ArticleWorld journal of gastroenterology2005
Activation of JAK-STAT pathway is required for platelet-derived growth factor-induced proliferation of pancreatic stellate cells.
Article in World journal of gastroenterology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 55 citations in OpenAlex.
- Review
- Nintedanib Alleviates Chronic Pancreatitis by Inhibiting the Activation of Pancreatic Stellate Cells via the JAK/STAT3 and ERK1/2 Pathways.Digestive diseases and sciences · 2023Article
- Fibrosis in Liver and Pancreas: a Review on Pathogenic Significance, Diagnostic Options, and Current Management Strategies.Inflammation · 2023Review
- Review
- Receptor Tyrosine Kinases and Their Signaling Pathways as Therapeutic Targets of Curcumin in Cancer.Frontiers in pharmacology · 2021Review
- The Effects of Tofacitinib-Mediated Janus Kinase/Signal Transducers and Activators of the Transcription Signal Pathway Inhibition on Collagen Biosynthesis in Hepatic and Skin Fibroblast Cell Culture.Archives of rheumatology · 2020Article
- Cathelicidin Modulates Vascular Smooth Muscle Cell Phenotypic Switching through ROS/IL-6 Pathway.Antioxidants (Basel, Switzerland) · 2020Article
- Molecular Mechanism of Pancreatic Stellate Cells Activation in Chronic Pancreatitis and Pancreatic Cancer.Journal of Cancer · 2020Review
- Potential therapeutic manipulations of the CXCR3 chemokine axis for the treatment of inflammatory fibrosing diseases.F1000Research · 2020Article
- Tumor microenvironment in chemoresistance, metastasis and immunotherapy of pancreatic cancer.American journal of cancer research · 2020Review
- Targeting Protein Kinases to Enhance the Response to anti-PD-1/PD-L1 Immunotherapy.International journal of molecular sciences · 2019Review
- Transgenic expression of cyclooxygenase-2 in pancreatic acinar cells induces chronic pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- PDGF‑BB promotes the differentiation and proliferation of MC3T3‑E1 cells through the Src/JAK2 signaling pathway.Molecular medicine reports · 2018Article
- "Do We Know Jack" About JAK? A Closer Look at JAK/STAT Signaling Pathway.Frontiers in oncology · 2018Review
- The tyrosine kinase inhibitor nintedanib activates SHP-1 and induces apoptosis in triple-negative breast cancer cells.Experimental & molecular medicine · 2017Article
- Mathematical model of chronic pancreatitis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Pancreatic stellate cell: Pandora's box for pancreatic disease biology.World journal of gastroenterology · 2017Review
- Natural Agents Used in Chemoprevention of Aerodigestive and GI Cancers.Current pharmacology reports · 2016Article
- Inflammation and pancreatic cancer: disease promoter and new therapeutic target.Journal of gastroenterology · 2014Review
- Combined targeting of STAT3/NF-κB/COX-2/EP4 for effective management of pancreatic cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo clarify the role of Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathway in platelet-derived growth factor (PDGF) induced proliferation in activated pancreatic stellate cells (PSCs).
methodsPSCs were isolated from rat pancreas tissue, and used in their culture-activated, myofibroblast-like phenotype. STAT-specific binding activity was assessed by electrophoretic mobility shift assay. Activation of Src, JAK2, STAT1, STAT3, and ERK was determined by Western blotting using anti-phospho-specific antibodies. Cell proliferation was assessed by measuring the incorporation of 5-bromo-2'-deoxyuridine.
resultsPDGF-BB induced STAT-specific binding activity, and activation of Src, JAK2, STAT1, STAT3, and ERK. Ethanol and acetaldehyde at clinically relevant concentrations decreased basal activation of JAK2 and STAT3. PDGF-induced activation of STAT1 and STAT3 was inhibited by a Src inhibitor PP1 and a JAK2 inhibitor AG490, whereas PDGF-induced activation of ERK was inhibited by PP1, and not by AG490. PDGF-induced proliferation was inhibited by PP1 and AG490 as well as by STAT3 antisense oligonucleotide.
conclusionPDGF-BB activated JAK2-STAT pathway via Src-dependent mechanism. Activation of JAK2-STAT3 pathway, in addition to ERK, may play a role in PDGF-induced proliferation of PSCs.
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