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 in | Neuroscience letters Vol. 508; no. 2; pp. 84 - 88 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Ireland
Elsevier Ireland Ltd
06.02.2012
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Subjects | |
Online Access | Get full text |
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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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Article-2 ObjectType-Feature-1 |
ISSN: | 0304-3940 1872-7972 1872-7972 |
DOI: | 10.1016/j.neulet.2011.12.024 |