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CircRNA expression profiles of fibroblasts: normal vs. NASH cirrhosis

ABSTRACT: circRNA expression profiles of fibroblasts: normal vs. NASH cirrhosis

PROVIDER: PRJNA554093 | ENA |

REPOSITORIES: ENA

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circRNA expression profiles of fibroblasts: normal vs. NASH cirrhosis

Project description:The progression from steatosis to nonalcoholic steatohepatitis (NASH) in nonalcoholic fatty liver disease (NAFLD) patients is one of the major causes of liver-related death worldwide and have limited effective therapies. We comparing the circular RNomics of liver fibroblasts isolated from patients with NAFLD-caused cirrhosis and the ones without NAFLD.

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Project description:Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of disease that ranges from simple steatosis, to inflammatory form non-alcoholic steatohepatitis (NASH), cirrhosis, and up to hepatocellular carcinoma. While NASH usually takes decades to develop at a rate of one stage per seven years, in the case of post-trasplant NASH (pt-NASH) develops fibrosis much more rapidly, with almost 50% of liver transplant recipients presenting stage 3 fibrosis by 5 years post-transplant. Archived fresh-frozen transplanted liver biopsy samples from four liver biopsy samples with evidence of NASH (2 recurrent and 2 de novo), two with simple steatosis (both de novo), and five with normal histology as controls had their transcriptome sequenced in two batches for deeper coverage.

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Exosomal microRNA expression profiles of NASH: normal vs. NASH

Project description:Exosomal microRNA expression profiles of NASH: normal vs. NASH

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Exosomal microRNA expression profiles of NASH: normal vs. NASH

Project description:Non-alcoholic fatty liver disease (NAFLD) is a predominant form of chronic liver disease, affecting nearly 25 % of the global population. The progression from steatosis to nonalcoholic steatohepatitis (NASH) in NAFLD patients is one of the major causes of liver-related death worldwide. We assessed the miRNA expression profiles of the exosomes derived from the peripheral blood of NASH patients or healthy controls.

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Tid1 Deficiency Disrupting Mitochondria to Drive NASH-Dependent Hepatocellular Carcinoma Progression

Project description:Non-alcoholic fatty liver disease/steatohepatitis (NAFLD/NASH) is a significant risk factor for hepatocellular carcinoma (HCC). However, a preclinical model of progressive NAFLD/NASH is largely lacking. Here, we report that mice with hepatocyte-specific deletion of Tid1, encoding a mitochondrial cochaperone, tended to develop NASH-dependent HCC. Mice with hepatic Tid1 deficiency showed impairing mitochondrial function and causing fatty acid metabolic dysregulation; meanwhile, sequentially developed fatty liver, NASH, and cirrhosis/HCC in a diethylnitrosamine (DEN) induced oxidative environment. The pathological signatures of human NASH, including cholesterol accumulation and activation of inflammatory and apoptotic signaling pathways, are also present in these mice. Clinically, low Tid1 expression was associated with unfavorable prognosis in patients with HCC. Empirically, hepatic Tid1 deficiency directly disrupts entire mitochondria that play a key role in the NASH-dependent HCC development. Overall, we established a new mouse model that develops NASH-dependent HCC and provides a promising approach to improve the treatment.

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To explore read-through circRNA profiles in human normal and NASH livers

Project description:To explore read-through circRNA profiles in human normal and NASH livers

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To explore read-through circRNA profiles in human normal and NASH livers

Project description:To investigate the function of read-through circRNAs in liver, we obtained human NASH liver tissues and normal liver tissues patients without NAFLD undergoing surgery for hepatic hemangioma.Patients with positive hepatitis B surface antigen or anti-hepatitis C virus (HCV) antibody with detectable HCV RNA, excessive alcohol consumption (20 g/day in men or 10 g/day in women), secondary fatty liver (e.g., use of systemic steroids or tamoxifen), or malignancies before baseline were excluded. We then performed exome capture mRNA sequencing using livers from three NASH patients and three patients with hepatic hemangioma.

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