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murine hepatocyte cell line aml12  (ATCC)


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    ATCC murine hepatocyte cell line aml12
    Murine Hepatocyte Cell Line Aml12, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1657 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/murine+hepatocyte+aml12+cell+line/AML12/pm42249087-64-1-6
    Average 98 stars, based on 1657 article reviews
    murine hepatocyte cell line aml12 - by Bioz Stars, 2026-09
    98/100 stars

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    Related Articles

    Cell Culture:

    Article Title: Clock mediates liver senescence by controlling ER stress
    Article Snippet: .. The murine hepatocyte AML12 cell line (ATCC CRL-2254) was cultured in a 1:1 mixture of Dulbecco's modified Eagle's medium and Ham's F12 medium with an insulin-transferrin-selenium mixture and 40 ng/ml dexamethasone and 10% FBS. (Gibco, life technologies) and incubated at 37°C under 5% CO 2 . ..

    Modification:

    Article Title: Clock mediates liver senescence by controlling ER stress
    Article Snippet: .. The murine hepatocyte AML12 cell line (ATCC CRL-2254) was cultured in a 1:1 mixture of Dulbecco's modified Eagle's medium and Ham's F12 medium with an insulin-transferrin-selenium mixture and 40 ng/ml dexamethasone and 10% FBS. (Gibco, life technologies) and incubated at 37°C under 5% CO 2 . ..

    Incubation:

    Article Title: Clock mediates liver senescence by controlling ER stress
    Article Snippet: .. The murine hepatocyte AML12 cell line (ATCC CRL-2254) was cultured in a 1:1 mixture of Dulbecco's modified Eagle's medium and Ham's F12 medium with an insulin-transferrin-selenium mixture and 40 ng/ml dexamethasone and 10% FBS. (Gibco, life technologies) and incubated at 37°C under 5% CO 2 . ..



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    H89 promotes extracellular vesicle (EV) production and release in hUCMSCs. (a) hUCMSCs were treated with 1 µM, 5 µM, or 10 µM H89 for 24 h, while cells in the control group received an equal volume of phosphate‐buffered saline (PBS). Immunofluorescence staining was used to visualize CD63 (red), and DAPI was used to stain nuclei (blue). The fluorescence intensity was quantified using ImageJ software ( n = 3). Scale bar: 100 µm. (b) Quantitative analysis of extracellular vesicle (EV) concentration by nanoflow cytometry (NanoFCM) in hUCMSCs pretreated with 10 µM H89 or mTORC1 inhibitors, as shown in Figure . The exact fold‐change for the H89 treatment group was 4.87‐fold compared to the control. (c) NanoFCM quantification of EV secretion by <t>AML12</t> cells, HepRG cells, MSCs, and PTMSCs after 48 h of treatment with 10 µM H89. (d) Western blot analysis of CD63 and TSG101 expression in cellular lysates and EV fractions isolated from hUCMSCs treated with PBS (negative control) or 10 µM H89 for 48 h. (e, f) NanoFCM quantification of the expression of CD63, CD9, and CD81 in EVs, along with the particle size distribution and concentration. (g) EVs were visualized by transmission electron microscopy (TEM). EV density was quantified in 15 random fields ( n = 3). All the data are presented as the mean ± SD. Unpaired two‐tailed Student's t tests and One‐way ANOVA followed by Dunnett's multiple comparisons test were used to test for statistical significance. ** p < 0.01, *** p < 0.001.
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    H89 promotes extracellular vesicle (EV) production and release in hUCMSCs. (a) hUCMSCs were treated with 1 µM, 5 µM, or 10 µM H89 for 24 h, while cells in the control group received an equal volume of phosphate‐buffered saline (PBS). Immunofluorescence staining was used to visualize CD63 (red), and DAPI was used to stain nuclei (blue). The fluorescence intensity was quantified using ImageJ software ( n = 3). Scale bar: 100 µm. (b) Quantitative analysis of extracellular vesicle (EV) concentration by nanoflow cytometry (NanoFCM) in hUCMSCs pretreated with 10 µM H89 or mTORC1 inhibitors, as shown in Figure . The exact fold‐change for the H89 treatment group was 4.87‐fold compared to the control. (c) NanoFCM quantification of EV secretion by <t>AML12</t> cells, HepRG cells, MSCs, and PTMSCs after 48 h of treatment with 10 µM H89. (d) Western blot analysis of CD63 and TSG101 expression in cellular lysates and EV fractions isolated from hUCMSCs treated with PBS (negative control) or 10 µM H89 for 48 h. (e, f) NanoFCM quantification of the expression of CD63, CD9, and CD81 in EVs, along with the particle size distribution and concentration. (g) EVs were visualized by transmission electron microscopy (TEM). EV density was quantified in 15 random fields ( n = 3). All the data are presented as the mean ± SD. Unpaired two‐tailed Student's t tests and One‐way ANOVA followed by Dunnett's multiple comparisons test were used to test for statistical significance. ** p < 0.01, *** p < 0.001.
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    H89 promotes extracellular vesicle (EV) production and release in hUCMSCs. (a) hUCMSCs were treated with 1 µM, 5 µM, or 10 µM H89 for 24 h, while cells in the control group received an equal volume of phosphate‐buffered saline (PBS). Immunofluorescence staining was used to visualize CD63 (red), and DAPI was used to stain nuclei (blue). The fluorescence intensity was quantified using ImageJ software ( n = 3). Scale bar: 100 µm. (b) Quantitative analysis of extracellular vesicle (EV) concentration by nanoflow cytometry (NanoFCM) in hUCMSCs pretreated with 10 µM H89 or mTORC1 inhibitors, as shown in Figure . The exact fold‐change for the H89 treatment group was 4.87‐fold compared to the control. (c) NanoFCM quantification of EV secretion by <t>AML12</t> cells, HepRG cells, MSCs, and PTMSCs after 48 h of treatment with 10 µM H89. (d) Western blot analysis of CD63 and TSG101 expression in cellular lysates and EV fractions isolated from hUCMSCs treated with PBS (negative control) or 10 µM H89 for 48 h. (e, f) NanoFCM quantification of the expression of CD63, CD9, and CD81 in EVs, along with the particle size distribution and concentration. (g) EVs were visualized by transmission electron microscopy (TEM). EV density was quantified in 15 random fields ( n = 3). All the data are presented as the mean ± SD. Unpaired two‐tailed Student's t tests and One‐way ANOVA followed by Dunnett's multiple comparisons test were used to test for statistical significance. ** p < 0.01, *** p < 0.001.
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    H89 promotes extracellular vesicle (EV) production and release in hUCMSCs. (a) hUCMSCs were treated with 1 µM, 5 µM, or 10 µM H89 for 24 h, while cells in the control group received an equal volume of phosphate‐buffered saline (PBS). Immunofluorescence staining was used to visualize CD63 (red), and DAPI was used to stain nuclei (blue). The fluorescence intensity was quantified using ImageJ software ( n = 3). Scale bar: 100 µm. (b) Quantitative analysis of extracellular vesicle (EV) concentration by nanoflow cytometry (NanoFCM) in hUCMSCs pretreated with 10 µM H89 or mTORC1 inhibitors, as shown in Figure . The exact fold‐change for the H89 treatment group was 4.87‐fold compared to the control. (c) NanoFCM quantification of EV secretion by <t>AML12</t> cells, HepRG cells, MSCs, and PTMSCs after 48 h of treatment with 10 µM H89. (d) Western blot analysis of CD63 and TSG101 expression in cellular lysates and EV fractions isolated from hUCMSCs treated with PBS (negative control) or 10 µM H89 for 48 h. (e, f) NanoFCM quantification of the expression of CD63, CD9, and CD81 in EVs, along with the particle size distribution and concentration. (g) EVs were visualized by transmission electron microscopy (TEM). EV density was quantified in 15 random fields ( n = 3). All the data are presented as the mean ± SD. Unpaired two‐tailed Student's t tests and One‐way ANOVA followed by Dunnett's multiple comparisons test were used to test for statistical significance. ** p < 0.01, *** p < 0.001.
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    Image Search Results


    H89 promotes extracellular vesicle (EV) production and release in hUCMSCs. (a) hUCMSCs were treated with 1 µM, 5 µM, or 10 µM H89 for 24 h, while cells in the control group received an equal volume of phosphate‐buffered saline (PBS). Immunofluorescence staining was used to visualize CD63 (red), and DAPI was used to stain nuclei (blue). The fluorescence intensity was quantified using ImageJ software ( n = 3). Scale bar: 100 µm. (b) Quantitative analysis of extracellular vesicle (EV) concentration by nanoflow cytometry (NanoFCM) in hUCMSCs pretreated with 10 µM H89 or mTORC1 inhibitors, as shown in Figure . The exact fold‐change for the H89 treatment group was 4.87‐fold compared to the control. (c) NanoFCM quantification of EV secretion by AML12 cells, HepRG cells, MSCs, and PTMSCs after 48 h of treatment with 10 µM H89. (d) Western blot analysis of CD63 and TSG101 expression in cellular lysates and EV fractions isolated from hUCMSCs treated with PBS (negative control) or 10 µM H89 for 48 h. (e, f) NanoFCM quantification of the expression of CD63, CD9, and CD81 in EVs, along with the particle size distribution and concentration. (g) EVs were visualized by transmission electron microscopy (TEM). EV density was quantified in 15 random fields ( n = 3). All the data are presented as the mean ± SD. Unpaired two‐tailed Student's t tests and One‐way ANOVA followed by Dunnett's multiple comparisons test were used to test for statistical significance. ** p < 0.01, *** p < 0.001.

    Journal: Journal of Extracellular Vesicles

    Article Title: The Small Molecule H89 Facilitates Mesenchymal Stem Cell‐derived Extracellular Vesicle Release and Optimizes Therapeutic Efficacy in Liver Regeneration

    doi: 10.1002/jev2.70285

    Figure Lengend Snippet: H89 promotes extracellular vesicle (EV) production and release in hUCMSCs. (a) hUCMSCs were treated with 1 µM, 5 µM, or 10 µM H89 for 24 h, while cells in the control group received an equal volume of phosphate‐buffered saline (PBS). Immunofluorescence staining was used to visualize CD63 (red), and DAPI was used to stain nuclei (blue). The fluorescence intensity was quantified using ImageJ software ( n = 3). Scale bar: 100 µm. (b) Quantitative analysis of extracellular vesicle (EV) concentration by nanoflow cytometry (NanoFCM) in hUCMSCs pretreated with 10 µM H89 or mTORC1 inhibitors, as shown in Figure . The exact fold‐change for the H89 treatment group was 4.87‐fold compared to the control. (c) NanoFCM quantification of EV secretion by AML12 cells, HepRG cells, MSCs, and PTMSCs after 48 h of treatment with 10 µM H89. (d) Western blot analysis of CD63 and TSG101 expression in cellular lysates and EV fractions isolated from hUCMSCs treated with PBS (negative control) or 10 µM H89 for 48 h. (e, f) NanoFCM quantification of the expression of CD63, CD9, and CD81 in EVs, along with the particle size distribution and concentration. (g) EVs were visualized by transmission electron microscopy (TEM). EV density was quantified in 15 random fields ( n = 3). All the data are presented as the mean ± SD. Unpaired two‐tailed Student's t tests and One‐way ANOVA followed by Dunnett's multiple comparisons test were used to test for statistical significance. ** p < 0.01, *** p < 0.001.

    Article Snippet: The murine hepatocyte cell line AML12 was purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China).

    Techniques: Control, Saline, Immunofluorescence, Staining, Fluorescence, Software, Concentration Assay, Cytometry, Western Blot, Expressing, Isolation, Negative Control, Transmission Assay, Electron Microscopy, Two Tailed Test

    Modulation of the content of hUCMSC‐EVs by H89. (a) Proteomic analysis revealing the percentage of proteins that remained unchanged, were upregulated (>1.5‐fold), or were downregulated (<0.75‐fold) in H‐EVs compared with C‐EVs. (b) Selected differentially expressed proteins associated with “cell cycle regulation,” “energy metabolism,” and “oxidative stress,” along with their fold changes. (c) CCK‐8 assay demonstrating the effect of siRNA knockdown on AML12 cell proliferation. (d) Heatmap illustrating the changes in the expression of differentially expressed miRNAs between H‐EVs and C‐EVs. (e) Volcano plot highlighting the differentially expressed miRNAs. (f) The top 10 highly expressed miRNAs. (g) CCK‐8 assay to assess the effect of miRNA knockdown on AML12 cell proliferation. (h) GO and KEGG pathway analyses to identify the biological functions and pathways regulated by the target genes of miR‐29a. All the data are presented as the mean ± SD ( n = 3). Unpaired two‐tailed Student's t test was used to test for statistical significance. * p < 0.05, ** p < 0.01, ns: not significant.

    Journal: Journal of Extracellular Vesicles

    Article Title: The Small Molecule H89 Facilitates Mesenchymal Stem Cell‐derived Extracellular Vesicle Release and Optimizes Therapeutic Efficacy in Liver Regeneration

    doi: 10.1002/jev2.70285

    Figure Lengend Snippet: Modulation of the content of hUCMSC‐EVs by H89. (a) Proteomic analysis revealing the percentage of proteins that remained unchanged, were upregulated (>1.5‐fold), or were downregulated (<0.75‐fold) in H‐EVs compared with C‐EVs. (b) Selected differentially expressed proteins associated with “cell cycle regulation,” “energy metabolism,” and “oxidative stress,” along with their fold changes. (c) CCK‐8 assay demonstrating the effect of siRNA knockdown on AML12 cell proliferation. (d) Heatmap illustrating the changes in the expression of differentially expressed miRNAs between H‐EVs and C‐EVs. (e) Volcano plot highlighting the differentially expressed miRNAs. (f) The top 10 highly expressed miRNAs. (g) CCK‐8 assay to assess the effect of miRNA knockdown on AML12 cell proliferation. (h) GO and KEGG pathway analyses to identify the biological functions and pathways regulated by the target genes of miR‐29a. All the data are presented as the mean ± SD ( n = 3). Unpaired two‐tailed Student's t test was used to test for statistical significance. * p < 0.05, ** p < 0.01, ns: not significant.

    Article Snippet: The murine hepatocyte cell line AML12 was purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China).

    Techniques: CCK-8 Assay, Knockdown, Expressing, Two Tailed Test