Macrophage migration inhibitory factor reduces apoptosis in cerebral arteriovenous malformations

被引:16
|
作者
Chen, Guangzhong [1 ,2 ]
Zheng, Meng [1 ,2 ]
Shu, Hang [1 ,2 ]
Zhan, Shengquan [1 ,2 ]
Wang, Hongqin [1 ,2 ]
Zhou, Dong [1 ,2 ]
Zeng, Shaojian [1 ,2 ]
Tang, Kai [1 ,2 ]
Feng, Lei [3 ]
机构
[1] Guangdong Gen Hosp, Dept Neurosurg, Guangzhou 510080, Guangdong, Peoples R China
[2] Guangdong Acad Med Sci, Inst Neurosci, Guangzhou 510080, Guangdong, Peoples R China
[3] Univ Calif Los Angeles, David Geffen Sch Med, Div Intervent Neuroradiol, Los Angeles, CA 90095 USA
关键词
Cerebral arteriovenous malformation; Macrophage migration inhibitory factor; Caspase-3; Apoptosis; ENDOTHELIAL-CELLS; UP-REGULATION; EXPRESSION; ATHEROSCLEROSIS; ANGIOGENESIS; BRAIN; PATHWAY; DISEASE; TARGET; GENE;
D O I
10.1016/j.neulet.2011.12.024
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Purpose: To investigate the expression of macrophage migration inhibitory factor (MIF) in human brain arteriovenous malformations (AVM). Materials and methods: Twelve AVM specimens were obtained from patients who did not received preoperative embolization. MIF levels were measured by Western blot and matrix metalloproteinase 9 (MMP9) levels were measured by reverse transcription PCR The expression of MIF in brain AVMs was also evaluated by immunohistochemistry and was correlated with apoptosis and the expression of cleaved caspase-3 and MMP9. Results: The expression of MIF. MMP9, and cleaved caspase-3 was elevated in brain AVM vessels. High levels of MIF were primarily found in the endothelium and adventitia, whereas apoptotic cells were concentrated in the smooth muscle layer. Conclusions: Abnormal apoptosis may be involved in the pathogenesis of brain AVM. In addition, increased MIF expression could play an important role regulating the homeostasis of AVM vessels. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:84 / 88
页数:5
相关论文
共 50 条
  • [1] Macrophage migration inhibitory factor induces cardiomyocyte apoptosis
    Dhanantwari, Preeta
    Nadaraj, Sumekala
    Lenessey, Agnes
    Chowdhury, Devyani
    Al-Abed, Yousef
    Miller, Edmund J.
    Ojamaa, Kaie
    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2008, 371 (02) : 298 - 303
  • [2] The cytokine macrophage migration inhibitory factor reduces pro-oxidative stress-induced apoptosis
    Nguyen, MT
    Lue, HQ
    Kleemann, R
    Thiele, M
    Tolle, G
    Finkelmeier, D
    Wagner, E
    Braun, A
    Bernhagen, J
    JOURNAL OF IMMUNOLOGY, 2003, 170 (06): : 3337 - 3347
  • [3] Inhibition of macrophage migration inhibitory factor reduces dengue virus replication
    Yeh, T. -M.
    CYTOKINE, 2012, 59 (03) : 529 - 529
  • [4] Genetic deletion of macrophage migration inhibitory factor reduces oral carcinogenesis
    Oghumu, Steve
    Knobloch, Thomas
    Terrazas, Cesar
    Varikuti, Sanjay
    Bollinger, Claire
    Iwenofu, Hans
    Weghorst, Christopher
    Satoskar, Abhay
    CANCER RESEARCH, 2016, 76
  • [5] DELETION OF MACROPHAGE MIGRATION INHIBITORY FACTOR REDUCES SEVERITY OF OSTEOARTHRITIS IN MICE
    Greene, M. A.
    Roland, A. L.
    Pritzker, L.
    Carlson, C. S.
    Bucala, R. J.
    Miller, R. A.
    Loeser, R. F., Jr.
    OSTEOARTHRITIS AND CARTILAGE, 2014, 22 : S58 - S59
  • [6] Macrophage migration inhibitory factor
    Leng, L
    Bucala, R
    CRITICAL CARE MEDICINE, 2005, 33 (12) : S475 - S477
  • [7] Macrophage migration inhibitory factor
    Lolis, E
    Bucala, R
    EXPERT OPINION ON THERAPEUTIC TARGETS, 2003, 7 (02) : 153 - 164
  • [8] Macrophage migration inhibitory factor
    Baugh, JA
    Bucala, R
    CRITICAL CARE MEDICINE, 2002, 30 (01) : S27 - S35
  • [9] Absence of macrophage migration inhibitory factor reduces proliferative retinopathy in a mouse model
    Wang, Jing
    Lin, Jihong
    Kaiser, Ulrike
    Wohlfart, Paulus
    Hammes, Hans-Peter
    ACTA DIABETOLOGICA, 2017, 54 (04) : 383 - 392
  • [10] Neutralization of macrophage migration inhibitory factor (MIF) reduces GVHD but preserves GVL
    Miklos, Sandra
    Mueller, Gunnar
    Lindner, Petra
    Chang, Ya-Yi
    Holler, Ernst
    Bucala, Richard
    Hildebrandt, Gerhard C.
    BLOOD, 2007, 110 (11) : 950A - 950A