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ATCC hepg2 human caucasian hepatocyte carcinoma cell line
Hepg2 Human Caucasian Hepatocyte Carcinoma Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 29817 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 99 stars, based on 29817 article reviews

hepg2 human caucasian hepatocyte carcinoma cell line - by Bioz Stars, 2026-09

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Article Title: Nano-bio interactions of Gum Arabic-stabilized lanthanide-based upconverting nanoparticles: in vitro and in vivo study.
Article Snippet: Lanthanide-based nanoparticles (Ln-NPs) are highly valued for their unique optical and magnetic properties, making them useful in various scientific fields, including materials science and biomedicine.. This study investigated the use of Gum Arabic (GA), a natural, non-toxic biopolymer, as capping agent for Ln-NPs to enhance their biocompatibility and chemical and colloidal stability.. Specifically, Er/Yb co-doped NaGdF4 Ln-NPs were modified with GA, followed by their characterization with respect to upconversion properties and in vitro as well as in vivo toxicity.

Cell Culture:

Article Title: Rapid, accurate mapping of transgene integration in viable rhesus macaque embryos using enhanced-specificity tagmentation-assisted PCR.
Article Snippet: .. Cell lines and cell culture Experiments used HepG2 cells, an immortalized human hepatocyte cell line (ATCC HB-8065), and HEK293 cells, an immortalized human kidney cell line (American Type Culture Collection [ATCC] CRL-1573). .. Cells were cultured in DMEM-F12 supplemented with 10% fetal bovine serum (FBS) and 1% penicillin/streptomycin. piggyBac-mediated stable transfection of HepG2 cells and generation of clonal cell lines HepG2 cells were transfected with a piggyBac-compatible vector containing an expression cassette that is under the control of the CAG promoter (GenBank: OK413188).

Article Title: Lavandula viridis L´Hér. Essential Oil Inhibits the Inflammatory Response in Macrophages Through Blockade of NF-KB Signaling Cascade
Article Snippet: HaCat, the human keratinocyte cell line and A549, the human alveolar epithelial cell line (ATCC-CCL-185) were cultured in DMEM medium supplemented with 10% (v/v) of heat inactivated FBS, 3.02 g/L sodium bicarbonate, 100 μg/mL streptomycin and 100 U/mL penicillin. .. HepG2, an human hepatocyte cell line (ATCC HB-8065) was cultured in DMEM medium supplemented with 10% (v/v) heat inactivated FBS, 1.5 g/L sodium bicarbonate, 100 μg/mL streptomycin and 100U/mL penicillin. ..

Article Title: Lavandula viridis L´Hér. Essential Oil Inhibits the Inflammatory Response in Macrophages Through Blockade of NF-KB Signaling Cascade.
Article Snippet: HaCat, the human keratinocyte cell line and A549, the human alveolar epithelial cell line (ATCC-CCL-185) were cultured in DMEMmedium supplemented with 10% (v/v) of heat inactivated FBS, 3.02 g/L sodium bicarbonate, 100 μg/mL streptomycin and 100 U/mL penicillin. .. HepG2, an human hepatocyte cell line (ATCC HB-8065) was cultured in DMEM medium supplemented with 10% (v/v) heat inactivated FBS, 1.5 g/L sodium bicarbonate, 100 μg/mL streptomycin and 100U/mL penicillin. ..

Retroviral:

Article Title: Hepatic lipids promote liver metastasis
Article Snippet: .. Mouse breast cancer cell lines PyMT-Bo1 (Bo1 – ), PyMT-Bo1-GFP-Luc (Bo1), and PyMT-B6 (B6) (estrogen receptor + cells) ( ); B16 murine melanoma cell line (ATCC); human hepatocyte cell line (HepG2, ATCC); and platinum-E (Plat-E, ATCC) retroviral packaging cell line were maintained at DMEM with 10% FBS. ..

Article Title: Hepatic lipids promote liver metastasis.
Article Snippet: .. Mouse breast cancer cell lines PyMT-Bo1 (Bo1–), PyMT-Bo1-GFP-Luc (Bo1), and PyMT-B6 (B6) (estrogen receptor+ cells) (33); B16 murine melanoma cell line (ATCC); human hepatocyte cell line (HepG2, ATCC); and platinum-E (Plat-E, ATCC) retroviral packaging cell line were maintained at DMEM with 10% FBS. ..

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MiR-300-3p was decreased in the livers of MAFLD mice and FFA-induced HepG2 cells. (A) MiR-300-3p was decreased in the livers of MAFLD mice. (B) MiR-300-3p was downregulated in the FFA-induced HepG2 cells. (C) MiR-300-3p was downregulated in HepG2 cells successfully. (D) MiR-300-3p was overexpressed in HepG2 cells successfully. Data in (A–D) are means±SDs (n = 3). *P < 0.05, **P < 0.01. NC, Healthy control; OC, over-expression control; IC, inhibition control.

Journal: Frontiers in Pharmacology

Article Title: Downregulation of microRNA-300-3p promotes steatosis-to-MASH progression by regulating STX17

doi: 10.3389/fphar.2026.1804415

Figure Lengend Snippet: MiR-300-3p was decreased in the livers of MAFLD mice and FFA-induced HepG2 cells. (A) MiR-300-3p was decreased in the livers of MAFLD mice. (B) MiR-300-3p was downregulated in the FFA-induced HepG2 cells. (C) MiR-300-3p was downregulated in HepG2 cells successfully. (D) MiR-300-3p was overexpressed in HepG2 cells successfully. Data in (A–D) are means±SDs (n = 3). *P < 0.05, **P < 0.01. NC, Healthy control; OC, over-expression control; IC, inhibition control.

Article Snippet: The human hepatocyte cell line HepG2 was procured from the American Type Culture Collection (ATCC, United States) and cultivated in a humidified incubator maintained at 37 °C with a 5% CO 2 atmosphere.

Techniques: Control, Over Expression, Inhibition

Downregulation of miR-300-3p promotes FFA-induced lipid accumulation and hepatic inflammation in HepG2 cells. (A) The experimental flow of the MAFLD cell model construction and miR-300-3p mimics, miR-300-3p inhibitors and as well as corresponding scrambled controls transfection in HepG2 cells. (B,C) Intercellular TG contents in miR-300-3p -inhibited and -overexpressing in HepG2 cells. (D) Oil Red O staining (400×) and the relative areas of lipid droplets in miR-300-3p-inhibited and -overexpressing in HepG2 cells. (E,F) mRNA levels of FASN, SREBP-1c, IL-6, IL-2 and TNF-αin miR-300-3p -inhibited and -overexpressing in HepG2 cells. (G) Protein levels of FASN, SREBP-1c and TNF-α in miR-300-3p -inhibited and -overexpressing in HepG2 cells. Data in (B,C) and (E–G) are means±SDs (n = 3). *P < 0.05, **P < 0.01, *** P < 0.001, **** P < 0.0001. OC, over-expression control; IC, inhibition control.

Journal: Frontiers in Pharmacology

Article Title: Downregulation of microRNA-300-3p promotes steatosis-to-MASH progression by regulating STX17

doi: 10.3389/fphar.2026.1804415

Figure Lengend Snippet: Downregulation of miR-300-3p promotes FFA-induced lipid accumulation and hepatic inflammation in HepG2 cells. (A) The experimental flow of the MAFLD cell model construction and miR-300-3p mimics, miR-300-3p inhibitors and as well as corresponding scrambled controls transfection in HepG2 cells. (B,C) Intercellular TG contents in miR-300-3p -inhibited and -overexpressing in HepG2 cells. (D) Oil Red O staining (400×) and the relative areas of lipid droplets in miR-300-3p-inhibited and -overexpressing in HepG2 cells. (E,F) mRNA levels of FASN, SREBP-1c, IL-6, IL-2 and TNF-αin miR-300-3p -inhibited and -overexpressing in HepG2 cells. (G) Protein levels of FASN, SREBP-1c and TNF-α in miR-300-3p -inhibited and -overexpressing in HepG2 cells. Data in (B,C) and (E–G) are means±SDs (n = 3). *P < 0.05, **P < 0.01, *** P < 0.001, **** P < 0.0001. OC, over-expression control; IC, inhibition control.

Techniques: Transfection, Staining, Over Expression, Control, Inhibition

Downregulation of miR-300-3p induces apoptosis in HepG2 cells to promote it. (A,B) The apoptosis rate in miR-300-3p -inhibited and -overexpressing in HepG2 cells. (C) mRNA levels of Bax, Bcl-2 and Caspase-3 in miR-300-3p -inhibited and -overexpressing in HepG2 cells. (D) Protein levels of Bax, Bcl-2 and Caspase-3 in miR-300-3p -overexpressing and -inhibited in HepG2 cells. Data in (A–D) are means±SDs (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. OC, over-expression control; IC, inhibition control.

Journal: Frontiers in Pharmacology

Article Title: Downregulation of microRNA-300-3p promotes steatosis-to-MASH progression by regulating STX17

doi: 10.3389/fphar.2026.1804415

Figure Lengend Snippet: Downregulation of miR-300-3p induces apoptosis in HepG2 cells to promote it. (A,B) The apoptosis rate in miR-300-3p -inhibited and -overexpressing in HepG2 cells. (C) mRNA levels of Bax, Bcl-2 and Caspase-3 in miR-300-3p -inhibited and -overexpressing in HepG2 cells. (D) Protein levels of Bax, Bcl-2 and Caspase-3 in miR-300-3p -overexpressing and -inhibited in HepG2 cells. Data in (A–D) are means±SDs (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. OC, over-expression control; IC, inhibition control.

Techniques: Over Expression, Control, Inhibition

MiR-300-3p regulates STX17 in HepG2 cells. (A,B) GO enrichment analysis (Biological Process category) and KEGG enrichment analysis diagrams of sixteen predicted target genes of miR-300-3p. (C) The predicted binding sites between miR-300-3p and STX17 were putatively identified via the TargetScan database. (D) Dual-luciferase reporter assay (DLRA) in HepG2 cells validated that STX17 is a direct target gene of miR-300-3p. (E,F) The mRNA and protein expression levels of STX17 in HepG2 cells with miR-300-3p inhibition or overexpression. Data in (A–D) are means±SDs (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. OC, overexpression control; IC, inhibition control.

Journal: Frontiers in Pharmacology

Article Title: Downregulation of microRNA-300-3p promotes steatosis-to-MASH progression by regulating STX17

doi: 10.3389/fphar.2026.1804415

Figure Lengend Snippet: MiR-300-3p regulates STX17 in HepG2 cells. (A,B) GO enrichment analysis (Biological Process category) and KEGG enrichment analysis diagrams of sixteen predicted target genes of miR-300-3p. (C) The predicted binding sites between miR-300-3p and STX17 were putatively identified via the TargetScan database. (D) Dual-luciferase reporter assay (DLRA) in HepG2 cells validated that STX17 is a direct target gene of miR-300-3p. (E,F) The mRNA and protein expression levels of STX17 in HepG2 cells with miR-300-3p inhibition or overexpression. Data in (A–D) are means±SDs (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. OC, overexpression control; IC, inhibition control.

Techniques: Binding Assay, Luciferase, Reporter Assay, Expressing, Inhibition, Over Expression, Control

P62 and LC3-II in miR-300-3p -inhibited and -overexpressing in HepG2 cells. (A) The protein levels of P62 and LC3-II in miR-300-3p -inhibited and -overexpressing in HepG2 cells. (B) P62 and LC3-II in miR-300-3p -inhibited and -overexpressing by Immunofluorescence assay. Data in (A-D) are means±SDs (n = 3). *P < 0.05, **P < 0.01,***P < 0.001,****P < 0.0001. OC, overexpression control; IC, inhibition control.

Journal: Frontiers in Pharmacology

Article Title: Downregulation of microRNA-300-3p promotes steatosis-to-MASH progression by regulating STX17

doi: 10.3389/fphar.2026.1804415

Figure Lengend Snippet: P62 and LC3-II in miR-300-3p -inhibited and -overexpressing in HepG2 cells. (A) The protein levels of P62 and LC3-II in miR-300-3p -inhibited and -overexpressing in HepG2 cells. (B) P62 and LC3-II in miR-300-3p -inhibited and -overexpressing by Immunofluorescence assay. Data in (A-D) are means±SDs (n = 3). *P < 0.05, **P < 0.01,***P < 0.001,****P < 0.0001. OC, overexpression control; IC, inhibition control.

Techniques: Immunofluorescence, Over Expression, Control, Inhibition

MiR-300-3p promoted autophagy by regulating STX17, reduces lipid accumulation, inflammatory response, and decreases hepatocyte apoptosis. (A) STX17 was inhibited or overexpressed in HepG2 cells successfully. (B) Protein levels of FASN, SREBP-1c and TNF-αin STX17 -inhibited and -overexpressing in HepG2 cells. (C,D) Intercellular TG contents in STX17-inhibited and -overexpressing in HepG2 cells. (E) Oil Red O staining (400×) and relative areas of lipid droplets in STX17-inhibited and -STX17 in HepG2 cells. (F) Protein levels of Bax, Capase-3 and Bcl-2 in STX17 -inhibited and -overexpressing in HepG2 cells. Data in (A–D) and (F) are means±SDs (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. OC, miR-300-3p overexpression control; IC,miR-300-3p inhibition control; Control, STX17-overexpression control or STX17-inhibition control; Si-STX17, STX17-inhibition; Over-STX17, STX17-overexpression.

Journal: Frontiers in Pharmacology

Article Title: Downregulation of microRNA-300-3p promotes steatosis-to-MASH progression by regulating STX17

doi: 10.3389/fphar.2026.1804415

Figure Lengend Snippet: MiR-300-3p promoted autophagy by regulating STX17, reduces lipid accumulation, inflammatory response, and decreases hepatocyte apoptosis. (A) STX17 was inhibited or overexpressed in HepG2 cells successfully. (B) Protein levels of FASN, SREBP-1c and TNF-αin STX17 -inhibited and -overexpressing in HepG2 cells. (C,D) Intercellular TG contents in STX17-inhibited and -overexpressing in HepG2 cells. (E) Oil Red O staining (400×) and relative areas of lipid droplets in STX17-inhibited and -STX17 in HepG2 cells. (F) Protein levels of Bax, Capase-3 and Bcl-2 in STX17 -inhibited and -overexpressing in HepG2 cells. Data in (A–D) and (F) are means±SDs (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. OC, miR-300-3p overexpression control; IC,miR-300-3p inhibition control; Control, STX17-overexpression control or STX17-inhibition control; Si-STX17, STX17-inhibition; Over-STX17, STX17-overexpression.

Techniques: Staining, Over Expression, Control, Inhibition

P62, LC3-II in STX17-inhibited and -overexpressing in HepG2 cells. (A) Protein levels of P62, LC3-II in STX17-inhibited and -overexpressing in HepG2 cells. (B) P62 and LC3-II in STX17-inhibited and -overexpressing by Immunofluorescence assay. Data in (A-D) are means±SDs (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. OC, overexpression control; IC, inhibition control.

Journal: Frontiers in Pharmacology

Article Title: Downregulation of microRNA-300-3p promotes steatosis-to-MASH progression by regulating STX17

doi: 10.3389/fphar.2026.1804415

Figure Lengend Snippet: P62, LC3-II in STX17-inhibited and -overexpressing in HepG2 cells. (A) Protein levels of P62, LC3-II in STX17-inhibited and -overexpressing in HepG2 cells. (B) P62 and LC3-II in STX17-inhibited and -overexpressing by Immunofluorescence assay. Data in (A-D) are means±SDs (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. OC, overexpression control; IC, inhibition control.

Techniques: Immunofluorescence, Over Expression, Control, Inhibition

(A) p107 protein levels in THLE2 cells transfected with siRNA p107 or siRNA control for 48 hours (n=3 per group). (B) Representative microphotographs of Oil Red O staining (left pannel) of THLE2 cells downregulating p107 (sip107) for 48 hours (n = 3 per group) and Oil Red O semiquantification (right pannel) (n = 3 per group). (C) Quantification of immunoblot analysis of de novo lipogenesis markers (n = 3 per group) and a representative immunoblot. (D) RNA expression of de novo lipogenesis markers (n = 3 per group. (E) De novo synthesis of free fatty acids (FFA) and triglycerides (TG) in THLE2 (n = 6 per group). (F) FAO activity in THLE2 cells transfected with siRNA p107 or siRNA control for 48 hours (n=5 per group). (G) Oxidation rate of palmitic acid (n = 6 per group). (H and I)) OCR and (I) ECAR of p107-silenced THLE2 (n = 17-19 per group). (J) Basal energetic metabolic states, based on quantification of ECAR and OCR during basal metabolism. (K) p107 protein levels in THLE2 after overexpressing p107 (n = 3 per group). (L) Representative microphotographs (left pannel) and semiquantification (right pannel) of Oil Red O staining of THLE2 cells overexpressing p107 (plasmid p107) for 24 hours. Oil Red O staining was quantified using ImageJ and normalized to the total number of nuclei per field (n = 4 per group). (M) Quantification of immunoblot analysis of de novo lipogenesis markers (n = 3 per group) and a representative immunoblot. (N) OCR of p107-overexpressed THLE2 (n =10 per group). GAPDH was used to normalize protein levels. Data are expressed as mean ±SEM. *p < 0.05, **p < 0.01, ***p <0.001, using a Student’s t test .

Journal: bioRxiv

Article Title: Inhibition of p107 alleviates liver steatosis by reducing de novo fatty acid synthesis

doi: 10.64898/2026.04.14.718271

Figure Lengend Snippet: (A) p107 protein levels in THLE2 cells transfected with siRNA p107 or siRNA control for 48 hours (n=3 per group). (B) Representative microphotographs of Oil Red O staining (left pannel) of THLE2 cells downregulating p107 (sip107) for 48 hours (n = 3 per group) and Oil Red O semiquantification (right pannel) (n = 3 per group). (C) Quantification of immunoblot analysis of de novo lipogenesis markers (n = 3 per group) and a representative immunoblot. (D) RNA expression of de novo lipogenesis markers (n = 3 per group. (E) De novo synthesis of free fatty acids (FFA) and triglycerides (TG) in THLE2 (n = 6 per group). (F) FAO activity in THLE2 cells transfected with siRNA p107 or siRNA control for 48 hours (n=5 per group). (G) Oxidation rate of palmitic acid (n = 6 per group). (H and I)) OCR and (I) ECAR of p107-silenced THLE2 (n = 17-19 per group). (J) Basal energetic metabolic states, based on quantification of ECAR and OCR during basal metabolism. (K) p107 protein levels in THLE2 after overexpressing p107 (n = 3 per group). (L) Representative microphotographs (left pannel) and semiquantification (right pannel) of Oil Red O staining of THLE2 cells overexpressing p107 (plasmid p107) for 24 hours. Oil Red O staining was quantified using ImageJ and normalized to the total number of nuclei per field (n = 4 per group). (M) Quantification of immunoblot analysis of de novo lipogenesis markers (n = 3 per group) and a representative immunoblot. (N) OCR of p107-overexpressed THLE2 (n =10 per group). GAPDH was used to normalize protein levels. Data are expressed as mean ±SEM. *p < 0.05, **p < 0.01, ***p <0.001, using a Student’s t test .

Article Snippet: THLE2 human hepatic cell line (American Type Culture Collection, ATCC) was cultured in bronchial epithelial cell basal medium (BEBM) supplemented with a growth factors BulleKit (Lonza/Clonetics Corporation), 70ng/mL phosphoethanolamine, 5 ng/mL epidermal growth factor, 10% (v/v) FBS and 1% (v/v) Glutamine-Penicillin-Streptomycin solution (MERCK).

Techniques: Transfection, Control, Staining, Western Blot, RNA Expression, Activity Assay, Plasmid Preparation

(A) Volcano plot of total protein expression in p107 liver KO mice compared to shLucif controls (n = 7). Red and blue points indicate significantly up- and downregulated proteins (p < 0.05). (B) Volcano plot of phosphosite abundance in p107 liver KO mice compared to shLucif controls (n = 7). Points represent individual phosphosites—annotated by their parent protein name—with red and blue indicating significant changes (p < 0.05). (C) Heatmap of total protein expression differences grouped by GO Biological Process terms, filtered by significance (p < 0.001). (D) Heatmap of robust total protein expression differences grouped by GO terms, utilizing strict filtering (> 3 combined razor and unique peptides, p < 0.001, absolute t-test difference > 0.58). (E) Quantification of p107 (left panel) and FAS (right panel) in THLE2 after overexpressing p107 (plasmid p107) and silencing FAS (siRNA FAS) during 24h (n = 3 per group) and representative immunoblot. (F) Representative microphotographs of Oil Red O staining of THLE2 cells overexpressing p107 (plasmid p107) and silencing FAS (siRNA FAS) for 24 hours. (G) Semiquantification of Oil Red O staining. Vinculin was used to normalize protein levels. Data are expressed as mean ±SEM. *p < 0.05, **p < 0.01, ***p <0.001, using a Student’s t test .

Journal: bioRxiv

Article Title: Inhibition of p107 alleviates liver steatosis by reducing de novo fatty acid synthesis

doi: 10.64898/2026.04.14.718271

Figure Lengend Snippet: (A) Volcano plot of total protein expression in p107 liver KO mice compared to shLucif controls (n = 7). Red and blue points indicate significantly up- and downregulated proteins (p < 0.05). (B) Volcano plot of phosphosite abundance in p107 liver KO mice compared to shLucif controls (n = 7). Points represent individual phosphosites—annotated by their parent protein name—with red and blue indicating significant changes (p < 0.05). (C) Heatmap of total protein expression differences grouped by GO Biological Process terms, filtered by significance (p < 0.001). (D) Heatmap of robust total protein expression differences grouped by GO terms, utilizing strict filtering (> 3 combined razor and unique peptides, p < 0.001, absolute t-test difference > 0.58). (E) Quantification of p107 (left panel) and FAS (right panel) in THLE2 after overexpressing p107 (plasmid p107) and silencing FAS (siRNA FAS) during 24h (n = 3 per group) and representative immunoblot. (F) Representative microphotographs of Oil Red O staining of THLE2 cells overexpressing p107 (plasmid p107) and silencing FAS (siRNA FAS) for 24 hours. (G) Semiquantification of Oil Red O staining. Vinculin was used to normalize protein levels. Data are expressed as mean ±SEM. *p < 0.05, **p < 0.01, ***p <0.001, using a Student’s t test .

Techniques: Expressing, Phospho-proteomics, Plasmid Preparation, Western Blot, Staining

Impaired mitochondrial fatty acid β-oxidation is a key metabolic defect contributing to cholesterol-induced hepatocellular fat accumulation. ( A, B ) Plasma glycerol and TAG levels in chow-fed mice supplemented with and without 2% cholesterol (w/w) for 4 weeks. ( C-E ) Extracellular TAG concentrations in the culture medium of AML12, HepaRG, and HepG2 cells following cholesterol. ( F, G ) Extracellular TAG concentrations in the culture medium of AML12 and HepG2 cells following LDL supplementation. ( H, I ) Heatmap visualization of representative lipid-related pathways in AML12 cells and in vivo . ( J, K ) qRT-PCR validation of mitochondrial fatty acid β-oxidation ( Pparα , Cpt1α , Acox1 , Hmgcs2 , and Cyp7a1 ) in vitro and in vivo . ( L-N ) Unaltered Srebp-1c pathway activation in AML12 cells following cholesterol exposure and in chow-fed mice supplemented with and without 2% cholesterol for 4 weeks, tested by Western-blot and qRT-PCR. ( O, P ) Fluorescence-based FAOBlue™ assay of fatty acid β-oxidation capacity (FAO) in AML12 and HepG2 cells after cholesterol loading (4 μM, 16 h). (40× objective). Chol, cholesterol; MβCD-chol, MβCD-cholesterol; LDL, low-density lipoprotein. * P < 0.05 and ** P < 0.01 represent statistical significance.

Journal: International Journal of Biological Sciences

Article Title: Cholesterol Overload Drives Hepatic Steatosis by Inhibiting OGT-dependent PPARα O-GlcNAcylation and Transactivation

doi: 10.7150/ijbs.135054

Figure Lengend Snippet: Impaired mitochondrial fatty acid β-oxidation is a key metabolic defect contributing to cholesterol-induced hepatocellular fat accumulation. ( A, B ) Plasma glycerol and TAG levels in chow-fed mice supplemented with and without 2% cholesterol (w/w) for 4 weeks. ( C-E ) Extracellular TAG concentrations in the culture medium of AML12, HepaRG, and HepG2 cells following cholesterol. ( F, G ) Extracellular TAG concentrations in the culture medium of AML12 and HepG2 cells following LDL supplementation. ( H, I ) Heatmap visualization of representative lipid-related pathways in AML12 cells and in vivo . ( J, K ) qRT-PCR validation of mitochondrial fatty acid β-oxidation ( Pparα , Cpt1α , Acox1 , Hmgcs2 , and Cyp7a1 ) in vitro and in vivo . ( L-N ) Unaltered Srebp-1c pathway activation in AML12 cells following cholesterol exposure and in chow-fed mice supplemented with and without 2% cholesterol for 4 weeks, tested by Western-blot and qRT-PCR. ( O, P ) Fluorescence-based FAOBlue™ assay of fatty acid β-oxidation capacity (FAO) in AML12 and HepG2 cells after cholesterol loading (4 μM, 16 h). (40× objective). Chol, cholesterol; MβCD-chol, MβCD-cholesterol; LDL, low-density lipoprotein. * P < 0.05 and ** P < 0.01 represent statistical significance.

Article Snippet: Murine AML12 and human HepG2 hepatocyte cell lines were obtained from the American Type Culture Collection (ATCC, VA, USA).

Techniques: Clinical Proteomics, In Vivo, Quantitative RT-PCR, Biomarker Discovery, In Vitro, Activation Assay, Western Blot, Fluorescence

OGT-mediated O-GlcNAcylation is essential for hepatic PPARα transactivation. AML12 cells were treated with OSMI-1. ( A ) qRT-PCR analysis of Ogt , Pparα , Hmgcs2 , and Cpt1a mRNA levels. AML12 and HepG2 cells were treated with OSMI-1, either alone or in combination with TMG. ( B, C ) Western blot analyses of PPARα protein. ( D, E ) qRT-PCR and ELISA analyses showing that Ogt silencing reduced Pparα , Hmgcs2 , and Cpt1α expression and decreased PPARα transcriptional activity in AML12 cells. ( F, G ) FAOBlue TM assay in AML12 and HepG2 cells. PPARα O-GlcNAcylation was examined by co-immunoprecipitation. ( H ) OGT association with PPARα (IB: OGT) and O-GlcNAc modification of PPARα (IB: O-GlcNAc; arrow). Right: effects of cholesterol treatment or si Ogt on PPARα O-GlcNAcylation. ( I, J ) qRT-PCR analysis of hepatic Pparα , Hmgcs2 , Cpt1α , Acox1 , and Cyp7a1 mRNA levels in liver-specific OGT- and OGA-deficient mice. O-GlcNAc, O-GlcNAcylation. * P < 0.05 and ** P < 0.01 represent statistical significance.

Journal: International Journal of Biological Sciences

Article Title: Cholesterol Overload Drives Hepatic Steatosis by Inhibiting OGT-dependent PPARα O-GlcNAcylation and Transactivation

doi: 10.7150/ijbs.135054

Figure Lengend Snippet: OGT-mediated O-GlcNAcylation is essential for hepatic PPARα transactivation. AML12 cells were treated with OSMI-1. ( A ) qRT-PCR analysis of Ogt , Pparα , Hmgcs2 , and Cpt1a mRNA levels. AML12 and HepG2 cells were treated with OSMI-1, either alone or in combination with TMG. ( B, C ) Western blot analyses of PPARα protein. ( D, E ) qRT-PCR and ELISA analyses showing that Ogt silencing reduced Pparα , Hmgcs2 , and Cpt1α expression and decreased PPARα transcriptional activity in AML12 cells. ( F, G ) FAOBlue TM assay in AML12 and HepG2 cells. PPARα O-GlcNAcylation was examined by co-immunoprecipitation. ( H ) OGT association with PPARα (IB: OGT) and O-GlcNAc modification of PPARα (IB: O-GlcNAc; arrow). Right: effects of cholesterol treatment or si Ogt on PPARα O-GlcNAcylation. ( I, J ) qRT-PCR analysis of hepatic Pparα , Hmgcs2 , Cpt1α , Acox1 , and Cyp7a1 mRNA levels in liver-specific OGT- and OGA-deficient mice. O-GlcNAc, O-GlcNAcylation. * P < 0.05 and ** P < 0.01 represent statistical significance.

Article Snippet: Murine AML12 and human HepG2 hepatocyte cell lines were obtained from the American Type Culture Collection (ATCC, VA, USA).

Techniques: Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing, Activity Assay, Immunoprecipitation, Modification

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hepg2 human caucasian hepatocyte carcinoma cell line (ATCC)

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