Membrane Proteome Analysis of Cerulein-Stimulated Pancreatic Acinar Cells: Implication for Early Event of Acute Pancreatitis
2
조회
0
다운로드
1
인용
0
참고문헌
초록
Background/Aims: Cerulein pancreatitis is similar to human edematous pancreatitis with dysregulation of the production and secretion of digestive enzymes,edema formation, cytoplasmic vacuolization and the death of acinar cells. We hypothesized that membrane proteins may be altered as the early event during the induction of acute pancreatitis. Present study aims to determine the differentially expressed proteins in the membranes of cerulein-treated pancreatic acinar cells. Methods: Pancreatic acinar AR42J cells were treated with 10−8 M cerulein for 1 hour. Membrane proteins were isolated from the cells and separated by two-dimensional electrophoresis using pH gradients of 5-8. Membrane proteins were identified by matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) analysis of the peptide digests. The differentially expressed proteins,whose expression levels were more or less than three-fold in cerulein-treated cells, were analyzed. Results: Two differentially expressed proteins (mannan-binding lectin-associated serine protease-2, heat shock protein 60) were up-regulated while four proteins (protein disulfide isomerase, γ-actin, isocitrate dehydrogenase 3, seven in absentia homolog 1A)were down-regulated by cerulein treatment in pancreatic acinar cells. These proteins are related to cell signaling, oxidative stress, and cytoskeleton arrangement. Conclusions: Oxidative stress may induce cerulein-induced cell injury and disturbances in defense mechanism in pancreatic acinar cells.
Abstract
Background/Aims: Cerulein pancreatitis is similar to human edematous pancreatitis with dysregulation of the production and secretion of digestive enzymes,edema formation, cytoplasmic vacuolization and the death of acinar cells. We hypothesized that membrane proteins may be altered as the early event during the induction of acute pancreatitis. Present study aims to determine the differentially expressed proteins in the membranes of cerulein-treated pancreatic acinar cells. Methods: Pancreatic acinar AR42J cells were treated with 10−8 M cerulein for 1 hour. Membrane proteins were isolated from the cells and separated by two-dimensional electrophoresis using pH gradients of 5-8. Membrane proteins were identified by matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) analysis of the peptide digests. The differentially expressed proteins,whose expression levels were more or less than three-fold in cerulein-treated cells, were analyzed. Results: Two differentially expressed proteins (mannan-binding lectin-associated serine protease-2, heat shock protein 60) were up-regulated while four proteins (protein disulfide isomerase, γ-actin, isocitrate dehydrogenase 3, seven in absentia homolog 1A)were down-regulated by cerulein treatment in pancreatic acinar cells. These proteins are related to cell signaling, oxidative stress, and cytoskeleton arrangement. Conclusions: Oxidative stress may induce cerulein-induced cell injury and disturbances in defense mechanism in pancreatic acinar cells.
참고문헌 (58)
- Shirohara H, "Plasma cholecystokinin levels in acute pancreatitis", Pancreas, 14, pp.249~254 (1997)
- Koide M, "Plasma cholecystokinin concentration in patients with chronic pancreatitis measured by bioassay", Nippon Shokakibyo Gakkai Zasshi, 86, pp.2419~2424 (1989)
- Mitchell CJ, "Functional recovery of the exocrine pancreas after acute pancreatitis", Scan J Gastroenterol, 18, pp.5~8 (1983)
- Gukovsky I, "Early NF-kappaB activation is associated with hormone-induced pancreatitis", J Physiol, 275, pp.G1402~G1414 (1998)
- Willemer S, "Hormone-induced pancreatitis", Eur Surg Res, 24(Suppl. 1), pp.29~39 (1992)
- Jensen RT, "Interaction of CCK with pancreatic acinar cells", Trends Pharmacol Sci, 10, pp.418~423 (1989)
- Sato S, "Receptor occupation, calcium mobilization, and amylase release in pancreatic acini: effect of CCKJMV-180", Am J Physiol, 257, pp.G202~G209 (1989)
- Lerch MM, "Experimental animal models of acute pancreatitis", Int J Pancreatol, 15, pp.159~170 (1994)
- Kanno T, "Ca2＋ signaling in the pancreatic acinus", Pancreas, 16, pp.273~276 (1998)
- Jungermann J, "Disassembly of rat pancreatic acinar cell cytoskeleton during supramaximal secretagogue stimulation", Am J Physiol, 268, pp.G328~G338 (1995)
- Dabrowski A, "Role of oxidative stress in the pathogenesis of caerulein-induced acute pancreatitis", Eur J Pharmacol, 377, pp.1~11 (1999)
- Yu JH, "Diphenyleneiodonium suppresses apoptosis in cerulein-stimulated pancreatic acinar cells", J Biochem Cell Biol, 39, pp.2063~2075 (2007)
- Yu JH, "Role of NADPH oxidase and calcium in cerulein-induced apoptosis: involvement of apoptosis-inducing factor", Ann N Y Acad Sci, 1090, pp.292~297 (2006)
- Yu JH, "NADPH oxidase and apoptosis in cerulein-stimulated pancreatic acinar AR42J cells", Free Radic Biol Med, 39, pp.590~602 (2005)
- Seo JY, "Oxidative stress induced cytokine production in isolated rat pancreatic acinar cells: effects of small-molecule antioxidants", Pharmacology, 64, pp.63~70 (2002)
- Kim H, "Suppression of NF-kappaB activation and cytokine production by N-acetylcysteine in pancreatic acinar cells", Free Radic Biol Med, 29, pp.674~683 (2000)
- Yu JH, "Proteome analysis of rat pancreatic acinar cells: implication for ceruleininduced acute pancreatitis", Proteomics, 3, pp.2446~2453 (2003)
- Santoni V, "Membrane proteins and proteomics: un amour impossible?", Electrophoresis, 21, pp.1054~1070 (2000)
- Paulsen IT, "Unified inventory of established and putative transporters encoded within the complete genome of Saccharomyces cerevisiae", FEBS Lett, 430, pp.116~125 (1998)
- Christophe J, "Pancreatic tumor cell line AR42J cell: an amphicrine model", Am J Physiol, 266, pp.G963~G971 (1994)
- Sata N, "Cytotoxicity of peroxynitrite in rat pancreatic acinar AR4-2J cells", Pancreas, 15, pp.278~284 (1997)
- Piiper A, "Subcellular distribution and function of Rab3A-D in pancreatic acinar AR42J cells", Biochem Biophys Res Commun, 287, pp.746~751 (2001)
- Masamune A, "Lysophosphatidylcholine induces apoptosis in AR42J cells", Pancreas, 22, pp.75~83 (2001)
- Okumura N, "Pancreatic endocrine function in experimental pancreatolithiasis in dogs", Am J Gastroenterol, 77, pp.392~396 (1982)
- Aho HJ, "Human acute pancreatitis: a light and electron microscopic study", Acta Pathol Microbiol Immunol Scand A, 90, pp.367~373 (1982)
- Neurath MF, "Role of NF-kappaB in immune and inflammatory responses in the gut", Gut, 43, pp.856~860 (1998)
- Takiguchi S, "Role of CCK-A receptor for pancreatic function in mice: a study in CCK-A receptor knockout mice", Pancreas, 24, pp.276~283 (2002)
- Evander A, "Influence of hormonal stimulation by caerulein on acute experimental pancreatitis in the rat", Eur Surg Res, 13, pp.257~268 (1981)
- Niederau C, "Beneficial effects of cholecystokinin-receptor blockade and inhibition of proteolytic enzyme activity in experimental acute hemorrhagic pancreatitis in mice. Evidence for cholecystokinin as a major factor in the development of acute pancreatitis", J Clin Invest, 78, pp.2056~1063 (1986)
- Gomez G, "Protective action of luminal bile salts in necrotizing acute pancreatitis in mice", J Clin Invest, 86, pp.323~331 (1990)
- Park BK, "Role of oxygen free radicals in patients with acute pancreatitis", World J Gastroenterology, 9, pp.2266~2269 (2003)
- Niederau C, "Effects of CCK on pancreatic function and morphology", Ann N Y Acad Sci, 713, pp.180~188 (1994)
- Smith JP, "Effects of cholecystokinin on cytosolic calcium in pancreatic duct segments and ductal cells", Am J Physiol, 264, pp.G1177~G1183 (1993)
- Li N, "Is NF-kappaB the sensor of oxidative stress?", FASEB J, 13, pp.1137~1143 (1999)
- Kaufmann SH, "Heat-shock protein 60: implications for pathogenesis of and protection against bacterial infections", Immunol Rev, 121, pp.67~90 (1991)
- Frossard JL, "Both thermal and non-thermal stress protect against caerulein induced pancreatitis and prevent trypsinogen activation in the pancreas", Gut, 50, pp.78~83 (2002)
- Tashiro M, "Hyperthermia induces multiple pancreatic heat shock proteins and protects against subsequent arginine-induced acute pancreatitis in rats", Digestion, 65, pp.118~126 (2002)
- Bhagat L, "Thermal stress-induced HSP70 mediates protection against intrapancreatic trypsinogen activation and acute pancreatitis in rats", Gastroenterology, 122, pp.156~165 (2002)
- Takacs T, "Comparative effects of water immersion pretreatment on three different acute pancreatitis models in rats", Biochem Cell Biol, 80, pp.241~251 (2002)
- Rakonczay Z Jr, "Water immersion pretreatment decreases pro-inflammatory cytokine production in cholecystokinin-octapeptide-induced acute pancreatitis in rats: possible role of HSP72", Int J Hyperthermia, 17, pp.520~535 (2001)
- Rakonczay Z Jr, "Induction of heat shock proteins fails to produce protection against trypsininduced acute pancreatitis in rats", Clin Exp Med, 2, pp.89~97 (2002)
- Schafer C, "Stress kinases and heat shock proteins in the pancreas: possible roles in normal function and disease", J Gastroenterol, 35, pp.1~9 (2000)
- Kimura E, "Regulation of HSP60 mRNA expression in a human ovarian carcinoma cell line", Cancer Chemother Pharmacol, 32, pp.279~285 (1993)
- Sakai J, "Proteomic analysis of rat heart in ischemia and ischemia-reperfusion using fluorescence two-dimensional difference gel electrophoresis", Proteomics, 3, pp.1318~1324 (2003)
- Turner MW, "The role of mannose-binding lectin in health and disease", Mol Immunol, 40, pp.423~429 (2003)
- Moller-Kristensen M, "Levels of mannan-binding lectin-associated serine protease-2 in healthy individuals", J Immunol Methods, 282, pp.159~167 (2003)
- Braakman I, "Manipulating disulfide bond formation and protein folding in the endoplasmic reticulum", EMBO J, 11, pp.1717~1722 (1992)
- van der Vlies D, "Endoplasmic reticulum resident proteins of normal human dermal fibroblasts are the major targets for oxidative stress induced by hydrogen peroxide", Biochem J, 366, pp.825~830 (2002)
- Cecconi D, "Proteomic analysis of pancreatic ductal carcinoma cells treated with 5-aza-2’-deoxycytidine", Electrophoresis, 24, pp.4291~4303 (2003)
- Goldsmith M, "Mechanics of motility: distinct dynein binding domains on alpha- and beta-tubulin", Biochem Cell Biol, 73, pp.665~671 (1995)
- Ogawa M, "Anticancer drugs and pharmacologic actions", Nippon Rinsho, 55, pp.1017~1023 (1997)
- Sarkar S, "Regulation of beta- and gamma- actin mRNA by thyroid hormone in the developing rat brain", Neuroreport, 8, pp.1267~1271 (1997)
- Lloyd C, "Beta- and gamma- Actin genes differ in their mechanisms of down-regulation during myogenesis", J Cell Biochem, 84, pp.335~342 (2002)
- Yang JH, "Oxalomalate, a competitive inhibitor of NADP＋-dependent isocitrate dehydrogenase, enhances lipid peroxidation-mediated oxidative damage in U937 cells", Arch Biochem Biophys, 416, pp.31~37 (2003)
- Lee JH, "Inactivation of NADP＋-dependent isocitrate dehydrogenase by peroxynitrite: implications for cytotoxicity and alcohol-induced liver injury", J Biol Chem, 278, pp.51360~51371 (2003)
- Jung UJ, "Effect of oxalomalate on lipid metabolism and antioxidant defense system in rats", J Biochem Mol Toxicol, 17, pp.295~302 (2003)
- Wheeler TC, "Regulation of synaptophysin degradation by mammalian homologues of seven in absentia", J Biol Chem, 277, pp.10273~10282 (2002)
- Ishikawa K, "Competitive interaction of seven in absentia homolog-1A and Ca2＋", calmodulin with the cytoplasmic tail of group 1 metabotropic glutamate receptors, 1999, pp.4, 381~390