Journal
SCIENTIFIC REPORTS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep32893
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Funding
- Swedish Medical Research Council
- Swedish National Stroke Foundation
- Pahlssons Foundation
- Sparbanken Foundation Fars Frosta
- Royal Physiographic Society
- Faculty of Medicine, Lund University
- China Scholarship Council
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In addition to brain injury stroke patients often suffer gastrointestinal complications. Neuroimmune interactions involving galectin-3, released from microglia in the brain, mediates the post-stroke pro-inflammatory response. We investigated possible consequences of stroke on the enteric nervous system and the involvement of galectin-3. We show that permanent middle cerebral artery occlusion (pMCAO) induces loss of enteric neurons in ileum and colon in galectin-3(+/+), but not in galectin-3(-/-), mice. In vitro we show that serum from galectin-3(+/+), but not from galectin-3(-/-), mice subjected to pMCAO, caused loss of C57BL/6J myenteric neurons, while myenteric neurons derived from TLR4(-/-) mice were unaffected. Further purified galectin-3 (10(-6) M) caused loss of cultured C57BL/6J myenteric neurons. Inhibitors of transforming growth factor beta-activated kinase 1 (TAK1) or AMP activated kinase (AMPK) counteracted both the purified galectin-3 and the galectin-3(+/+) pMCAO serum-induced loss in vitro. Combined we show that stroke (pMCAO) triggers central and peripheral galectin-3 release causing enteric neuronal loss through a TLR4 mediated mechanism involving TAK1 and AMPK. Galectin-3 is suggested a target for treatment of post-stroke complications.
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