Galectin-1 is an inductor of pancreatic stellate cell activation

Autor: Gisela Sparmann, Stefan Liebe, Brit Fitzner, Jörg Emmrich, Robert Jaster, Hermann Walzel
Rok vydání: 2005
Předmět:
Male
medicine.medical_specialty
Time Factors
Galectin 1
Proline
medicine.medical_treatment
Becaplermin
Oligonucleotides
Pancreatic stellate cell
Gene Expression
Electrophoretic Mobility Shift Assay
Biology
Culture Media
Serum-Free
Pancreatic cancer
Internal medicine
medicine
Extracellular
Animals
Phosphorylation
Promoter Regions
Genetic
Pancreas
Transcription factor
Cells
Cultured
Cell Proliferation
Mitogen-Activated Protein Kinase 1
Platelet-Derived Growth Factor
Mitogen-Activated Protein Kinase 3
Tumor Necrosis Factor-alpha
Kinase
Growth factor
NF-kappa B
Transcription Factor RelA
Proteins
Proto-Oncogene Proteins c-sis
Cell Biology
medicine.disease
Actins
Rats
Cell biology
Transcription Factor AP-1
Endocrinology
medicine.anatomical_structure
Rats
Inbred Lew
Galectin-1
Hepatic stellate cell
Collagen
Protein Binding
Signal Transduction
Zdroj: Cellular Signalling. 17:1240-1247
ISSN: 0898-6568
DOI: 10.1016/j.cellsig.2004.12.012
Popis: Pancreatic stellate cells (PSCs) play a key role in the development of pancreatic fibrosis, a pathological feature of chronic pancreatitis and pancreatic cancer. Here, we show that activation of rat PSCs in vitro is associated with increased expression of galectin-1 (gal-1) and that gal-1 modulates PSC function. Expression of the lectin was stimulated by fetal calf serum and platelet-derived growth factor. PSCs exposed to exogenous gal-1 proliferated at a higher rate and synthesised more collagen than controls. Gal-1-dependent collagen synthesis was blocked by lactose but not by cellobiose, suggesting that gal-1 acts on PSCs through targeting beta-galactoside-containing glycoconjugates. Analysis of gal-1 signalling in PSCs revealed an activation of the extracellular signal-regulated kinases 1 and 2 and enhanced DNA binding of AP-1 transcription factors. Together, our data implicate gal-1 in PSC activation and suggest further studies to analyse the role of endogenous lectins in the development of pancreatic fibrosis in vivo.
Databáze: OpenAIRE
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