Related Experiment Video
Updated: Jan 13, 2026
Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line
Published on: April 11, 2025
Expression of transforming growth factor beta1, beta2, and beta3 in chronic, cancer-associated, obstructive
Yuki Fukumura1, Toshio Kumasaka, Keiko Mitani
1Department of Pathology I, Juntendo University, School of Medicine, Tokyo, Japan. yfuku@med.juntendo.ac.jp
Context:
Myofibroblasts are considered to play central roles in pancreatic fibrosis. The potent fibrogenic capacities of transforming growth factor betas (TGF-betas) have been emphasized in vitro and in animal studies. However, the roles of TGF-betas in human chronic pancreatitis have not been fully clarified.
Objective:
To investigate whether expressions of TGF-betas are related to myofibroblast distribution in chronic, cancer-associated, obstructive pancreatitis (COP).
Design:
Histopathologic studies using hematoxylin-eosin and Elastica-Masson trichrome and immunohistochemical studies using antibodies against alpha-smooth muscle actin (SMA); CD68; TGF-beta1, -beta2, and -beta3; and TGF-beta soluble receptor type II were performed in 19 COP cases and 6 controls. By classifying COP tissues into 3 fibrosis phases by the amount of collagen deposits, immunoreactivities for TGF-betas, histopathologic changes, and myofibroblast distribution were examined for each fibrosis phase.
Results:
Six cases were categorized in the early stage of fibrosis, 8 in the intermediate stage, and 5 in the advanced stage. Immunoreactivities for all 3 isoforms of TGF-beta were observed in occasional myofibroblasts. In the early and intermediate stages, TGF-beta1-expressing macrophages and neutrophils were distributed in the midst of myofibroblasts. TGF-beta2 and TGF-beta3 expressions were observed in ductal structures, sometimes even in sites where no or few myofibroblasts were seen. TGF-beta soluble receptor type II was immunoreactive for myofibroblasts, endothelium, and ductal structures.
Conclusions:
All 3 isoforms of TGF-betas may contribute to fibrosis in COP. Macrophages and neutrophils may be sources of fibrogenic TGF-beta1. Infiltration of these cells appears to play an important role in the progression of COP fibrosis.
