Sudan III dye strongly induces CYP1A1 mRNA expression in HepG2 cells

2012 ◽  
Vol 26 (1) ◽  
pp. 16-22 ◽  
Author(s):  
Marumi Ohno ◽  
Yoshinori Ikenaka ◽  
Mayumi Ishizuka
Keyword(s):  
Mrna Expression ◽  
Hepg2 Cells ◽  
Sudan Iii ◽  
Cyp1a1 Mrna

scholarly journals Side-effects of resveratrol in HepG2 cells: Reduced pten and increased bcl-xl mRNA expression

2012 ◽  
Vol 6 (6) ◽  
pp. 1367-1370 ◽  
Author(s):  
MIN ZHENG ◽  
RUIFU CHEN ◽  
HONGYUAN ZHONG ◽  
QIUYAN LIN ◽  
XIAOQIN WANG ◽  
...  
Keyword(s):  
Side Effects ◽  
Mrna Expression ◽  
Hepg2 Cells

scholarly journals Iron elevates mesenchymal and metastatic biomarkers in HepG2 cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Kosha J. Mehta ◽  
Paul A. Sharp
Keyword(s):  
Transcription Factors ◽  
Mrna Expression ◽  
Hepg2 Cells ◽  
Cellular Mechanisms ◽  
Intracellular Iron ◽  
Liver Iron ◽  
Mesenchymal Transition ◽  
Excess Iron ◽  
Epithelial Marker ◽  
E Cadherin

AbstractLiver iron excess is observed in several chronic liver diseases and is associated with the development of hepatocellular carcinoma (HCC). However, apart from oxidative stress, other cellular mechanisms by which excess iron may mediate/increase HCC predisposition/progression are not known. HCC pathology involves epithelial to mesenchymal transition (EMT), the basis of cancer phenotype acquisition. Here, the effect of excess iron (holo-transferrin 0–2 g/L for 24 and 48 h) on EMT biomarkers in the liver-derived HepG2 cells was investigated. Holo-transferrin substantially increased intracellular iron. Unexpectedly, mRNA and protein expression of the epithelial marker E-cadherin either remained unaltered or increased. The mRNA and protein levels of metastasis marker N-cadherin and mesenchymal marker vimentin increased significantly. While the mRNA expression of EMT transcription factors SNAI1 and SNAI2 increased and decreased, respectively after 24 h, both factors increased after 48 h. The mRNA expression of TGF-β (EMT-inducer) showed no significant alterations. In conclusion, data showed direct link between iron and EMT. Iron elevated mesenchymal and metastatic biomarkers in HepG2 cells without concomitant decrement in the epithelial marker E-cadherin and altered the expression of the key EMT-mediating transcription factors. Such studies can help identify molecular targets to devise iron-related adjunctive therapies to ameliorate HCC pathophysiology.

scholarly journals RNA interference-mediated URG4 gene silencing diminishes cyclin D1 mRNA expression in HepG2 cells

2010 ◽  
Vol 9 (3) ◽  
pp. 1557-1567 ◽  
Author(s):  
N.L. Satiroglu-Tufan ◽  
Y. Dodurga ◽  
D. Gok ◽  
A. Cetinkaya ◽  
M.A. Feitelson
Keyword(s):  
Rna Interference ◽  
Gene Silencing ◽  
Cyclin D1 ◽  
Mrna Expression ◽  
Hepg2 Cells

Effect of cadmium on uptake of iron, zinc and copper and mRNA expression of metallothioneins in HepG2 cells in vitro

2017 ◽  
Vol 44 ◽  
pp. 372-376 ◽  
Author(s):  
Sabine Sampels ◽  
Hana Kocour Kroupova ◽  
Pavla Linhartova
Keyword(s):  
Mrna Expression ◽  
Hepg2 Cells

scholarly journals Oestrogen receptor α is required for biochanin A-induced apolipoprotein A-1 mRNA expression in HepG2 cells

2007 ◽  
Vol 98 (3) ◽  
pp. 534-539 ◽  
Author(s):  
Ming Yan Chan ◽  
Gho Wai Man ◽  
Zhen-yu Chen ◽  
Jun Wang ◽  
Lai K. Leung
Keyword(s):  
Mrna Expression ◽  
Hepg2 Cells ◽  
Oestrogen Receptor ◽  
Transcriptional Control ◽  
Plasma Lipid ◽  
Firefly Luciferase ◽  
Mrna Abundance ◽  
Biochanin A ◽  
Luciferase Reporter ◽  
Postmenopausal Symptoms

Epidemiological studies have indicated that soya consumption may produce a better plasma lipid profile. The effect may be attributed to the phyto-oestrogens in soya. The red clover (Trifolium pratense) isoflavone biochanin A has a chemical structure similar to those phyto-oestrogens found in soya beans, and is marketed as a nutraceutical for alleviating postmenopausal symptoms. In the present study we investigated the effect of biochanin A on the mRNA expression of ApoA-1 in the hepatic cell line HepG2. Real-time PCR revealed that biochanin A increased ApoA-1 mRNA abundance in cells expressing oestrogen receptor (ER) α. Without ERα transfection, biochanin A had no effect on mRNA abundance. In order to study the transcriptional control, a fragment of the 5′-flanking region of the ApoA-1 gene was amplified and inserted in a firefly luciferase reporter plasmid. The reporter assay indicated that the transactivation of the ApoA-1 promoter was induced by biochanin A in HepG2 cells transfected with the ERα expression plasmid. This induction was reduced by the anti-oestrogen ICI 182,780, whereas the inhibitors of protein kinase (PK) C, PKA, or mitogen-activated kinase (ERK) had no suppressive effect. The present study illustrated that biochanin A might up regulate hepatic apoA-1 mRNA expression through an ER-dependent pathway.

scholarly journals CHEMICAL INVESTIGATION AND ANTIPROLIFERATIVE STUDIES OF ISOLATED POLYISOPRENYLATED BENZOPHENONES FROM STEM-BARK OF Garcinia maingayi

2021 ◽  
Vol 9 (Spl-1- GCSGD_2020) ◽  
pp. S71-S84
Author(s):  
Sangeetha Arullappan ◽  
◽  
Wong Fai Chu ◽  
Lim Chan Kiang ◽  
Vivien Jong Yi Mian ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mrna Expression ◽  
Hepg2 Cells ◽  
Optical Rotation ◽  
Stem Bark ◽  
Antiproliferative Effect ◽  
Mechanistic Study ◽  
Native Plant ◽  
Guttiferone F ◽  
Mcf 7

In the current study, sequential solvents extraction from the stem bark of Garcinia maingayi, a native plant to Malaysia has led to the isolation of four polyisoprenylated benzophenones: 30-epi-cambogin (GB 1), 14-deoxy-30-epi-cambogin (GB 2), guttiferone F (GB 3), and 14-deoxy-guttiferone F (GB 4). The structures were elucidated using IR, optical rotation, and NMR spectral data. The compounds were evaluated for antiproliferative effect using MTT assay, apoptosis using Annexin V/7-AAD flow cytometry, cell cycle progression, and activation of caspases 3/7, 8 and 9 and BCL2 mRNA expression in MCF-7, HeLa, and HepG2 cancer cell lines. Compounds GB 1 to GB 4 exhibited a remarkable antiproliferative effect on HeLa, MCF-7, and HepG2 cells with IC50 values ranging from 5 to 45 µM. Compounds GB 1 to GB 4 induced significant cell cycle arrest in the G1 phase corroborated with the decrease in the number of MCF-7 and HepG2 cells in S and G2/M phases (P<0.05). Compounds GB 1 to GB 4 induced apoptosis at 48 h. Further, among these, compounds GB 1 and GB 2 induced significant levels of caspases 3 and 9 in HeLa cells, while GB 3 induced caspase 9 activities in both MCF-7 and HepG2 cells. No significant induction of caspase 8 was observed suggesting that the apoptotic effects are mainly mediated through the intrinsic pathway. Only compound GB 1 inhibited the BCL2 mRNA expression significantly in all treated cancer cells. In conclusion, these compounds possess anticancer properties and thus further investigation is crucial on the mechanistic study, structure-activity relationship, and identification of putative molecular targets.

scholarly journals The Ashwell-Morell Receptor Regulates Hepatic Thrombopoietin Production Via JAK2-STAT3 Signaling in Vivo and in Vitro

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 2-2
Author(s):  
Renata Grozovsky ◽  
Antonija Jurak Begonja ◽  
John H. Hartwig ◽  
Herve Falet ◽  
Karin M Hoffmeister
Keyword(s):  
Bone Marrow ◽  
Sialic Acid ◽  
Mrna Expression ◽  
Hepg2 Cells ◽  
Mrna Levels ◽  
Platelet Production ◽  
Platelet Survival ◽  
Post Infusion

Abstract The human body produces and removes 1011 platelets daily to maintain a normal steady-state platelet count, and the level of production can be greatly increased under conditions of platelet destruction. Thrombopoietin (TPO) is the primary regulator of platelet production, supporting the survival, proliferation and differentiation of platelet precursors, bone marrow megakaryocytes. Hepatocytes are a major source of production and secretion of circulating TPO. However, mechanisms regulating circulating TPO levels have been debated for decades. Here, we provide experimental evidence that platelets lacking sialic acid (desialylated platelets) are removed by the hepatic Ashwell-Morell receptor (AMR or asialoglycoprotein receptor), thereby regulating platelet survival and hepatic TPO levels. These conclusions are based on the following evidence: 1) Mice lacking the AMR Asgr2 subunit had increased platelet survival, compared to wild type (WT) mice. Platelets from Asgr2-null mice showed increased loss of sialic acid, as evidenced by flow cytometry using the galactose specific lectins RCAI and ECL, showing that removal of desialylated platelets by the AMR regulates in vivo platelet survival. 2) Livers isolated from Asgr2-null mice had TPO mRNA levels decreased by 40%, compared to WT mice. In contrast, liver TPO mRNA levels were increased by 30% in St3gal4-null mice lacking the sialyltransferase ST3GalIV, where desialylated platelet clearance is increased and specifically mediated by the AMR. Both plasma TPO levels and platelet TPO contents were similarly altered in both mutant mice. Thus, desialylated platelet uptake by the AMR regulated liver TPO levels. 3) Desialylated platelets isolated from St3gal4-null or Asgr2-null mice infused into WT mice increased hepatic TPO mRNA levels as early as 12h post-infusion. Plasma TPO concentrations and bone marrow megakaryocyte numbers increased in parallel with TPO mRNA levels, peaking by day 2 post-infusion, followed by new platelet release at day 10 post-infusion. In contrast, desialylated platelets infused into Asgr2-null mice had no effect on TPO mRNA synthesis, TPO plasma levels and bone marrow megakaryocyte numbers. 4) Incubation of human hepatoma cell line, HepG2 cells, with human desialylated platelets by sialidase treatment resulted in TPO mRNA expression increase by 2.2 and 2.9-fold after 4 and 6h, respectively, followed by significant increase in TPO secretion. 5) The signaling pathways activated by uptake of desialylated platelets by the AMR to induce TPO mRNA transcription were investigated in vivo and in vitro. Major polypeptides of 60-70 and 125 kDa were highly tyrosine phosphorylated in WT liver cells, as evidenced by SDS-PAGE. Using a specific antibody directed against JAK2, we identified the 125-kDa phosphoprotein as the tyrosine kinase JAK2 in mouse liver cells and human HepG2 cells. Analysis of liver samples revealed a marked reduction in JAK2 phosphorylation in Asgr2-null mice and significant increase in St3gal4-null mice. 6) The JAK1/2 inhibitor AZD1480 significantly decreased phosphorylation of JAK2, phosphorylation and translocation to the nucleus of the acute phase response transcription factor STAT3, TPO mRNA expression and TPO secretion in HepG2 cells incubated with desialylated platelets. In vivo treatment of WT mice with AZD1480 blocked TPO mRNA increase promoted by injection of endogenously desialylated platelets. Therefore we conclude that platelets desialylate as they circulate, thereby becoming the primary AMR ligand and providing a novel physiological feedback mechanism to regulate plasma TPO levels and platelet production in vivo and in vitro. Disclosures No relevant conflicts of interest to declare.

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