Journal: Poultry Science

Article Title: Overexpression of irisin reduces embryonic and diet-induced hepatic lipid accumulation in chickens

doi: 10.1016/j.psj.2026.106831

Figure Lengend Snippet: Lipid accumulation in the liver of 19-day chicken embryos was reduced by lentivirus-mediated overexpression of irisin. A Schematic diagram of the lentiviral vector structure. B Effects of lentivirus -mediated overexpression of irisin on chicken hatchability. Data analysis was performed using the chi-square test. C The levels of exogenous irisin in plasma were measured in 19-day-old chicken embryos. D Triglyceride (TG) and total cholesterol (TC) content in chicken embryonic liver. E H&E and Oil Red O staining of chicken embryonic liver. In the Control group, numerous lipid droplets were observed within hepatocytes, accompanied by extensive cytoplasmic vacuolization and indistinct hepatic cord architecture. Compared to the Control group, the Irisin group exhibited a significant reduction in lipid droplets, marked improvement in cytoplasmic vacuolization, and clear, intact hepatic cord structure. F Effects of irisin on the expression levels of lipid-related genes in chicken embryonic liver.

Article Snippet: Hepatic and plasma triglycerides (TG) and total cholesterol (TC) levels were measured using commercial kits (Nanjing Jiancheng Bioengineering Institute, China) according to the manufacturer's protocols.

Techniques: Over Expression, Plasmid Preparation, Clinical Proteomics, Staining, Control, Expressing

Journal: Frontiers in Immunology

Article Title: NPC1 promotes HTNV replication by controlling innate immune response

doi: 10.3389/fimmu.2026.1811629

Figure Lengend Snippet: NPC1 disrupts cellular cholesterol distribution. (A) Wild-type and NPC1 knockout HeLa cells were treated with U18666A (10 µM) and HTNV (MOI = 10), cellular cholesterol levels were measured at 48 h post-infection. Non-treatment, U18666A treatment only or HTNV infection only were all parallel control. (B) Wild-type and NPC1 knockout HeLa cells were treated with cholesterol (10 µM) and HTNV (MOI = 1) or not, and viral genome copies within medium and cells of each group were quantified using qPCR. (C) The cellular cholesterol distribution of each group was visualized by Filipin staining following the same treatment as (A) . (D) The represented captures of Filipin staining for each group. WT: wild type HeLa cells, KO: NPC1 knockout HeLa cells. Mock+DMSO: cells were treated with the same amount of DMSO and without HTNV infection; Mock+U18666A: cells were treated with10 μM U18666A and without HTNV infection; HTNV+DMSO: cells treated with the same amount of DMSO and with HTNV infection for 48 hours (MOI=1); HTNV+U18666A: cells were treated with10 μM U18666A andwith HTNV infection for 48 hours (MOI=1).

Article Snippet: Wild-type and NPC1 knockout HeLa cells were grown on a six-well plate for 12 h, 10 μM U18666A and HTNV (MOI = 1) were added to the cells, and the cellular cholesterol level was measured using Tissue Total Cholesterol (TC) Content Assay Kit (APPLYGEN) at 48 h post-infection.

Techniques: Knock-Out, Infection, Control, Staining

Journal: Frontiers in Immunology

Article Title: NPC1 promotes HTNV replication by controlling innate immune response

doi: 10.3389/fimmu.2026.1811629

Figure Lengend Snippet: Diagram of NPC1 functioning in HTNV life cycle. HTNV infection triggers cellular cholesterol redistribution, which requires NPC1. Cholesterol extensively accumulated in late-endosome, thereby amplifying the innate immune response, when HTNV infected NPC1 defective cells. Consequently, NPC1 avoids abnormal endosomal cholesterol accumulation to mitigate innate immune response and promote HTNV replication.

Article Snippet: Wild-type and NPC1 knockout HeLa cells were grown on a six-well plate for 12 h, 10 μM U18666A and HTNV (MOI = 1) were added to the cells, and the cellular cholesterol level was measured using Tissue Total Cholesterol (TC) Content Assay Kit (APPLYGEN) at 48 h post-infection.

Techniques: Infection