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murine hepatocyte cell line aml 12  (ATCC)


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    Structured Review

    ATCC murine hepatocyte cell line aml 12
    Murine Hepatocyte Cell Line Aml 12, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1667 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/murine+hepatocyte+cell+line+aml12/AML12/pm42835072-75-5-21
    Average 98 stars, based on 1667 article reviews
    murine hepatocyte cell line aml 12 - by Bioz Stars, 2026-10
    98/100 stars

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    Related Articles

    Incubation:

    Article Title: ABCC4 impairs the clearance of plasma LDL cholesterol through suppressing LDLR expression in the liver
    Article Snippet: .. Murine hepatocyte cell line AML12 (Alpha Mouse Liver 12, ATCC CRL-2254) and human embryonic kidney (HEK) 293 T cell line (ATCC CRL-3216) were originally obtained from American Tissue Culture Collection Biobank (Manassas, VA, USA) and were incubated at 37°C with 5% CO2. .. Human hepatocyte cell line LO2 were originally purchased from QuiCell Biotechnology (QuiCell-L090, Shanghai, China).

    Cell Culture:

    Article Title: DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease
    Article Snippet: .. Treatment of cells with palmitate, lipopolysaccharide, and 5-aza-2′-deoxycytidine (AZA) The murine hepatocyte cell line AML12 (#CRL-2254) was purchased from American Type Culture Collection and cultured in Dulbecco’s Modified Eagle Medium/F12 media (Welgene, Korea) supplemented with 10% fetal bovine serum (Welgene), 1% penicillin-streptomycin (Welgene), 40 ng/mL dexamethasone (Sigma-Aldrich) and 1×ITS solution (Thermo Scientific). ..

    Article Title: DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease.
    Article Snippet: .. Treatment of cells with palmitate, lipopolysaccharide, and 5-aza-2′-deoxycytidine (AZA) The murine hepatocyte cell line AML12 (#CRL-2254) was purchase from American Type Culture Collection and cultured in Dulbecco’s Modified Eagle Medium/F12 media (Welgene, Korea) supplemented with 10% fetal bovine serum (Welgene), 1% penicillin-streptomycin (Welgene), 40 ng/mL dexamethasone (Sigma-Aldrich) and 1 ITS solution (Thermo scientific). ..

    Article Title: DN203316, a novel PPARδ agonist, suppresses ferroptotic signaling and fibrogenesis in metabolic dysfunction-associated steatohepatitis.
    Article Snippet: .. The murine hepatocyte cell line AML12 (ATCC) was cultured in DMEM–F12 medium (Gibco) containing 10% fetal bovine serum (FBS), 5 mg/ml insulin, 5 μg/ml transferrin, 5 ng/ml selenium (ITS mix, Thermo Fisher Scienfitic), 40 ng/ml dexamethasone (Sigma-Aldrich) and 1% penicillin–streptomycin (Gibco). .. The HepG2 (ATCC) cells were cultured in Eagle’s minimum essential medium (ATCC) supplemented with 10% FBS and 1% penicillin–streptomycin.

    Modification:

    Article Title: DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease
    Article Snippet: .. Treatment of cells with palmitate, lipopolysaccharide, and 5-aza-2′-deoxycytidine (AZA) The murine hepatocyte cell line AML12 (#CRL-2254) was purchased from American Type Culture Collection and cultured in Dulbecco’s Modified Eagle Medium/F12 media (Welgene, Korea) supplemented with 10% fetal bovine serum (Welgene), 1% penicillin-streptomycin (Welgene), 40 ng/mL dexamethasone (Sigma-Aldrich) and 1×ITS solution (Thermo Scientific). ..

    Article Title: DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease.
    Article Snippet: .. Treatment of cells with palmitate, lipopolysaccharide, and 5-aza-2′-deoxycytidine (AZA) The murine hepatocyte cell line AML12 (#CRL-2254) was purchase from American Type Culture Collection and cultured in Dulbecco’s Modified Eagle Medium/F12 media (Welgene, Korea) supplemented with 10% fetal bovine serum (Welgene), 1% penicillin-streptomycin (Welgene), 40 ng/mL dexamethasone (Sigma-Aldrich) and 1 ITS solution (Thermo scientific). ..



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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 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