![]() ![]() Constitutive phosphorylation of p38 MAPK and JNK was observed in these glioma cells. Inhibitors of p38 MAPK and/or JNK significantly suppressed VEGF secretion both in the presence and absence of IL-1beta, while inhibitors of COX-2, ERK1/2, and PI3-K did not. ![]() ![]() IL-1beta significantly stimulated VEGF secretion in these glioma cells. The basal levels of VEGF secretion were significantly higher in U87MG, U373MG, and T98G, than HFL. Phosphorylation of MAPK was examined by immunoblotting. Inhibitors of COX-2, MAPK, and phosphatidyl inositol 3-kinase (PI3-K), and blocking antibodies to TGF-beta II and TNF-alpha, or IL-1 receptor antagonist, were used to examine their effects on VEGF secretion. VEGF mRNA levels were estimated by RT-PCR. VEGF, IL-1, IL-6, and TNF-alpha were measured with ELISA. Human malignant glioma cell lines, T98G, U373MG, U87MG, and A172, and human fetal lung fibroblasts (HFL) were cultured both with and without IL-1beta under normoxic conditions. In this study, we examined intracellular signaling pathways involved in the secretion of VEGF in glioma cells under normoxic conditions. ![]() However, malignant gliomas express high levels of VEGF in both hypoxic perinecrotic and vital tumor areas. Hypoxia has been identified as an important regulator of VEGF. Malignant gliomas are typically angiogenic and secrete high levels of VEGF. ![]()
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