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2022 ◽  
Vol 47 (1) ◽  
pp. 13-18
Author(s):  
Chika Yamamoto ◽  
Akinori Takemura ◽  
Sanae Ishii ◽  
Atsushi Doi ◽  
Isao Saito ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Sangsoo Daniel Kim ◽  
Larry Morgan ◽  
Elyse Hargreaves ◽  
Xiaoying Zhang ◽  
Zhihui Jiang ◽  
...  

Jaundice is a potentially fatal condition resulting from elevated serum bilirubin levels. For centuries, herbal remedies containing Artemisia capillaris Thunb. including the compound 6,7-dimethylesculetin (DE) have been used in Asia to prevent and treat jaundice in neonates. DE activates an important regulator of bilirubin metabolism, the constitutive androstane receptor (CAR), and increases bilirubin clearance. In addition, murine cytochrome P450 2a5 (Cyp2a5) is known to be involved in the oxidative metabolism of bilirubin. Moreover, treatment of mice with phenobarbital, a known inducer of both CAR and Cyp2a5, increases expression of Cyp2a5 suggesting a potential relationship between CAR and Cyp2a5 expression. The aim of this study is to investigate the influence of Artemisia capillaris and DE on the expression and regulatory control of Cyp2a5 and the potential involvement of CAR. Treatment of mouse hepatocytes in primary culture with DE (50 μM) significant increased Cyp2a5 mRNA and protein levels. In mice, Artemisia capillaris and DE treatment also increased levels of hepatic Cyp2a5 protein. Luciferase reporter assays showed that CAR increases Cyp2a5 gene transcription through a CAR response element in the Cyp2a5 gene promoter. Moreover, DE caused nuclear translocation of CAR in primary mouse hepatocytes and increased Cyp2a5 transcription in the presence of CAR. These results identify a potential CAR-mediated mechanism by which DE regulates Cyp2a5 gene expression and suggests that DE may enhance bilirubin clearance by increasing Cyp2a5 levels. Understanding this process could provide an opportunity for the development of novel therapies for neonatal and other forms of jaundice.


PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e12358
Author(s):  
Barbara Kramar ◽  
Dušan Šuput ◽  
Irina Milisav

Background One of the most frequently deleted genes in cancer is CDKN2A encoding p16. This protein is often overexpressed in senescent cells, while its suppression can bypass the oncogene-induced senescence to enable transformation and tumorigenesis. The roles of the protein p16 are recently being expanded from the cell cycle progression regulator to the cellular regulator interacting in several different pathways. Yet data on its liver and liver cells’ expression are inconclusive. Methods The expression of the p16 gene in liver and liver cells was determined by RT-qPCR and compared to its protein amounts by western blotting. Results p16 is expressed at low levels in the liver and rat hepatocytes. Its expression varies from none to the considerable levels in the examined hepatocellular carcinoma cell lines (FaO and HepG2) and in immortalized mouse hepatocytes. Such significant expression differences of an important cellular regulator warrant the need to closely examine the differences in biochemical pathways correlated with the p16 expression when using hepatocytes and hepatoma liver models.


2021 ◽  
Vol 25 ◽  
pp. 100339
Author(s):  
Arturo Simoni-Nieves ◽  
Denise Clavijo-Cornejo ◽  
Soraya Salas-Silva ◽  
Alejandro Escobedo-Calvario ◽  
Leticia Bucio ◽  
...  

2021 ◽  
Author(s):  
Natalia Nunez ◽  
Aurelie Derre-Bobillot ◽  
Goran Lakisic ◽  
Alexandre Lecomte ◽  
Francoise Mercier-Nome ◽  
...  

Enterococcus faecalis is a bacterial species present at a sub-dominant level in the human gut microbiota. This commensal turns into an opportunistic pathogen under specific conditions involving dysbiosis and host immune deficiency. E. faecalis is also the only intestinal pathobiont identified to date as contributing to liver damage in alcoholic liver disease. We have previously observed that E. faecalis is internalized in hepatocytes. Here, the survival and fate of E. faecalis was examined in hepatocytes, the main epithelial cell type in the liver. Although referred to as an extracellular pathogen, we demonstrate that E. faecalis is able to survive and divide in hepatocytes, and form intracellular clusters in two distinct hepatocyte cell lines, in primary mouse hepatocytes, as well as in vivo. This novel process extends to kidney cells. Unravelling the intracellular lifestyle of E. faecalis, our findings contribute to the understanding of pathobiont-driven diseases.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jeong-Rang Jo ◽  
Seungwon An ◽  
Swati Ghosh ◽  
Balachandar Nedumaran ◽  
Yong Deuk Kim

AbstractGrowth hormone (GH) is one of the critical factors in maintaining glucose metabolism. B-cell translocation gene 2 (BTG2) and yin yang 1 (YY1) are key regulators of diverse metabolic processes. In this study, we investigated the link between GH and BTG2–YY1 signaling pathway in glucose metabolism. GH treatment elevated the expression of hepatic Btg2 and Yy1 in primary mouse hepatocytes and mouse livers. Glucose production in primary mouse hepatocytes and serum blood glucose levels were increased during GH exposure. Overexpression of hepatic Btg2 and Yy1 induced key gluconeogenic enzymes phosphoenolpyruvate carboxykinase 1 (PCK1) and glucose-6 phosphatase (G6PC) as well as glucose production in primary mouse hepatocytes, whereas this phenomenon was markedly diminished by knockdown of Btg2 and Yy1. Here, we identified the YY1-binding site on the Pck1 and G6pc gene promoters using reporter assays and point mutation analysis. The regulation of hepatic gluconeogenic genes induced by GH treatment was clearly linked with YY1 recruitment on gluconeogenic gene promoters. Overall, this study demonstrates that BTG2 and YY1 are novel regulators of GH-dependent regulation of hepatic gluconeogenic genes and glucose production. BTG2 and YY1 may be crucial therapeutic targets to intervene in metabolic dysfunction in response to the GH-dependent signaling pathway.


Author(s):  
Schuyler D. Vickers ◽  
Dominique C. Saporito ◽  
Roberta Leonardi
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2021 ◽  
Vol 2 (3) ◽  
pp. 100616
Author(s):  
Yuqian Shen ◽  
Wenhua Liu ◽  
Jian Zuo ◽  
Junhai Han ◽  
Zi Chao Zhang

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