Irisin Regulates the Functions of Hepatic Stellate Cells
Autor: | Eun Hee Cho, So Young Park, Hanh Nguyen Dong, Cong Thuc Le, Daehee Choi |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
Lipopolysaccharides
Liver Cirrhosis Irisin Endocrinology Diabetes and Metabolism medicine.medical_treatment Down-Regulation 030209 endocrinology & metabolism lcsh:Diseases of the endocrine glands. Clinical endocrinology Cell Line Contractility Transforming Growth Factor beta1 03 medical and health sciences 0302 clinical medicine Endocrinology Fibrosis Hepatic stellate cells Myokine medicine Renal fibrosis Humans Cell Proliferation lcsh:RC648-665 biology Chemistry Transforming growth factor beta medicine.disease Recombinant Proteins Cell biology Fibronectins Cytokine 030220 oncology & carcinogenesis Hepatic stellate cell biology.protein Original Article Hepatic fibrosis |
Zdroj: | Endocrinology and Metabolism Endocrinology and Metabolism, Vol 35, Iss 3, Pp 647-655 (2020) |
ISSN: | 2093-5978 2093-596X |
Popis: | Background Hepatic stellate cells (HSCs) are known to play a fundamental role in the progression of liver fibrosis. Once HSCs are activated, they are involved in proliferation, migration, and contractility which are characteristics of liver fibrogenesis. Recent studies have shown that irisin, a myokine secreted during physical exercise, has a protective effect in various metabolic diseases, especially in renal fibrosis. However, whether irisin is involved in HSC activation and other processes associated with liver fibrosis has not yet been investigated. In this study, we reveal the role of irisin in HSC activation as well as in proliferation, migration, and contractile properties of HSCs in vitro. Methods LX-2 cells, immortalized human HSCs, were treated with transforming growth factor beta 1 (TGF-β1), a core regulator of HSC fibrosis, with or without irisin, and markers of the aforementioned processes were analyzed. Further, an inflammatory response was stimulated with TGF-β1 and lipopolysaccharide (LPS) in combination with irisin and the expression of cytokines was measured. Results Recombinant irisin significantly suppressed the expression of TGF-β1-stimulated fibrosis markers including alpha-smooth muscle actin and collagen type 1 alpha 1 and prevented the TGF-β1-induced proliferation, migration, and contractility of LX-2 cells. Additionally, irisin ameliorated the production of interleukin-6 (IL-6) and IL-1β induced by TGF-β1 and LPS treatments. Conclusion These findings suggested that irisin potently improved the progression of hepatic fibrosis by regulating HSC activation, proliferation, migration, contractility, and HSC-mediated production of inflammatory cytokine. |
Databáze: | OpenAIRE |
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