TY - JOUR
T1 - Galectin-1 and galectin-3 in chronic pancreatitis
AU - Wang, Li
AU - Friess, Helmut
AU - Zhu, Zhaowen
AU - Frigeri, Luciano
AU - Zimmermann, Arthur
AU - Korc, Murray
AU - Berberat, Pascal O.
AU - Büchler, Markus W.
N1 - Funding Information:
This work was supported in part by the DKF research grant, University of Bern, Switzerland, and SNF Grant 32–49494.96, Swiss National Foundation. Address reprint requests to: Dr. Helmut Friess, Department of Visceral and Transplantation Surgery, University of Bern, Inselspital, CH-3010 Bern, Switzerland. Fax: 41 31 632 9732; E-mail: [email protected]
PY - 2000
Y1 - 2000
N2 - Galectin-1 and galectin-3 have important functions in cell-cell interactions, cell adhesion to extracellular matrix, the organization of extracellular matrix, and tissue remodeling. To assess their potential role in chronic pancreatitis (CP), we examined their expression by Northern blot analysis, in situ hybridization, immunohistochemistry, and Western blot analysis in normal and CP pancreatic tissues. Northern blot analysis revealed a 4.5-fold increase of galectin-1 mRNA (p < 0.01) and a 3.8-fold increase of galectin-3 mRNA (p < 0.01) in CP samples compared with normal controls. In situ hybridization analysis of normal pancreas indicated low abundance of galectin-1 mRNA in fibroblasts, whereas galectin-3 mRNA was moderately present in ductal cells. CP samples exhibited moderate to intense galectin-1 mRNA signals in fibroblasts, whereas galectin-3 mRNA signals were intense in the ceils of ductular complexes and weak in the degenerating acinar cells, in addition, intense galectin-1 and galectin-3 mRNA signals were present in nerves of normal and CP samples. Immunohistochemistry showed a distribution pattern of galectin-1 and galectin-3 similar to that described for in situ hybridization. Relative quantification of galectin-1 and galectin-3 protein by immunoblotting revealed an increase of 3.2-fold and 3.0-fold, respectively, in CP compared with normal controls. There was a significant correlation between galectin-1 and fibrosis and between galectin-3 and fibrosis and the density of ductular complexes. Up-regulation of galectin-1 in fibroblasts and galectin-3 in ductular complexes suggests a role of these lectins in tissue remodeling in CP. Galectin-1 might participate in ECM Changes, whereas galectin-3 seems to be involved in both ECM changes and ductular complex formation.
AB - Galectin-1 and galectin-3 have important functions in cell-cell interactions, cell adhesion to extracellular matrix, the organization of extracellular matrix, and tissue remodeling. To assess their potential role in chronic pancreatitis (CP), we examined their expression by Northern blot analysis, in situ hybridization, immunohistochemistry, and Western blot analysis in normal and CP pancreatic tissues. Northern blot analysis revealed a 4.5-fold increase of galectin-1 mRNA (p < 0.01) and a 3.8-fold increase of galectin-3 mRNA (p < 0.01) in CP samples compared with normal controls. In situ hybridization analysis of normal pancreas indicated low abundance of galectin-1 mRNA in fibroblasts, whereas galectin-3 mRNA was moderately present in ductal cells. CP samples exhibited moderate to intense galectin-1 mRNA signals in fibroblasts, whereas galectin-3 mRNA signals were intense in the ceils of ductular complexes and weak in the degenerating acinar cells, in addition, intense galectin-1 and galectin-3 mRNA signals were present in nerves of normal and CP samples. Immunohistochemistry showed a distribution pattern of galectin-1 and galectin-3 similar to that described for in situ hybridization. Relative quantification of galectin-1 and galectin-3 protein by immunoblotting revealed an increase of 3.2-fold and 3.0-fold, respectively, in CP compared with normal controls. There was a significant correlation between galectin-1 and fibrosis and between galectin-3 and fibrosis and the density of ductular complexes. Up-regulation of galectin-1 in fibroblasts and galectin-3 in ductular complexes suggests a role of these lectins in tissue remodeling in CP. Galectin-1 might participate in ECM Changes, whereas galectin-3 seems to be involved in both ECM changes and ductular complex formation.
UR - http://www.scopus.com/inward/record.url?scp=0033870239&partnerID=8YFLogxK
U2 - 10.1038/labinvest.3780131
DO - 10.1038/labinvest.3780131
M3 - Article
C2 - 10950114
AN - SCOPUS:0033870239
SN - 0023-6837
VL - 80
SP - 1233
EP - 1241
JO - Laboratory Investigation
JF - Laboratory Investigation
IS - 8
ER -