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STAT3 phosphorylation induced by vascular endothelial growth factor is associated with regulation of immune responses by dendritic cells
Author(s) -
Zhang Wenguang,
Hauke Ralph
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1076.19
Subject(s) - vascular endothelial growth factor , stat3 , phosphorylation , immune system , lncap , chemistry , western blot , cancer research , microbiology and biotechnology , biology , vegf receptors , immunology , medicine , cancer cell , cancer , biochemistry , gene
OBJECTS The expression of phosphorylated signal tranducer and activators of transcription 3 (p‐STAT3) is correlated with expressions of vascular endothelial growth factor (VEGF) in some carcinomas. The mechanism of the immunomodulatory effects of VEGF on human dendritic cells (DCs) is not clearly understood. This study seeks to investigate the effects of VEGF on STAT3 phosphorylation and its correlation with immune regulation by human DCs. METHODS: Monocytes‐derived immature DCs were incubated with VEGF. We detected expression of p‐STAT3 in DCs induced by VEGF with different concentrations and for different effect times by immunohistochemistry and Western blot. The cytotoxicity of DC‐activated T cells against LNCaP prostate cancer cells was determined by lactate dehydrogenase (LDH) activity assay. RESULTS: A concentration of 100 ng/ml of VEGF was enough to increase phosphorylation of STAT3 and showed nuclear translocation of p‐STAT3 from the cytoplasm to the nucleus. The cytotoxicity of T cells was significantly decreased after co‐culture with VEGF‐treated DCs. CONCLUSIONS: VEGF plays a key role in immunoregulation of human DCs. VEGF‐induced phosphorylation and nuclear translocation of STAT3 is correlated with DCs activation decreased, suggesting that VEGF decreased DC‐activated T cells cytotoxity activation by phosphorylation of STAT3. Supported by: UNMC Internal Medicine Research Support .