Sentences with phrase «mouse hepatocyte»

In contrast, primary mouse hepatocytes from Ldlr — / — Lrp1fl / fl Alb - Cre + mice did not show a significant difference in binding or uptake between ApoC - III — depleted and ApoC - III — bearing TRLs (Figure 10).

Not exact matches

They transplanted the hepatocyte - like cells into mice; 14 days later, some of the corrected cells had integrated into the rodent liver and were able to produce human A1AT.

Gandhi's research team is the first to develop a mouse model with depleted levels of a protein called augmenter of liver regeneration (ALR), which is essential for the survival of liver cells called hepatocytes.

To address this, Lagasse has injected hepatocytes into lymph nodes in peripheral parts of a mouse's body — under the knee or arm — because that requires less invasive surgery.

They found that hepatitis in these «human hepatocyte chimeric mice» was caused by white blood cells known as cytotoxic T lymphocytes (CTLs) that were specifically targeted to hepatitis B virus.

Hepatocyte - specific Sqle transgenic expression in mice accelerated the development of high - fat, high - cholesterol diet — induced HCC.

Immunohistochemical stainings of Ki67 and pancytokeratin (Ki67 is stained brown, pancytokeratin is stained pink) indicate proliferation of hepatocytes (arrowheads) and biliary epithelial cells (arrows) in TAK1 / RIP3 - deficient mice.

To validate their computer modeling predictions, researchers performed experiments in human cancer cell lines, mouse liver samples and primary human hepatocytes.

They found that the starvation - induced accumulation of p53 was indeed detectable in hepatocytes, irrespective of whether these cells were of mouse or human origin.

When Lin engineered the telomerase - expressing hepatocytes to die in response to a chemical signal and gave the mice with a liver - damaging chemical, he found that those animals in which the telomerase cells had been killed exhibited much more severe liver scarring than those in which the cells were functional.

Many conventional hepatocyte cells that are transplanted to mice for in vivo testing last for only two or three days, but the drug and its various metabolites might take weeks to metabolize, so toxic effects might not be apparent in such testing.

«We have shown that an endogenous peptide, catestatin, can directly suppress glucose production from hepatocytes and can indirectly suppress lipid accumulation in liver as well as macrophage - mediated inflammation in obese mice,» said Sushil K. Mahata, PhD, professor of medicine at UC San Diego School of Medicine.

In our previous study we found that a high fat diet containing comparable amounts of soybean oil to what Americans are currently consuming caused mice to become obese, diabetic and insulin resistant and to have large lipid droplets and hepatocyte ballooning in their livers.

We combine experimental and computational approaches to investigate the molecular mechanisms underlying hepatocyte polarity as well as the 3D organization of the bile canaliculi and sinusoidal networks in the mouse and human liver tissue.

They developed a simple system that allows them to transplant human hepatocytes into immunodeficient mice, which can now be used to test how drugs affect the liver.

Within three months of transplantation, up to 20 percent of the mouse liver is repopulated by human hepatocytes.

Taking away NBTC allows human hepatocytes to take hold and populate the mouse liver with human cells.

An enzymatic defect in the tyrosine catabolism results in a toxic accumulation of byproducts within hepatocytes unless the mice are treated with a drug called NBTC.

One way to get around the altered properties of the stranded cells is to populate mouse livers with human hepatocytes in the hope of creating a natural environment, which is exactly what researchers at the Salk Institute for Biological Studies did.

Myeloid - Mixed Lineage Kinase 3 contributes to chronic ethanol - induced inflammation and hepatocyte injury in mice.

Overall binding of both [3H] TRL preparations was significantly reduced in hepatocytes isolated from Ldlr — / — Lrp1fl / fl Alb - Cre + mice compared with hepatocytes isolated from Ndst1fl / fl Alb - Cre + mice (Figure 10).

In a second approach, [3H] retinol - radiolabeled ApoC - III — depleted and ApoC - III — bearing TRLs (Figure 9A and Supplemental Figure 6) were evaluated for their uptake by primary hepatocytes isolated from Ndst1fl / fl Alb - Cre + and Ldlr — / — Lrp1fl / fl Alb - Cre + mice.

Binding and uptake of isolated [3H] TRLs (50 μg / ml) from control ASO - and ApoC - III ASO — treated Ldlr — / — Ndst1fl / fl Alb - Cre + mice in primary hepatocytes isolated from Ndst1fl / fl Alb - Cre + and Ldlr — / — Lrp1fl / fl Alb - Cre — mice after a 4 - hour incubation at 37 °C (n = 3 / condition).

These results support the notion that the increased clearance of ApoC - III — depleted [3H] TRLs in Ndst1fl / fl Alb - Cre + mice, and not in Ldlr — / — Lrp1fl / fl Alb - Cre + mice, is a consequence of increased uptake by LDLR / LRP1 on hepatocytes.

Binding and uptake of radiolabeled ApoC - III — depleted TRLs was significantly increased in hepatocytes isolated from Ndst1fl / fl Alb - Cre + mice (i.e., in mice expressing both LDLR and LRP1) when compared with ApoC - III — bearing TRLs (Figure 10).