Dataset Information

Human HNF1A KI mice liver proteome analysis

ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is a pathological condition caused by excessive fat accumulation in liver. HNF1A is the pathogenic cause of hepatocellular adenoma and HCC. It is an important transcription factor in liver. We constructed a knock-in mice expressing a human dominant negative HNF1α P291fsinsC mutation to explore how the pathogenic mutant affected lipid metabolism. Three liver samples of control group and four liver samples of KI group were used to do proteome analysis.

ORGANISM(S): Mus Musculus

SUBMITTER: Jiajun Zhao

PROVIDER: PXD040561 | iProX | Thu Mar 02 00:00:00 GMT 2023

REPOSITORIES: iProX

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Dominant-negative HNF1α mutant promotes liver steatosis and inflammation by regulating hepatic complement factor D.

Liu Moke M Liu Luna L Guo Honglin H Fan Xiude X Liu Tianbao T Xu Chao C He Zhao Z Song Yongfeng Y Gao Ling L Shao Shanshan S Zhao Jiajun J Lu Peng P

iScience 20230922 10

Patients with HNF1A variants may develop liver steatosis, while the underlying mechanism is still unclear. Here, we established a mouse model carrying the dominant-negative HNF1α P291fsinsC mutation (hHNF1Amut/-) and found that the mutant mice developed liver steatosis spontaneously under the normal chow diet. Transcriptome analysis showed significant upregulation of Cfd and other genes related to innate immune response in the liver of hHNF1Amut/-</sup ...[more]

PMID: 37841581

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Project description:Nonalcoholic fatty liver disease (NAFLD) has become the most common cause of liver disease affecting 20-30% of the population in developed countries. NAFLD is strongly associated with abdominal obesity and is recognized as the hepatic manifestation of the metabolic syndrome. In a subgroup of patients with NAFLD inflammation and fibrosis develops, this so-called Non-Alcoholic Steatohepatitis (NASH) may progress to cirrhosis and hepatocellular carcinoma. A multi-hit hypothesis has been proposed in which during the first “hit” fat accumulation occurs in hepatocytes from excessive delivery of fatty acids from adipose tissue, in addition there is an imbalance in lipid synthesis and export. However, the reason why fat accumulation is subsequently followed by inflammation and fibrosis in some patients is poorly understood. We studied the role of inflammatory processes in visceral and subcutaneous fat at the transcriptional level using microarray in bariatric patients from whom the liver histology was available. Patients scheduled for bariatric surgery were recruited in two centers (Pretoria/South-Africa and Antwerpen/Belgium). At the time of the procedure, tissue samples of the visceral and subcutaneous fat were taken for molecular analysis as well as liver tissue for histology, also full biochemical data was collected. Patients were grouped according histology: group I (<5% steatosis), group II (NAFLD, 30-50% steatosis), group III (NASH) and group IV (NASH + fibrosis F2-F3). The following samples were used for microarray (number of 'patients' respectively for stages I-II-III-IV): visceral fat (9-7-7-5), subcutaneous fat (6-6-6-5). Microarrays were run in two batches (15xxx versus 17xxx CEL file samples; indicated in the description field). Samples from two patients (FN61; FN76) were put twice on array (15078+17881; 15064+17877) to verify and exclude batch effects. Please note that, due to technical repeats with two patient samples, the number of 'visceral fat samples' for stages I-II-III-IV is 10-7-8-5.

Dataset Information

Human HNF1A KI mice liver proteome analysis

Publications

Dominant-negative HNF1α mutant promotes liver steatosis and inflammation by regulating hepatic complement factor D.

Similar Datasets

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