Galectin-3 is upregulated in microglial cells in response to ischemic brain lesions, but not to facial nerve axotomy.

Authors: Walther, M  Kuklinski, S  Pesheva, P  Guntinas-Lichius, O  Angelov, DN  Neiss, WF  Asou, H  Probstmeier, R 
Citation: Walther M, etal., J Neurosci Res. 2000 Aug 15;61(4):430-5.
Pubmed: (View Article at PubMed) PMID:10931529
DOI: Full-text: DOI:10.1002/1097-4547(20000815)61:4<430::AID-JNR9>3.0.CO;2-3

We have recently demonstrated that the beta-galactoside-specific lectin galectin-3 is expressed by microglial cells in vitro, but not by normal resting microglia in vivo. In the present study, we have analyzed the expression of galectin-3 by microglia under traumatic conditions in vivo using two experimental rat models which substantially differ in the severity of lesion related to a breakdown of the blood-brain barrier (BBB) and the occurrence of inflammatory processes. These two features are absent after peripheral nerve lesion and present after cerebral ischemia. Here we show that, following facial nerve axotomy under conditions allowing (nerve anastomosis) or not subsequent regeneration (nerve resection), galectin-3 is not expressed by microglia in the corresponding facial nucleus 1-112 days after lesion. Galectin-3 is also absent in microglia at sites of a defective BBB in the normal brain, such as the circumventricular organs. Following experimental ischemia (i.e., permanent occlusion of the middle cerebral artery), in contrast, galectin-3 becomes strongly expressed by activated microglia as early as 48 hours after trauma, as determined by immunohistochemistry and Western blot analysis. Our findings suggest that the expression of galectin-3 by microglia in vivo correlates with the state of microglial activation.

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CRRD ID: 9685227
Created: 2014-12-30
Species: All species
Last Modified: 2014-12-30
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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.