Oncostatin M-enhanced vascular endothelial growth factor expression in human vascular smooth muscle cells involves PI3K-, p38 MAPK-, Erk1/2- and STAT1/STAT3-dependent pathways and is attenuated by interferon-γ
| العنوان: | Oncostatin M-enhanced vascular endothelial growth factor expression in human vascular smooth muscle cells involves PI3K-, p38 MAPK-, Erk1/2- and STAT1/STAT3-dependent pathways and is attenuated by interferon-γ |
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| المؤلفون: | Gersina Rega, Christoph Kaun, Kathrin Rychli, Matthias Paireder, Kurt Huber, Valery N. Bochkov, Igor Huk, Svitlana Demyanets, Stefan Pfaffenberger, Taras Afonyushkin, Stefan P. Kastl, Katharina M. Katsaros, Philipp J. Hohensinner, Johann Wojta, Gerald Maurer |
| المصدر: | Basic Research in Cardiology. 106:217-231 |
| بيانات النشر: | Springer Science and Business Media LLC, 2010. |
| سنة النشر: | 2010 |
| مصطلحات موضوعية: | Adult, Male, STAT3 Transcription Factor, Vascular Endothelial Growth Factor A, Vascular smooth muscle, MAP Kinase Signaling System, Physiology, Angiogenesis, medicine.medical_treatment, Myocytes, Smooth Muscle, Oncostatin M, p38 Mitogen-Activated Protein Kinases, Muscle, Smooth, Vascular, Interferon-gamma, Phosphatidylinositol 3-Kinases, chemistry.chemical_compound, Physiology (medical), medicine, Humans, RNA, Messenger, STAT3, Protein kinase B, Cells, Cultured, Aged, Mitogen-Activated Protein Kinase 1, biology, fungi, Atherosclerosis, Glycoprotein 130, Coronary Vessels, Interleukin-10, Up-Regulation, Vascular endothelial growth factor, STAT1 Transcription Factor, Cytokine, chemistry, biology.protein, Cancer research, Female, Interleukin-4, Cardiology and Cardiovascular Medicine |
| الوصف: | The pleiotropic cytokine oncostatin M (OSM), a member of the glycoprotein (gp)130 ligand family, plays a key role in inflammation and cardiovascular disease. As inflammation precedes and accompanies pathological angiogenesis, we investigated the effect of OSM and other gp130 ligands on vascular endothelial growth factor (VEGF) production in human vascular smooth muscle cells (SMC). Human coronary artery SMC (HCASMC) and human aortic SMC (HASMC) were treated with different gp130 ligands. VEGF protein was determined by ELISA. Specific mRNA was detected by RT-PCR. Western blotting was performed for signal transducers and activators of transcription1 (STAT1), STAT3, Akt and p38 mitogen-activated protein kinase (p38 MAPK). OSM mRNA and VEGF mRNA expression was analyzed in human carotid endaterectomy specimens from 15 patients. OSM increased VEGF production in both HCASMC and HASMC derived from different donors. OSM upregulated VEGF and OSM receptor-specific mRNA in these cells. STAT3 inhibitor WP1066, p38 MAPK inhibitors SB-202190 and BIRB 0796, extracellular signal-regulated kinase1/2 (Erk1/2) inhibitor U0126, and phosphatidylinositol 3-kinase (PI3K) inhibitors LY-294002 and PI-103 reduced OSM-induced VEGF synthesis. We found OSM expression in human atherosclerotic lesions where OSM mRNA correlated with VEGF mRNA expression. Interferon-γ (IFN-γ), but not IL-4 or IL-10, reduced OSM-induced VEGF production in vascular SMC. Our findings that OSM, which is present in human atherosclerotic lesions and correlates with VEGF expression, stimulates production of VEGF by human coronary artery and aortic SMC indicate that OSM could contribute to plaque angiogenesis and destabilization. IFN-γ reduced OSM-induced VEGF production by vascular SMC. |
| تدمد: | 1435-1803 0300-8428 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::11f5828c1f2f0d4e07ceabe6b3a18a6cTest https://doi.org/10.1007/s00395-010-0141-0Test |
| حقوق: | CLOSED |
| رقم الانضمام: | edsair.doi.dedup.....11f5828c1f2f0d4e07ceabe6b3a18a6c |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14351803 03008428 |
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