Macrophage migration inhibitory factor reduces apoptosis in cerebral arteriovenous malformations

► We used the human AVM specimens as the research objects. ► We investigated the relationship between MIF, apoptosis and cleaved caspase-3 expression. ► It is the first time to show the abnormal apoptosis may be involved in the pathogenesis of brain AVM. ► The increased MIF expression may play an im...

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Published inNeuroscience letters Vol. 508; no. 2; pp. 84 - 88
Main Authors Chen, Guangzhong, Zheng, Meng, Shu, Hang, Zhan, Shengquan, Wang, Hongqin, Zhou, Dong, Zeng, Shaojian, Tang, Kai, Feng, Lei
Format Journal Article
LanguageEnglish
Published Ireland Elsevier Ireland Ltd 06.02.2012
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Summary:► We used the human AVM specimens as the research objects. ► We investigated the relationship between MIF, apoptosis and cleaved caspase-3 expression. ► It is the first time to show the abnormal apoptosis may be involved in the pathogenesis of brain AVM. ► The increased MIF expression may play an important role regulating the homeostasis of AVM vessels. 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.
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ISSN:0304-3940
1872-7972
1872-7972
DOI:10.1016/j.neulet.2011.12.024