November 12, 2014
Notes: Gompertz, Macarena
Miranda, Juan Pablo
Rev Med Chil. 2013 May;141(5):562-7. doi: 10.4067/S0034-98872013000500002.
Author Address: Seccion de Gastroenterologia, Departamento de Medicina Interna, Hospital Clinico, Universidad de Chile, Santiago, Chile.
Reference Type: Journal Article
Record Number: 4955Author: Gong, J., Wang, Y., Jiang, R., Zhang, G. and Tian, F.
Title: The naive effector cells of collagen type I during acute experimental pancreatitis are acinar cells and not pancreatic stellate cells
Journal: Biochem Biophys Res Commun
Date: Oct 4
Short Title: The naive effector cells of collagen type I during acute experimental pancreatitis are acinar cells and not pancreatic stellate cells
Alternate Journal: Biochemical and biophysical research communications
ISSN: 1090-2104 (Electronic)
Accession Number: 24036265
Keywords: Acinar Cells/*metabolism/pathology
Collagen Type I/genetics/metabolism
Pancreatic Stellate Cells/*metabolism/pathology
Real-Time Polymerase Chain Reaction
Transforming Growth Factor beta1/genetics/metabolism
Abstract: OBJECTIVE: The purpose of this study was to investigate the expression of collagen type I and the mRNA level of its regulatory factor, TGF-beta1, in tissue samples of acute pancreatitis and to determine the significance of collagen type I in predisposition to pancreatic fibrosis during acute pancreatitis. METHODS: Sprague-Dawley rats were divided into an experimental group (30 rats) and a control group (12 rats). The rats in the experimental group were intraperitoneally injected with cerulein to induce acute pancreatitis. The distribution and expression of collagen type I in the pancreatic tissues were examined by immunohistochemical staining. The mRNA level of TGF-beta1 was determined by real-time polymerase chain reaction (PCR). RESULTS: (1) Collagen type I was localized in the cytoplasm of pancreatic acinar cells. With pancreatitis progressed, strong positive staining for collagen type I covered whole pancreatic lobules, whereas, the islet tissue, interlobular area, and pancreatic necrotic area were negative for collagen type I. (2) The level of TGF-beta1 mRNA in rats from the experimental group increased gradually the establishment of acute pancreatitis, and was significantly higher than that in the control group at every time point. CONCLUSIONS: (1) During acute pancreatitis, pancreatic acinar cells, not pancreatic stellate cells as traditionally believed, were the naive effector cells of collagen type I. (2) TGF-beta1 played a key role in regulating collagen I expression during acute pancreatitis.