期刊文献+

信号传导与转录活化因子3及其磷酸化在颅内动静脉畸形中的表达与临床相关因素分析

Correlation study of express of STAT3 and phosphorylated STAT3 in cerebral arteriovenous malformation with clinical factors
原文传递
导出
摘要 目的 明确颅内动静脉畸形(AVM)病灶内信号转导与转录活化因子3(STAT3)及其磷酸化形式的表达.方法 35例颅内AVM患者行开颅脑AVM切除术,留取手术切除标本,5例脑外伤行内减压患者脑组织为正常对照.应用免疫组化方法检测STAT3及其磷酸化形式P-STAT3(Tyr705)、P-STAT3(Ser727)的表达,并比较出血和未出血、术前栓塞和未栓塞以及Sptzer-Martin分级低级别和高级别患者STAT3及其磷酸化形式表达是否存在差异.结果 对照组中仅2例有STAT3弱表达,35例AVM患者STAT3、P-STAT3(Tyr705)和P-STAT3(Ser727)表达阳性率分别为100%、74%(26/35)和77%(27/35).P-STAT3(Tyr705)在栓塞组表达高于未栓塞组(P<0.05).结论 STAT3及其磷酸化形式在颅内AVM中表达增高,STAT3通路激活可能参与颅内AVM的病理发展过程;栓塞可能促使颅内AVM病灶内STAT3活化. Objective To investigate the expression of STAT3 (signal transducers and activators of transcription-3) and phosphorylated STAT3 in patients of cerebral arteriovenous malformation (AVM).Methods 35 patients who underwent cerebral AVM removal had been enrolled in this study.Five patients who underwent decompression for brain trauma were normal control.The resected AVM nidus and control tissue were under immunohistochemisty analysis for STAT3,P-STAT3(Tyr705) and P-STAT3(Ser727).Results The expression of STAT3,P-STAT3 (Tyr705) and P-STAT3 (Ser727) were 100% (35/35),74% (24/35) and 77% (24/35) respectively in AVM group.except weakly positive express of STAT3 in two patient,P-STAT3 (Tyr705) and P-STAT3 (Ser727) were all negative in control group.the expression of P-STAT3 (Tyr705) showed more intensive level in thrombosis group than unthrombosis group (P < 0.05).Conclusions STAT3 was overexpressed and activated in cerebral AVM.The activation of STAT3 signal transduction way may mediate the blood vessels remolding and neovasculization in cerebral AVM.Thrombosis maybe increase STAT3 phosphorylation.
出处 《中华神经外科杂志》 CSCD 北大核心 2014年第11期1097-1100,共4页 Chinese Journal of Neurosurgery
基金 国家自然科学基金(81171102)
关键词 颅内动静脉畸形 信号转导与转录活化因子3 免疫组织化学 Cerebral arteriovenous malformation Signal transducers and activators of transcription-3 Immunohistochemistry
  • 相关文献

参考文献20

  • 1Ruiz-Sandoval JL,Cantu C,Barinagarrementeria F.Intracerebral hemorrhage in young people:analysis of risk factors,location,causes,and prognosis[J].Stroke,1999,30:537-541.
  • 2Moftakhar P,Hauptman JS,Malkasian D,et al.Cerebral arteriovenous malformations.Part 1:cellular and molecular biology[J].Neurosurg Focus,2009,26:E10.
  • 3Moftakhar P,Hauptman JS,Malkasian D,et al.Cerebral arteriovenous malformations.Part 2:physiology[J].Neurosurg Focus,2009,26:E11.
  • 4Chen Z,Han ZC.STAT3:a critical transcription activator in angiogenesis[J].Med Res Rev,2008,28:185-200.
  • 5Ng I,Tan WL,Ng PY,et al.Hypoxia inducible factor-1alpha and expression of vascular endothelial growth factor and its receptors in cerebral arteriovenous malformations[J].J Clin Neurosci,2005,12:794-799.
  • 6Chen Y,Pawlikowska L,Yao JS,et al.Interleukin-6 involvement in brain arteriovenous malformations[J].Ann Neurol,2006,59:72-80.
  • 7Boscolo E,Pavesi G,Zampieri P,et al.Endothelial cells from human cerebral aneurysm and arteriovenous malformation release ET-1 in response to vessel rupture[J].Int J Mol Med,2006,18:813-819.
  • 8Sammons V,Davidson A,Tu J,et al.Endothelial cells in the context of brain arteriovenous malformations[J].J Clin Neurosci,2011,18:165-170.
  • 9Giraud AS,Menheniott TR,Judd LM.Targeting STAT3 in gastric cancer[J].Expert Opin Ther Targets,2012,16:889-901.
  • 10Hilfiker-Kleiner D,Hilfiker A,Fuchs M,et al.Signal transducer and activator of transcription 3 is required for myocardial capillary growth,control of interstitial matrix deposition,and heart protection from ischemic injury[J].Circ Res,2004,95:187-195.

二级参考文献20

  • 1Zhang, Jian-Guo,Zhao, Jing,Xin, Yan.Significance and relationship between Cripto-1 and p-STAT3 expression in gastric cancer and precancerous lesions[J].World Journal of Gastroenterology,2010,16(5):571-577. 被引量:12
  • 2Mellinghoff IK, Lassman AB, Wen PY. Signal transduction inhi- bitors and antiangiogenic therapies for malignant glioma [ J]. Glia, 2011,59 : 1205-1212.
  • 3Ltsch D, Steiner E, Holzmann K, et al. Major vault protein supports glioblastoma survival and migration by upregulating the EGFR/PI3K signalling axis [ J ]. Oncotarget, 2013, 4: 1904-1918.
  • 4England B, Huang T, Karsy M. Current understanding of the role and targeting of tumor suppressor p53 in glioblastoma muhiforme[ J]. Tumour Biol, 2013, 34:2063-2074.
  • 5Gately S, Soft GA, Brem S. The potential role of basic fibroblast growth factor in the transformation of cultured primary human fetal astrocytes and the proliferation of human glioma ( U-87 ) cells [ J]. Neurosurgery, 1995,37:723-730.
  • 6Fukui S, Nawashiro H, Otani N, et al. Nuclear accumulation of basic fibroblast growth factor in human astrocytic tumors [ J ]. Cancer, 2003,97:3061-3067.
  • 7Weissenberger J, Loeffler S, Kappeler A. IL6 is required for giioma development in a mouse model[J ]. Oncogene, 2004, 23:3308-3316.
  • 8Tchirkov A, Khalil T, Chautard EE. Interleukin-6 gene am- plification and shortened survival in glioblastoma patients[ J]. Br J Cancer, 2007, 96:474-476.
  • 9Garner JM, Fan M, Yang CH, et al. Constitutive activation of signal transducer and activator of transcription 3 ( STAT3 ) and nuclear factor B signaling in glioblastoma cancer stem cells regulates the Notch pathway [ J ]. J Biol Chem, 2013, 288 : 26167-26176.
  • 10Fouse SD, Costello JF. Cancer Stem Cells Activate STAT3 the EZWay[J]. Cancer Cell, 2013, 23:711-713.

共引文献14

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部