【摘 要】
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AIM The present study was designed to obverse whether c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) regulates the angiogenesis of human umbilical vein endothelial cells (HUVEC) in
【机 构】
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The MOE Key Laboratory for Standardization of Chinese Medicines and The SATCM Key Laboratory for New
【出 处】
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第二届世界天然药物和传统药物药理学学术会议
论文部分内容阅读
AIM The present study was designed to obverse whether c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) regulates the angiogenesis of human umbilical vein endothelial cells (HUVEC) induced by angiogenic growth factors.METHODS Cell proliferation, migration and tube formation were observed in HUVEC, and in vivo Matrigel plug assay was used.Western-blotting analysis was used to observe the related signals.RESULTS Vascular endothelial growth factor (VEGF) and basic fibroblastic growth factor (bFGF) both stimulated HUVEC proliferation, migration and tube formation in a concentration-dependent manner.Further results showed that VEGF and bFGF induced the activation of JNK/SAPK, p38 kinase and extracellular signal-regulated kinase 1 and 2 (ERK1/2), while JNK/SAPK inhibitor SP600125 and specific siRNA both blocked all those angiogenic effects induced by VEGF or bFGF.Additionally, in vivo matrigel plug assay showed that SP600125 inhibited VEGF-induced angiogenesis.Furthermore,JNK/SAPK inhibitor SP600125 and specific siRNA inhibited VEGF or bFGF-induced JNK/SAPK signal cascade activation.Further results showed that SP600125 and JNK/SAPK siRNA decreased VEGF-induced VEGFR2 (Flk-1/KDR) sustained phosphorylation in HUVEC.CONCLUSION Taken together, all these results indicates that JNK/SAPK signal pathway plays an important role in mediating growth factors-induced angiogenic responses, and thus JNK/SAPK is a potential target for drug development in angiogenesisrelated diseases such as cancer, diabetic retinopathy, etc.
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