摘要
目的探讨HIV-1Nef蛋白能否通过调控PTEN／P13K信号通路促进卡波氏肉瘤病毒（KSHV）vIL-6诱导血管生成。方法用脂质体转染的方法将pPTEN．cDNA、P13K．DN及其对照空载体质粒分别转染稳定表达KSHVvIL-6和HIV-1Nef蛋白的内皮细胞，采用微管形成试验观察微管形成状况，将这些细胞接种鸡胚绒毛尿囊膜（CAM）检测血管生成情况。Westernblot进一步检测转染了上述质粒后细胞内源性VrEN和P13K信号分子的表达水平。结果过表达PTEN或抑制P13K表达均可抑制Nef促进vIL-6诱导的内皮细胞微管形成和CAM血管生成。结论HIV-1Nef蛋白通过调控PTEN／P13K信号通路促进KSHVvIL-6诱导血管生成。
Objective To investigate whether HIV-1 Nef could promote the angiogenesis and tu- morigenesis induced by KSHV vIL-6 through regulating PTEN/PI3K signaling pathway. Methods Lipo- some transfection was used to transfect cDNA of pPTEN, dominant-negative （DN） construct of PI3K and control vector into endothelial cells, which stably express KSHV vIL-6 and HIV-1 Nef. Microtubule forma- tion assay and chicken chorioallantoic membrane（CAM） assay were used to evaluate microtubule formation and angiogenesis , respectively. Expressions of PTEN and PI 3 K were measured by Western blot. Results Both overexpression of PTEN and inhibited expression of PI3K suppressed the vIL-6-induced microtubule for- mation and angiogenesis in CAM mediated by Nef. Conclusion HIV-1 Nef enhances vIL-6-induced angio- genesis and tumorigenesis through regulating PTEN/PI3K signaling pathway.
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
2013年第8期627-633,共7页
Chinese Journal of Microbiology and Immunology
基金
国家自然科学基金（81171552）
浙江省教育厅科技计划项目（Y201328970）o
浙江省教育厅高校访问学者教师专业发展项目（FX2012120）
