Hostname: page-component-6b989bf9dc-476zt Total loading time: 0 Render date: 2024-04-12T21:18:38.741Z Has data issue: false hasContentIssue false

E-Selectin Expression Increased in Human Ruptured Cerebral Aneurysm Tissues

Published online by Cambridge University Press:  02 December 2014

Wenqing Jia
Affiliation:
Department of Neurosurgery, Capital Medical University
Rong Wang
Affiliation:
Department of Neurosurgery, Capital Medical University
Jizong Zhao*
Affiliation:
Department of Neurosurgery, Capital Medical University
Isabelle Yisha Liu
Affiliation:
School of Medicine, Washington University, St. Louis, Missouri
Dong Zhang
Affiliation:
Department of Neurosurgery, Capital Medical University
Xuejiang Wang
Affiliation:
Department of Pathology, TianTan Hospital, School of Basic Medical Sciences, Capital Medical University
Xiaodi Han
Affiliation:
Department of Neurosurgery, Beijing Tiantan Puhua Hospital, Beijing China Department of Neurosurgery, University of Rochester Medical Center, New York, New York, USA
*
Department of Neurosurgery, TianTan Hospital, Capital Medical University, Beijing China, 100050.
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Objectives:

The purpose of the present study is to investigate the expression of inflammation factor endothelial-leukocyte adhesion molecule (E-selectin, CD62E) in cerebral aneurysm walls and its relationship with aneurysm rupture.

Methods:

Cerebral aneurysm tissue samples were collected at the time of surgical clipping of nine patients with history of subarachnoid hemorrhage, and then compared with control artery tissues from the superficial temporal arteries (STA) of five patients with intracranial tumors. Immunohistochemistry (IHC) was performed to reveal and localize E-selectin expression in the aneurysms and artery tissues. Western blot analysis was used to relatively quantify the level of E-selectine protein expression in cerebral aneurysms when compared with normal arteries.

Results:

E-selectin was detected in the wall of all the aneurysm tissue samples and was rarely found in normal control arteries by IHC, and it was concentrated in proliferating and disorganized epithelia cells. Moreover, with the Western blot method, the E-selectin protein level increased significantly in aneurysm tissues compared to normal STA.

Conclusions:

E-selectin might be an important factor involved in the process of cerebral aneurysm formation and rupture, by promoting inflammation and weakening cerebral artery walls.

Type
Original Articles
Copyright
Copyright © The Canadian Journal of Neurological 2011

References

1.Chyatte, D.The epidemiology, genetics and clinical behavior of intracranial aneurysms. In: Awad, IA, editor. Current management of cerebral aneurysms. Park Ridge: AANS; 1995. p. 120.Google Scholar
2.Stehbens, WE.Aneurysms and anatomical variations of cerebral arteries. Arch Pathol. 1963; 75: 4564.Google Scholar
3.Berenstein, A, Flamm, ES, Kupersmith, MJ.Unruptured intracranial aneurysms. N Engl J Med. 1999; 340: 143940.Google Scholar
4.Laroux, FS.Mechanisms of inflammation: the good, the bad and the ugly. Front Biosci. 2004; 9: 315662.Google Scholar
5.Chyatte, D, Bruno, G, Desai, S, Todor, DR.Inflammation and intracranial aneurysms. Neurosurgery. 1999; 45: 113746.Google Scholar
6.Frosen, J, Piippo, A, Paetau, A, et al.Remodeling of saccular cerebral artery aneurysm wall is associated with rupture: Histological analysis of 24 unruptured and 42 ruptured cases. Stroke. 2004; 35: 228793.Google Scholar
7.Yang, PY, Rui, YC.Intercellular adhesion molecule and vascular endothelial growth factor expression kinetics in macrophage derived foam cells. Life Sci. 2003; 74: 47180.Google Scholar
8.Hansson, GK.Immune and inflammatory mechanisms in the pathogenesis of atherosclerosis. J Atheroscler Thromb [Suppl 1]. 1994; 69.Google Scholar
9.Henry, PD, Chen, CH.Inflammatory mechanisms of atheroma formation: influence of fluid mechanics and lipid-derived inflammatory mediators. Am J Hypertens. 1993; 6: 32834.Google Scholar
10.Ross, R.Atherosclerosis: an inflammatory disease. N Engl J Med. 1999; 340: 11526.Google Scholar
11.Freestone, T, Turner, RJ, Coady, A, et al.Inflammation and matrix metalloproteinases in the enlarging abdominal aortic aneurysm. Arterioscler Thromb Vasc Biol. 1995; 15: 114551.Google Scholar
12.Koch, AE, Haines, GK, Rizzo, RJ, et al.Human abdominal aortic aneurysms: immunophenotypic analysis suggesting an immunemediated response. Am J Pathol. 1990; 137: 1199213.Google Scholar
13.Pearce, WH, Koch, AE.Cellular components and features of immune response in abdominal aortic aneurysms. Ann NY Acad Sci. 1996; 800: 17585.Google Scholar
14.Weyand, CM, Hicok, KC, Hunder, GG.The HLA-DRB1 locus as a genetic component in giant cell arteritis: Mapping of a diseaselinked sequence motif to the antigen binding site of the HLA-DR molecule. J Clin Invest. 1992; 90: 235561.Google Scholar
15.Polin, RS, Bavbek, M, Shaffrey, ME.Detection of soluble E-selectin, ICAM-1, VCAM-1 and L-selectin in the cerebrospinal fluid of patients after subarachnoid haemorrhage. J Neurosurg. 1998; 89: 55967.Google Scholar
16.Virchow, VR.Uber die akute Entzundung der Arterien. Virchows Arch A Pathol Anat Histopathol. 1947; 1: 272378.Google Scholar
17.Handler, FP, Blumenthal, HT.Inflammatory factors in the pathogenesis of cerebrovascular aneurysms. JAMA. 1954; 155: 147983.Google Scholar
18.Ryba, M, Jarzabek-Chorzelska, M, Chorzelski, T, et al.Is vascular angiopathy following intracranial aneurysm rupture immunologically mediated? Acta Neurochir (Wien). 1992; 117: 347.Google Scholar
19.Kosierkiewicz, TA, Factor, SM, Dickson, DW.Immunocytochemical studies of atherosclerotic lesions of cerebral berry aneurysms. J Neuropathol Exp Neurol. 1994; 53: 399406.Google Scholar
20.Schievink, WI.Intracranial aneurysms. N Engl J Med. 1997; 336: 2840.Google Scholar
21.Stehbens, WE.Etiology of intracranial berry aneurysms. J Neurosurg. 1989; 70: 82331.Google Scholar
22.Chyatte, D, Bruno, G.Inflammation and intracranial aneurysms. Neurosurgery. 1999; 45: 113756.Google Scholar
23.Frijns, CJM, Kasiu, KM, Algra, A.Endothelial cell activation markers and delayed cerebral ischaemia in patients with subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry. 2006; 77: 8637.Google Scholar
24.Nissen, JJ.Serum concentration of adhesion molecules in patients with delayed ischemic neurological deficit after aneurysmal subarachnoid hemorrhage: the immunoglobulin and selectin superfamilies. J Neurol Neurosurg Psychiatry. 2001; 71: 32933.Google Scholar
25.Tanriverdi, T, Sanus, GZ, Ulu, MOet al.Serum and cerebrospinal fluid concentrations of E-selectin in patients with aneurismal subarachnoid hemorrhage. Braz J Med Biol Res. 2005; 38: 170310.Google Scholar