BACKGROUND/AIMS: Several studies have suggested that pancreatic exocrine cells are able to differentiate into endocrine cells. REG I has been shown to be crucial for induction of ductal epithelial cells to differentiate into insulin producing cells. To date, however, there has been no study which examined the expression of REG I along with other differentiation markers in patients with chronic pancreatitis. METHODOLOGY: Six cases with chronic pancreatitis and the pancreata from the age-matched autopsy cases of unrelated diseases (n=2) were included in this study and examined by immunostaining methods using antibodies against human REG I protein, trypsin, insulin, chromogranin A, cytokeratin 19 and Ki-67. RESULTS: In chronic pancreatitis, REG I was found in acinar and acinoductular cells and the latter were also characterized by cytokeratin 19 positivity. The acinoductular cells showed the budding of REG I-positive cells which were also trypsin- and chromogranin A-positive. MIB-1 antibody against Ki-67 was found negative in the ductal, acinoductular and islet cells reflecting low proliferation in these cells. CONCLUSIONS: The current study revealed that acinoductular cells characterized by dual expression of REG I and cytokeratin 19 also express insulin, chromogranin A and trypsin and therefore supports the hypothesis that transdifferentiation of fully differentiated (acinar) cells may be the main source of islet neogenesis in patients with chronic pancreatitis. However, low proliferation rate in these cells limits the regeneration capacity of the pancreatic tissue in these cases. The present results of double staining of REG I with cytokeratin 19, chromogranin A and insulin in the acinoductular cells indicate that REG I may be used as a marker for these cells.
BACKGROUND/AIMS: Several studies have suggested that pancreatic exocrine cells are able to differentiate into endocrine cells. REG I has been shown to be crucial for induction of ductal epithelial cells to differentiate into insulin producing cells. To date, however, there has been no study which examined the expression of REG I along with other differentiation markers in patients with chronic pancreatitis. METHODOLOGY: Six cases with chronic pancreatitis and the pancreata from the age-matched autopsy cases of unrelated diseases (n=2) were included in this study and examined by immunostaining methods using antibodies against humanREG I protein, trypsin, insulin, chromogranin A, cytokeratin 19 and Ki-67. RESULTS: In chronic pancreatitis, REG I was found in acinar and acinoductular cells and the latter were also characterized by cytokeratin 19 positivity. The acinoductular cells showed the budding of REG I-positive cells which were also trypsin- and chromogranin A-positive. MIB-1 antibody against Ki-67 was found negative in the ductal, acinoductular and islet cells reflecting low proliferation in these cells. CONCLUSIONS: The current study revealed that acinoductular cells characterized by dual expression of REG I and cytokeratin 19 also express insulin, chromogranin A and trypsin and therefore supports the hypothesis that transdifferentiation of fully differentiated (acinar) cells may be the main source of islet neogenesis in patients with chronic pancreatitis. However, low proliferation rate in these cells limits the regeneration capacity of the pancreatic tissue in these cases. The present results of double staining of REG I with cytokeratin 19, chromogranin A and insulin in the acinoductular cells indicate that REG I may be used as a marker for these cells.
Authors: Yarong Lu; André Ponton; Hiroshi Okamoto; Shin Takasawa; Pedro L Herrera; Jun-Li Liu Journal: Am J Physiol Endocrinol Metab Date: 2006-01-31 Impact factor: 4.310
Authors: Martin Tobi; Mijin Kim; Douglas H Weinstein; Mary Ann Rambus; James Hatfield; N Volkan Adsay; Edi Levi; Douglas Evans; Michael J Lawson; Suzanne Fligiel Journal: Dig Dis Sci Date: 2012-09-22 Impact factor: 3.199
Authors: Domenico Viterbo; Gordon E Callender; Theresa DiMaio; Cathy M Mueller; Tamar Smith-Norowitz; Michael E Zenilman; Martin H Bluth Journal: JOP Date: 2009-01-08