP-1 resulted in a gradual decrease in p-Akt protein levels of in Min6 cells compared to the Ctrl group ( n = 5). K Compared to the Ctrl + PBS group, OP9-CM/HG-OP9-CM + 100 ng/mL Mcp-1 significantly decreased the proliferation of Min6 cells. Conversely, pretreatment of Min6 cells with the MCP-1 receptor CCR2 antagonist RS (100 µM), followed by co-culture with OP9A-CM/HG-OP9A-CM for 24 or 48 h, did not significantly alter cell viability ( n = 12). L The protein level of p-Akt in Min6 cells after OP9-CM/HG-OP9-CM + 100 ng/mL MCP-1 intervention was obviously decreased compared to the Ctrl group, while the p-Akt protein level of Min6 cells regained to a level comparable to that of the Ctrl group when RS was added to block MCP-1 pathway ( n = 5). * p < 0.05, ** p < 0.01, ns means no statistical difference.

    Journal: Cell Death Discovery

    Article Title: Pathological roles of bone marrow adipocyte-derived monocyte chemotactic protein-1 in type 2 diabetic mice

    doi: 10.1038/s41420-023-01708-3

    Figure Lengend Snippet: A , B The MCP-1 levels in OP9A-CM/BMA-CM were overtly higher than those in OP9-CM/BMSCs-CM, with further increases observed in HG-OP9A-CM/HG-BMA-CM compared to OP9A-CM/BMA-CM ( n = 16 and 12). C , D Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly inhibited the proliferation of Min6 cells at 24 h and 48 h of co-culture, and HG-OP9A-CM/HG-BMA-CM further inhibited Min6 cells proliferation ( n = 12). E , F Compared to OP9-CM/BMSCs-CM, OP9A-CM/BMA-CM significantly aggravated the apoptosis of Min6 cells, and HG-OP9A-CM/HG-BMA-CM exacerbated the apoptosis of Min6 cells ( n = 6). G GSIS in Min6 cells increased by 2-fold under Ctrl condition, 1.6-fold with OP9-CM intervention, and 1.3, 0.4 and 0.2-fold with HG-OP9-CM, OP9A-CM and HG-OP9A-CM interventions, respectively ( n = 12). H GSIS in Min6 cells increased by 2.2-fold after BMSCs-CM intervention, while HG-BMSCs-CM, BMA-CM and HG-BMA-CM interventions resulted in increases of 0.7, 0.4 and 0.09-fold, respectively ( n = 8). I The expression levels of t-Akt in Min6 cells in different intervention groups did not change dramatically compared to each other. Whereas the protein levels of p-Akt in Min6 cells were obviously decreased in the OP9A-CM/HG-OP9A-CM intervention group compared to the OP9-CM intervention group ( n = 5). J Treatment with 10, 50 and 100 ng/mL of MCP-1 resulted in a gradual decrease in p-Akt protein levels of in Min6 cells compared to the Ctrl group ( n = 5). K Compared to the Ctrl + PBS group, OP9-CM/HG-OP9-CM + 100 ng/mL Mcp-1 significantly decreased the proliferation of Min6 cells. Conversely, pretreatment of Min6 cells with the MCP-1 receptor CCR2 antagonist RS (100 µM), followed by co-culture with OP9A-CM/HG-OP9A-CM for 24 or 48 h, did not significantly alter cell viability ( n = 12). L The protein level of p-Akt in Min6 cells after OP9-CM/HG-OP9-CM + 100 ng/mL MCP-1 intervention was obviously decreased compared to the Ctrl group, while the p-Akt protein level of Min6 cells regained to a level comparable to that of the Ctrl group when RS was added to block MCP-1 pathway ( n = 5). * p < 0.05, ** p < 0.01, ns means no statistical difference.

    Article Snippet: The mouse bone marrow stromal cell line OP9 was obtained from American Type Culture Collection (ATCC) and they were recently authenticated by STR profiling and tested for mycoplasma contamination.

    Techniques: Co-Culture Assay, Expressing, Blocking Assay