Significance of cyclooxygenase-2 elevation in middle cerebral artery for patients with hemorrhagic moyamoya disease.
10.1007/s11596-016-1563-1
- Author:
Jian-jian ZHANG
1
;
Zhong-wei XIONG
1
;
Sheng WANG
2
;
Shou-jia SUN
2
;
Hao WANG
2
;
Xiao-lin WU
2
;
Long WANG
2
;
Hua-qiu ZHANG
2
;
Chao YOU
2
;
Yu WANG
2
;
Jin-cao CHEN
3
Author Information
1. Department of Neurosurgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
2. Department of Neurosurgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
3. Department of Neurosurgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China. chenjincao2012@hotmail.com.
- Publication Type:Journal Article
- Keywords:
COX-2;
hemorrhage;
inflammation;
middle cerebral artery;
moyamoya disease
- MeSH:
Adult;
Case-Control Studies;
Cyclooxygenase 2;
genetics;
metabolism;
Female;
Humans;
Intracranial Hemorrhages;
enzymology;
etiology;
Male;
Middle Aged;
Middle Cerebral Artery;
metabolism;
Moyamoya Disease;
complications;
enzymology
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2016;36(2):181-185
- CountryChina
- Language:English
-
Abstract:
The etiology and pathogenesis of moyamoya disease (MMD) remain elusive. Some inflammatory proteins, such as cyclooxygenase (COX)-2, are believed to be implicated in the development of MMD. So far, the relationship between COX-2 and MMD is poorly understood and reports on the intracranial vessels of MMD patients are scanty. In this study, tiny pieces of middle cerebral artery (MCA) and superficial temporal artery (STA) from 13 MMD patients were surgically harvested. The MCA and STA samples from 5 control patients were also collected by using the same technique. The expression of COX-2 was immunohistochemically detected and the average absorbance (A) of positively-stained areas was measured. High-level COX-2 expression was found in all layers of the MCA samples from all 5 hemorrhagic MMD patients, while positive but weak expression of COX-2 was observed only in the endothelial layer of the MCA samples from most ischemic MMD patients (6/8, 75%). The average A values of COX-2 in the hemorrhagic MMD patients were substantially higher than those in their ischemic counterparts (t=4.632, P=0.001). There was no significant difference in the COX-2 expression among the "gender" groups, or "radiographic grade" groups, or "lesion location" groups (P>0.05 for all). The COX-2 expression was detected neither in the MCA samples from the controls nor in all STA specimens. Our results suggested that COX-2 was up-regulated in the MCA of MMD patients, especially in hemorrhagic MMD patients. We are led to speculate that COX-2 may be involved in the pathogenesis of MMD and even contribute to the hemorrhagic stroke of MMD patients.
