Publications by authors named "Kinuyo Ida"
Article Synopsis
- Progressive familial intrahepatic cholestasis (PFIC) is a serious liver disease in children that can lead to the need for liver transplantation and is linked to mutations in the ABCB4 gene, which is important for bile production.
- Mice lacking the Abcb4 gene (Abcb4-deficient mice) typically display milder symptoms than humans due to the presence of less harmful bile acids, but researchers created CYPDKO mice with a more human-like bile acid profile to improve disease modeling.
- By inducing the Abcb4 deletion in CYPDKO mice, researchers found these animals experienced more severe liver injury and inflammation, making them a better model for studying PFIC and
The liver is a crucial organ for maintaining homeostasis in living organisms and is the center of various metabolic functions. Therefore, abnormal metabolic activity, as in metabolic syndrome, leads to pathological conditions, such as abnormal accumulation of lipids in the liver. Inflammation and cell death are induced by several stresses in the fatty liver, namely steatohepatitis.
View Article and Find Full Text PDFThe liver is an important metabolic organ that controls homeostasis in the body. Moreover, it functions as a hematopoietic organ, while its metabolic function is low during development. Hepatocytes, which are parenchymal cells of the liver, acquire various metabolic functions by the maturation of hepatic progenitor cells during the fetal period; however, this molecular mechanism is still unclear.
View Article and Find Full Text PDFSexual dimorphism in gene regulation, including DNA methylation, is the main driver of sexual dimorphism in phenotypes. However, the questions of how and when sex shapes DNA methylation remain unresolved. Recently, using mice with different combinations of genetic and phenotypic sex, we identified sex-associated differentially methylated regions (sDMRs) that depended on the sex phenotype.
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- NASH prevalence rises with metabolic disorders like high blood pressure and diabetes, prompting investigation into its causes.
- Bcl6, a key protein for immune cell development, was studied in mice to see how it influences liver diseases related to NASH.
- Results showed that mice lacking Bcl6 had less liver damage and tumor formation when fed a high-fat diet, suggesting Bcl6 plays a significant role in worsening NASH and its complications.
In the developing liver, bile duct structure is formed through differentiation of hepatic progenitor cells (HPC) into cholangiocytes. A subtype of polycystic liver diseases characterized by uncontrolled expansion of bile ductal cells is caused by genetic abnormalities such as in that of protein kinase C substrate 80 K-H (PRKCSH). In this study, we aimed to mimic the disease process in vitro by genome editing of the PRKCSH locus in human inducible pluripotent stem (iPS) cells.
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- The liver plays a crucial role in maintaining balance in the body, but its functions and how it processes drugs can vary between sexes due to differences in enzyme expression.
- The study identifies B-cell lymphoma 6 (Bcl6) as a key factor influencing these sex-biased differences in liver enzymes (CYPs) that metabolize drugs.
- Results show that knocking out Bcl6 in male mice alters their liver enzyme expression to resemble that of females, indicating Bcl6's critical role in regulating sex differences in drug metabolism without affecting overall sex characteristics.
Liver consists of parenchymal hepatocytes and other cells. Liver progenitor cell (LPC) is the origin of both hepatocytes and cholangiocytic cells. The analyses of mechanism regulating differentiation of LPCs into these functional cells are important for liver regenerative therapy using progenitor cells.
View Article and Find Full Text PDFHepatic stem/progenitor cells in liver development have a high proliferative potential and the ability to differentiate into both hepatocytes and cholangiocytes. In this study, we focused on the cell surface molecules of human induced pluripotent stem (iPS) cell-derived hepatic progenitor-like cells (HPCs) and analyzed how these molecules modulate expansion of these cells. Human iPS cells were differentiated into immature hepatic lineage cells by cytokines.
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