Recently, the identification of pancreatic stellate cells (PSCs) was reported by Bachem et al. [22, 23], and these cells, also known as vitamin A-storing cells, that were isolated from the pancreas were shown to differentiate into myofibroblast-like cells expressing a-SMA and producing collagen type I and III, laminin, and fibronectin. Most of these studies, however, were performed using animal models, such as WBN/Kob rats [24, 25], Otsuka Long Evans Tokushima Fatty (OLETF) rats  and Aly mice , which are known to develop pancreatitis spontaneously, as well as experimental pancreatitis induced by ethanol feeding , arginine injection  or trinitrobenzene sul-foric acid (TNBS) infusion  in rats or mice. These animal model studies and a cell-culture study used activated periacinar, not perilobular, PSCs in fibroge-nesis [31-33] that has histological features different from those of chronic pancreatitis in humans .
According to Kuroda et al. , the myofibroblasts play an important role in pancreatic fibrosis in alcoholics. Based on their diameter and location, the fine filaments (8-15 nm in diameter) presenting between the myofibroblasts and collagen fibrils are considered to probably be collagen filaments in nature (fig. 8). The presence of collagen filaments around the myofibroblasts may indicate that myofibroblasts produce the collagen filaments and fibers. Hence, they suggest that alcohol has an effect on the initial stage of periacinar collage-nization in intralobular fibrosis via the activation of myofibroblasts.
Prolyl hydroxylase (PH), located in microsomes, is an enzyme that hydrox-ylates peptide-bound proline in the process of collagen biosynthesis . Our previous study  showed that the immunoreactivity of PH in the pancreas is mainly localized in the acinar cells (fig. 9), and seems to play a role in pancreatic fibrosis. Moreover, Kuroda et al.  also notes that protein transport blockage, which is represented by leakage of the contents of zymogen granules, rough endoplasmic reticulum and lysosomes to the cytoplasm and around aci-nar cells, is preceded by alcohol intake and may contribute to severe damage to acinar cells and the development of periacinar collagenization (fig. 10).
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