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hepatocytes

Mimicking Native Liver Lobule Microarchitecture In Vitro with Parenchymal and Non-Parenchymal Cells Using 3D Bioprinting for Drug Toxicity and Drug Screening Applications

[ACS Applied Materials & interfaces] A physiologically relevant human vascularized liver model was bioprinted with a novel liver extracellular matrix-based bioink laden with human adipose mesenchymal stem cell-derived hepatocyte-like cells, human umbilical vein endothelial cells, and human hepatic stellate cells.

Extracellular Microparticles Derived from Hepatic Progenitor Cells Deliver a Death Signal to Hepatoma-Initiating Cells

[Journal of Nanobiotechnology] Researchers isolated extracellular microparticles derived from apoptotic hepatic progenitor cells and tested their ability to inhibit hepatocarcinogenesis.

Generation and Transplantation of Hepatocytes-Like Cells Using Human Origin Hepatogenic Serum for Acute Liver Injury Treatment

[Xenotransplantation] Human MSCs derived from umbilical cord tissue were transdifferentiated into hepatocyte-like cells using patient-derived serum along with dimethyl sulfoxide.

Dicer Deletion in Hepatocytes Promotes Macrophages M1 Polarization through Dysregulated miR-192-3p/IGF2 in Non-Alcoholic Steatohepatitis and Hepatocellular Carcinoma

[Cancer Gene Therapy] In hepatic cells, Dicer deletion delivered distinct lipid profile and increased lipid oxidation. Mechanically, Dicer deletion caused declined miR-192-3p and increased IGF2 in hepatocytes.

Ionizable Liposomal siRNA Therapeutics Enables Potent and Persistent Treatment of Hepatitis B

[Signal Transduction and Targeted Therapy] A novel ionizable lipidoid nanoparticle and a state-of-the-art lyophilization technology were developed, enabling to deliver small interfering RNA (siRNA) targeting apolipoprotein B into the hepatocytes with an ED50 of 0.05 mg/kg after intravenous injection.

MEHP Promotes Liver Fibrosis by Down-Regulating STAT5A in BRL-3A Hepatocytes

[Chemosphere] The authors demonstrated that mono-2-ethylhexyl phthalate (MEHP) exposure inhibited the expression of STAT5A by causing oxidative damage in BRL-3A hepatocytes, thus accelerating the expression of key molecules in fibrosis and promoting the occurrence of liver fibrosis.

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