基础研究

人颞叶内侧癫痫海马组织星形胶质细胞Syntrophin的表达变化

  • 王晓璇 ,
  • 孙振荣 ,
  • 吴敏 ,
  • 师忠芳 ,
  • 闫旭 ,
  • 徐立新 ,
  • 董丽萍 ,
  • 杨少华 ,
  • 袁芳
展开
  • 1.首都医科大学北京市神经外科研究所病理生理室,首都医科大学附属北京天坛医院,北京市 100050;
    2.首都医科大学附属北京天坛医院神经外科,北京市 100050;
    3.北德克萨斯大学医学中心神经与药理系,美国德克萨斯州沃思堡 76107。
王晓璇(1993-),女,汉族,山东聊城市人,硕士研究生,主要研究方向:难治性癫痫的发病机制研究。

收稿日期: 2016-12-21

  网络出版日期: 2017-03-31

基金资助

北京市自然科学基金项目(No. 7152027)

Distribution of Astrocytic Syntrophin in Hippocampus from Human Mesial Temporal Lobe Epilepsy

  • WANG Xiao-xuan ,
  • SUN Zhen-rong ,
  • WU Min ,
  • SHI Zhong-fang ,
  • YAN Xu ,
  • XU Li-xin ,
  • DONG Li-ping ,
  • YANG Shao-hua ,
  • YUAN Fang
Expand
  • 1. Department of Pathophysiology, Beijing Neurosurgical Institute, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China;
    2. Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China;
    3. Department of Pharmacology and Neuroscience, University of North Texas Health Science Center, Fort Worth, Texas 76107, USA

Received date: 2016-12-21

  Online published: 2017-03-31

摘要

目的观察人颞叶内侧癫痫(MTLE)海马组织星形胶质细胞syntrophin的表达变化。方法2015年4月至2016年7月,17例癫痫患者手术切除的海马组织,依据苏木素-伊红(HE)染色及胶质原纤维酸性蛋白、神经元核抗原免疫组织化学染色结果,分为MTLE组13例和非MTLE组4例。免疫荧光双重组织化学法及免疫荧光组织化学法观察syntrophin的表达。结果MTLE组星形胶质细胞大量增生,神经元明显减少。syntrophin在星形胶质细胞膜及足突处表达。与非MTLE组相比,MTLE组syntrophin在血管周围星形胶质细胞足突处分布减少,在其他部位分布增加。图像分析显示,与非MTLE组相比,MTLE组syntrophin蛋白量显著增多(t=5.421, P<0.001)。结论海马组织syntrophin在星形胶质细胞上的分布及其整体表达变化可能与MTLE发生相关。

本文引用格式

王晓璇 , 孙振荣 , 吴敏 , 师忠芳 , 闫旭 , 徐立新 , 董丽萍 , 杨少华 , 袁芳 . 人颞叶内侧癫痫海马组织星形胶质细胞Syntrophin的表达变化[J]. 中国康复理论与实践, 2017 , 23(3) : 292 -297 . DOI: 10.3969/j.issn.1006-9771.2017.03.009

Abstract

ObjectiveTo investigate the expression changes of astrocytic syntrophin in hippocampus from human mesial temporal lobe epilepsy (MTLE). MethodsFrom April, 2015 to July, 2016, 17 cases of hippocampus, collected from temporal lobectomy, were divided into MTLE group (n=13) and non-MTLE group (n=4) according to hematoxylin and eosin staining, glial fibrillary acidic protein and neuronal nuclei immunohistochemical staining. Immunofluorescence double labeling and immunofluorescence histochemistry were used to observe the expression of syntrophin. ResultsThe proliferation of astrocytes increased and neurons reduced in the hippocampus of MTLE group. Syntrophin was found in the membrane and foot processes of astrocyte, that was enriched along perivascular astrocyte end-feet domain in non-MTLE group, but lost in MTLE group. While the whole expression of syntrophin was more in MTLE group than in non-MTLE group (t=5.421, P<0.001). ConclusionThe distribution of syntrophin in hippocampus astrocytes may be related to the development of MTLE.

参考文献

[1] Joe MK, Kee C, Tomarev SI. Myocilin interacts with syntrophins and is member of dystrophin-associated protein complex [J]. J Biol Chem, 2012, 287(16): 13216-13227.
[2] Connors NC, Adams ME, Froehner SC, et al. The potassium channel Kir4.1 associates with the dystrophin-glycoprotein complex via alpha-syntrophin in glia [J]. J Biol Chem, 2004, 279(27): 28387-28392.
[3] Guadagno E, Moukhles H. Laminin-induced aggregation of the inwardly rectifying potassium channel, Kir4.1, and the water-permeable channel, AQP4, via a dystroglycan-containing complex in astrocytes [J]. Glia, 2004, 47(2): 138-149.
[4] 徐仟,孙振荣,李桂林,等. 人颞叶内侧癫痫海马组织星形胶质细胞水通道蛋白4和内向整流性钾离子通道4.1的再分布[J]. 中国康复理论与实践, 2012, 18(3): 215-218.
[5] Amiry-Moghaddam M, Williamson A, Palomba M, et al. Delayed K + clearance associated with aquaporin-4 mislocalization: Phenotypic defects in brains of α-syntrophin-null mice [J]. Proc Natl Acad Sci U S A, 2003, 100(23): 13615-13620.
[6] Sinha S, Danish SF. History and technical approaches and considerations for ablative surgery for epilepsy [J]. Neurosurg Clin N Am, 2016, 27(1): 27-36.
[7] 吴敏,方庆,师忠芳,等. 亚甲基蓝对大鼠局灶性脑缺血再灌注血脑屏障的保护作用[J]. 中国康复理论与实践, 2016, 22(2): 125-131.
[8] Blumcke I, Thom M, Aronica E, et al. International consensus classification of hippocampal sclerosis in temporal lobe epilepsy: a Task Force report from the ILAE Commission on Diagnostic Methods [J]. Epilepsia, 2013, 54(7): 1315-1329.
[9] Steinhauser C, Grunnet M, Carmignoto G. Crucial role of astrocytes in temporal lobe epilepsy [J]. Neuroscience, 2016, 323: 157-169.
[10] Allen NJ, Barres BA. Glia–more than just brain glue [J]. Nature, 2009, 457(7230): 675-677.
[11] Coulter DA, Steinhauser C. Role of astrocytes in epilepsy [J]. Cold Spring Harb Perspect Med, 2015, 5(3): a022434.
[12] Gumerson JD, Michele DE. The dystrophin-glycoprotein complex in the prevention of muscle damage [J]. J Biomed Biotechnol, 2011, 2011: 210797.
[13] Waite A, Brown SC, Blake DJ. The dystrophin-glycoprotein complex in brain development and disease [J]. Trends Neurosci, 2012, 35(8): 487-496.
[14] Haenggi T, Fritschy JM. Role of dystrophin and utrophin for assembly and function of the dystrophin glycoprotein complex in non-muscle tissue [J]. Cell Mol Life Sci, 2006, 63(14): 1614-1631.
[15] 赵蕾,胡超平,王艺,等. Duchenne型肌营养不良症患儿肌膜抗肌萎缩蛋白-糖蛋白复合物表达研究[J]. 中国现代神经疾病杂志, 2015, 15(6): 448-452.
[16] van den Bergen JC, Wokke BH, Hulsker MA, et al. Studying the role of dystrophin-associated proteins in influencing Becker muscular dystrophy disease severity [J]. Neuromuscul Disord, 2015, 25(3): 231-237.
[17] 付雅,吴士文. Duchenne型肌营养不良认知障碍机制研究进展[J]. 中国康复理论与实践, 2014, 20(5): 451-454.
[18] D'Angelo MG, Lorusso ML, Civati F, et al. Neurocognitive profiles in Duchenne muscular dystrophy and gene mutation site [J]. Pediatr Neurol, 2011, 45(5): 292-299.
[19] Anastasi G, Tomasello F, DiMauro D, et al. Expression of sarcoglycans in the human cerebral cortex: an immunohistochenical and molecular study [J]. Cells Tissues Organs, 2012, 196(5): 470-480.
[20] Blake DJ, Hawkes R, Benson MA, et al. Different dystrophin-like complexes are expressed in neurons and glia [J]. J Cell Biol, 1999, 147(3): 645-658.
[21] Pilgram GS, Potikanond S, Baines RA, et al. The roles of the dystrophin-associated glycoprotein complex at the synapse [J]. Mol Neurobiol, 2010, 41(1): 1-21.
[22] Nagelhus EA, Ottersen OP. Physiological roles of aquaporin-4 in brain [J]. Physiol Rev, 2013, 93(4): 1543-1562.
[23] Nwaobi SE, Cuddapah VA, Patterson KC, et al. The role of glial-specific Kir4.1 in normal and pathological states of the CNS [J]. Acta Neuropathol, 2016, 132(1): 1-21.
[24] Dmytrenko L, Cicanic M, Anderova M, et al. The impact of alpha-syntrophin deletion on the changes in tissue structure and extracellular diffusion associated with cell swelling under physiological and pathological conditions [J]. PLoS One, 2013, 8(7): e68044.
[25] Heuser K, Eid T, Lauritzen F, et al. Loss of perivascular Kir4.1 potassium channels in the sclerotic hippocampus of patients with mesial temporal lobe epilepsy [J]. J Neuropathol Exp Neurol, 2012, 71(9): 814-825.
文章导航

/