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低氧条件下鼻息肉细胞中HIF-1α基因对VEGF表达的影响 被引量:1

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摘要 目的探讨鼻息肉上皮细胞中HIF-1α与VEGF表达相互作用。方法采用体外原代低氧培养鼻息肉细胞,运用RNA干扰技术(RNAi)特异性沉默HIF-1α基因,Real-time PCR和Western blot方法检测HIF-1α干扰效率,同时Western blot检测VEGF的表达。结果 HIF-1α瞬时干扰效果显著,HIF-1α的m RNA和蛋白表达均显著性下降(P<0.05),选取干扰效果最佳的序列HIF-1α-si RNA2作为后续实验的RNAi干扰序列,进行瞬时干扰HIF-1α;鼻息肉细胞中si RNA瞬时干扰HIF-1a后,VEGF表达下调。结论在低氧培养条件下,鼻息肉细胞中HIF-1α可以调控VEGF的表达情况。
出处 《哈尔滨医药》 2018年第2期131-133,共3页 Harbin Medical Journal
基金 黑龙江省自然科学基金资助项目(QC2010076)
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  • 1[1]Huang LE,Gu J,Schau M,et al.Regulation of hypoxiainducible factor 1alpha is mediated by an O2-dependent degradation domain via the ubiquitin-proteasome pathway.Proc Natl Acad Sci U S A,1998,95:7987-7992.
  • 2[2]Zhong H,De Marzo AM,Laughner E,et al.Overexpression of hypoxia-inducibIe factor 1alpha jn common human cancers and their metastases.Caner Res,1999,59:5830-5835.
  • 3[3]Wu R,Yankaskas J,Cheng E,et al.Growth and differentiation of human nasal epithelial cells in culture.Serum-free,hormone-supplemented medium and proteoglycan synthesis.Am Rev Respir Dis,1985,132:311-320.
  • 4[4]Semenza GL,Agani F,Booth G,et al.Structural and functional analysis of hypoxia-inducible factor 1.Kidney Int,1997,51:553-555.
  • 5[5]Choi KS,Bae MK,Jeong JW,et al.Hypoxia-induced angiogenesis during carcinogenesis.J Biochem Mol Biol,2003,36:120-127.
  • 6[6]Cremer T,Yamanishj Y,Clauseen BE,et al.HIF-1alpha is essential for myeloid call-mediated inflammation.Cell,2003,112:645-657.
  • 7[7]Walmsley SR,Print C,Farahi N,et al.Hypoxia-induced neutrophil survival is mediated by HIF-1alpha-dependent NF-kappaB activity.J Exp Med,2005,201:105-115.
  • 8[8]Dong Z,Yang Z,Wang C.Expression of TLR2 and TLR4 messenger RNA in the epithelial calls of the nasal airway.Am J Rhinol,2005,19:236-239.
  • 9[9]Zarember KA,Malech HL.HIF-1alpha:a master regulator of innate host deferises?J Clin Invest,2005,115:1702-1704.
  • 10[10]Blouin CC,Pagé EL,Soucy GM,et al.Hypoxic gene activation by lipopolysaccharide in macrophages: implication of hypoxia-inducible factor 1alpha.Blood,2004,103:1124-1130.

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