An article by researchers from the Jagiellonian University Department of General Biochemistry has been published in Cellular and Molecular Gastroenterology and Hepatology journal, issued by the American Gastroenterological Association. The title of the paper is 'MCPIP1 inhibits hepatic stellate cell activation in autocrine and paracrine manners, preventing liver fibrosis'.
Liver fibrosis is a process of scar formation accompanying all chronic liver conditions, regardless of their aetiology. It is a complex process, involving many different types of cells and is characterised by disorders of extracellular martix (ECM) structure and content. During a chronic liver injury an inflammatory reaction occurs and hepatic stellate cells (HSCs) are activated and transdifferentiatied into myofibroblast-like cells, aquiring proinflammatory and profibrogenic properties. The monocyte chemoattractant protein-induced protein (MCPIP1) is an important inflammation regulator, whose RNase activity inhibits the inflammation by degrading a wide variety of transcripts, including those coding proinflammatory cytokines.
The results showed that MCPIP1 expression levels are increased in fibrotic livers as compared to the healthy ones. The MCPIP1 levels are also higher in MSC cells and hepatocytes in mouse liver fibrosis models. Additionally, hepatocytes with MCPIP1 deletion trigger HSC activation via the release of connective tissue growth factor. Moreover, the overexpression of MCPIP1 in HSC cells inhibits their activation through the redution of TGFB1 expression and this phenotype is reversed upon MCPIP1 silencing. The research indicates that MCPIP1 plays an important role in liver fibrisis process.
The study was funded by the National Science Centre. The paper was authored by Dr Natalia Pydyn, Anna Ferenc, Katarzyna Trzos, Dr Mateusz Wilamowski, Dr Olga Mucha, Justyna Kadłuczka, Prof. Jolanta Jura, and Dr Jerzy Kotlinowski from the Department of General Biochemistry of the JU Faculty of Biochemistry, Biophysics and Biotechnology. The article content is available on the journal website.
