title: Opposite Expression of SPARC between the Liver and Pancreas in Streptozotocin-Induced Diabetic Rats.
abstract: Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein that regulates several cellular events, including inflammation and tissue remodelling. In this study, we investigated the tissue-specific expression of SPARC in streptozotocin (STZ)-induced diabetes, and found that SPARC was significantly up-regulated in the liver while down-regulated in the pancreas of STZ-induced diabetic rats. Chronic inflammation occurred in the diabetic pancreas accompanied by up-regulation of CCAAT/enhancer-binding protein beta (C/EBPβ) and its targets (TNFα, Il6, CRP, and Fn1) as well as myeloperoxidase (Mpo) and C-X-C chemokine receptor type 2 (Cxcr2). Diabetic liver showed significant up-regulation of Tgfb1 as well as moderately less up-regulated TNFα and reduced Fn1, resulting in elevated fibrogenesis. PARP-1 was not up-regulated during CD95-mediated apoptosis, resulting in restoration of high ATP levels in the diabetic liver. On the contrary, CD95-dependent apoptosis was not observed in the diabetic pancreas due to up-regulation of PARP-1 and ATP depletion, resulting in necrosis. The cytoprotective machinery was damaged by pancreatic inflammation, whereas adequate antioxidant capacity indicates low oxidative stress in the diabetic liver. High and low cellular insulin content was found in the diabetic liver and pancreas, respectively. Furthermore, we identified six novel interacting partner proteins of SPARC by co-immunoprecipitation in the diabetic liver and pancreas, and their interactions with SPARC were predicted by bioinformatics tools. Taken together, opposite expression of SPARC in the diabetic liver and pancreas may be related to inflammation and immune cell infiltration, degrees of apoptosis and fibrosis, cytoprotective machinery, and cellular insulin levels.
authors.affiliation: Department of Biotechnology, Daegu University, Kyungsan, Kyungbuk, 712-714, Republic of Korea.
authors.forename: Kanikkai Raja
authors.initials: KR
authors.lastname: Aseer
authors.affiliation: Department of Biotechnology, Daegu University, Kyungsan, Kyungbuk, 712-714, Republic of Korea.
authors.forename: Sang Woo
authors.initials: SW
authors.lastname: Kim
authors.affiliation: Center for Food and Nutritional Genomics Research & Department of Food Science and Nutrition, Kyungpook National University, Daegu, 702-701, Republic of Korea.
authors.forename: Myung-Sook
authors.initials: MS
authors.lastname: Choi
authors.affiliation: Department of Biotechnology, Daegu University, Kyungsan, Kyungbuk, 712-714, Republic of Korea.
authors.forename: Jong Won
authors.initials: JW
authors.lastname: Yun
mesh_terms: D000818:Animals; D017209:Apoptosis; D003921:Diabetes Mellitus, Experimental / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D005260:Female; D007328:Insulin / Q000378:metabolism; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008297:Male; D025261:Mitochondrial Proton-Translocating ATPases / Q000235:genetics / Q000378:metabolism; D009336:Necrosis; D015676:Osteonectin / Q000235:genetics* / Q000378:metabolism*; D010179:Pancreas / Q000378:metabolism* / Q000473:pathology; D000071137:Poly (ADP-Ribose) Polymerase-1; D011065:Poly(ADP-ribose) Polymerases / Q000235:genetics / Q000378:metabolism; D060066:Protein Interaction Maps; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D014018:Tissue Distribution; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation; D019014:fas Receptor / Q000235:genetics / Q000378:metabolism
chemical_list: D007328:Insulin; D015676:Osteonectin; D012333:RNA, Messenger; C508962:Tgfb1 protein, rat; D053773:Transforming Growth Factor beta1; D019014:fas Receptor; C499322:Parp1 protein, rat; D000071137:Poly (ADP-Ribose) Polymerase-1; D011065:Poly(ADP-ribose) Polymerases; D025261:Mitochondrial Proton-Translocating ATPases