Comparative proteome analysis of TGF‐β1‐induced fibrosis processes in normal rat kidney interstitial fibroblast cells in response to ascofuranone |
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Authors: | Jeong‐Han Kang Hyun‐Ji Cho In‐Seon Lee Moonkyu Kim In‐Kyu Lee Young‐Chae Chang |
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Institution: | 1. Department of Pathology, Research Institute of Biomedical Engineering, Catholic University of Daegu School of Medicine, Daegu, Korea;2. The Center for Traditional Microorganism Resources, Keimyung University, Daegu, Korea;3. Department of Immunology, Kyungpook National University School of Medicine, Daegu, Korea;4. Department of Internal Medicine, Kyungpook National University School of Medicine, Daegu, Korea |
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Abstract: | Transforming growth factor‐β1 (TGF‐β1) has a wide range of biological functions such as the regulation of cell growth, differentiation, and immunological response in various types of cells. Particularly, TGF‐β1 induces plasminogen activator inhibitor‐1 (PAI‐1) as a major target protein. PAI‐1 is associated with fibrosis, thrombosis, and metabolic disorders. In this study, to identify proteins potentially involved in TGF‐β1‐induced fibrosis processes, we performed a proteomic analysis of TGF‐β1‐induced normal rat kidney cells exposed to ascofuranone (AF). In these cells, we detected 1500 proteins, with 74 differentially expressed proteins identified by MALDI‐TOF and reference to the NCBI and Swiss‐Prot databases, including PAI‐1, peroxisome prdifesator‐activated receptor, prohibitin, glutamate formyltransferase, LIM domain protein 1, LASP‐1, porphobilinogen deaminase, and peroxiredoxin 2. We also found that AF suppresses expression of profibrotic factors induced by TGF‐β in renal fibroblasts, including matrix proteins and PAI‐1. AF was also shown to inhibit selectively phosphorylation of epidermal growth factor receptor, and downstream kinases such as extracellular signal‐regulated kinase 1/2 (ERK‐1/2). Further ongoing analysis of fibrosis‐related proteins will determine AF's potential for application in fibrotic diseases and therapeutics. |
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Keywords: | 2‐DE Cell biology Fibrosis Plasminogen activator inhibitor‐1 |
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