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结构蛋白及血管形成因子在体表海绵状静脉畸形中的表达及意义(英文) 被引量:3

Expression and significance of structural proteins and vascular growth factors in cavernous venous malformation on body surface
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摘要 背景:体表海绵状静脉畸形,又称为海绵状血管瘤,是一种较常见而难治的血管疾病,目前对其发病机制了解甚少。目的:研究结构蛋白及血管形成因子在体表海绵状静脉畸形(cavernousvenousmalformation,CVM)中的表达及意义。设计:研究CVM病理标本中的结构蛋白和血管形成因子的表达,用正常中型静脉和小静脉标本作为对照,半定量分析结果。地点和对象:解放军第二军医大学附属长海医院1996/2000间手术切除的CVM病理标本25例,正常中型静脉和小静脉标本各12例。干预:采用Envision法免疫组化染色观察CVM、正常中型静脉和小静脉标本中的Ⅳ-型胶原、纤维连接蛋白(Fn)、层粘连蛋白(Ln)等结构蛋白及血管内皮细胞生长因子(VEGF)、血管生成素-1(Ang-1)等血管形成因子的表达。主要观察指标:观察Ⅳ-型胶原、Fn、Ln、VEGF、Ang-1在各个标本中的表达强度,分为“-、+、”3个等级。结果:Ⅳ型胶原、Fn和Ln在海绵状静脉畸形与在中小静脉中的分布类似,但表达量明显少。畸形组织和小静脉的VEGF表达明显强于中型静脉,小静脉的Ang-1表达明显强于静脉畸形和中型静脉。结论:结构蛋白及血管形成因子表达变化可能是海绵状静脉畸形形成发展的重要因素。Ang-1表达减少可能参与海绵状静脉畸形的血管塑型障碍的发生。 BACKGROUND:Cavernous venous malformation(CVM),also called cavernous hemangioma,is a common kind of vascular disease and hard to cure.At present we know little about the pathogenesis of it. OBJECTIVE:To study the expression and significance of structural proteins and vascular growth factors in cavernous venous malformation of body surface. DESIGN:The expression of structural proteins and vascular growth factors in the CVM specimens was studied.The normal medium sized veins and small veins were used as the control. A semi quantitative analysis was used to analyze the result. SETTING and PARTICIPANTS:Twenty five specimens of cavernous venous malformation,12 specimens of medium sized veins and 12 specimens of small veins were abtained from Changhai Hospital affiliated to the Second Military Medical University during the year of 1996 to 2000. INTERVENTION:Envision method was used to observe the expression of Ⅳ collagen,fibronectin(Fn),Laminin(Ln), vascular endothelial growth factor(VEGF) and angiogenin 1(Ang 1) in the above mentioned specimens. MAIN OUTCOME MEASURE:The expression intensity of Ⅳ collagen,Fn,Ln,VEGF and Ang 1 in these specimens was observed.The intensity was divided into three levels:-,+and . RESULTS: The distribution of Ⅳ collagen,Fn and Ln in specimens of CVM is similar to that in specimens of moderate and small veins, but the expression of Ⅳ collagen,Fn and Ln in specimens of CVM is less obviously. The expression of VEGF in specimens of malformations and small veins was significantly higher than that in medium sized veins. The expression of Ang 1 in specimens of small veins was significantly higher than that in specimens of venous malformation and medium sized veins. CONCLUSION:The changes of the expression of structural proteins and vascular growth factors may be one of the important factors in the formation and development of CVM. The decreased expression of Ang 1 may be related to the disturbance of vascular remodeling in CVM.
出处 《中国临床康复》 CSCD 2004年第8期1587-1589,共3页 Chinese Journal of Clinical Rehabilitation
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  • 1[1]Garzon M.Hemangioma:Update on classification,clinical presentation,and associated anomalies.Cutis 2000;66(5):325-8
  • 2[2]Song J,Rolfe BE,Hayward IP,et al.Effects of collagen gel configuration on behavior of vascular smooth muscle cells in vitro: association with vascular morphogenesis.In Vitro Cell Dev Biol Anim 2000;36(9):600-10
  • 3[3]Stroeva OG,Dol'nikova AE,Sologub AA,et al.Immunohistochemical study of fibronectin localization during the formation ofthe vascular coat under the influence of the pigment epithelium in chick embryos.Ontogenez 1989;20(4):350-6
  • 4[4]Ponce ML,Hibino S,Lebioda AM,et al.Identification of a potent peptide antagonist to an active laminin-1 sequence that blocks angiogenesis and tumor growth.Cancer Res 2003;63(16):5060-4
  • 5[5]Rothbart D,Awad IA,Lee J,et al.Expression of angiogenic factors and structural proteins in central nervous system vascular malformations.Neurosurgery 1996;38(5):915-24.discussion 924-5
  • 6[6]Ferrara N,Gerber HP,LeCouter J.The biology of VEGF and its receptors.Nat Med 2003;9(6):669-76
  • 7[7]Kilic T,Pamir MN,Kullu S,et al.Expression of structural proteins and angiogenic factors in cerebrovascular malformations.Neurosurgery 2000;46(5):1179-91,discussion 1191-2
  • 8[8]Vikkula M,Boon L,Carraway K,et al.Vascular dysmorphogenesis caused by an activating mutation in the receptor tyrosine kinase TIE-2.Cell 1996;87:1181-90

同被引文献47

  • 1欧阳天祥,郭恩覃.海绵状血管瘤内压监测指导栓塞及硬化剂注射治疗[J].中华整形烧伤外科杂志,1997,13(3):171-174. 被引量:25
  • 2Garzon M. Hemangioma: update on classification, clinical presentation, and associated anomalies. Cutis 2000; 66(5): 325 - 8.
  • 3Mulliken JB, Zetter BR, Folkman J. In vitro characteristics of endothelium from hemangiomas and vascular malformations Surgry 1982; 92(2): 348 - 53.
  • 4Allen KE, Varty K, Jones L, et al. Human venous endothelial can promote intimal hyperplasia in a paracrine manner. J Vasc Surg 1994; 19:577 -84.
  • 5Korff T, Kimmina S, Martiny-Baron G, et al. Blood vessel maturation in a 3- dimensional spheroidal the spheroid's coculture model: direct contact with smooth muscle cells regulates endothelial cell quiescence and The abrogates represses the VEGF responsiveness. FASEB J 2001; 15 (2): 447 - 57.
  • 6Nicosia RF, Villaschi S. Autoregulation of angiogenesis by cells of the vessel wall. Int Rev Cytol 1999; 185: 1 -43.
  • 7Malinda KM, Ponce L, Kleinman HK, et al. Gp38k, a protein synthesized by vascular smooth muscle cells, stimulatesdirectional migration of human umbilical vein endothelial cells. Exp Cell Res 1999; 250( 1 ): 168 -73.
  • 8Drake C J, Hungerford JE, Little CD. Morphogenesis of the first blood vessels. Ann N Y Acad Sci 1998; 857:155 -79.
  • 9Powell R J, Cronenwett JL, Fillinger MF, et al. Endothelial cell modulation of smooth muscle cell morphorlogy and organizational growth pattern. Ann Vasc Surg 1996; 10:4 - 10.
  • 10Vikkula M, Boon LM, Carraway KL 3rd, et al. Vascular dysmorphogenesis caused by an activating mutation in the receptor tyrosine kinase TIE-2. Cell 1996; 87:181 -90.

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