Galectin-3 causes enteric neuronal loss in mice after left sided permanent middle cerebral artery occlusion, a model of stroke
(2016) In Scientific Reports 6.- Abstract
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)... (More)
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 β-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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- author
- Cheng, Xiaowen LU ; Boza-Serrano, Antonio LU ; Turesson, Michelle Foldschak ; Deierborg, Tomas LU ; Ekblad, Eva LU and Voss, Ulrikke LU
- organization
- publishing date
- 2016-09-09
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Scientific Reports
- volume
- 6
- article number
- 32893
- publisher
- Nature Publishing Group
- external identifiers
-
- scopus:84986880504
- pmid:27612206
- wos:000391987700001
- ISSN
- 2045-2322
- DOI
- 10.1038/srep32893
- language
- English
- LU publication?
- yes
- id
- fa96fa73-ec97-4ce6-92cc-c08c236ee883
- date added to LUP
- 2016-11-04 14:19:50
- date last changed
- 2024-04-05 07:58:38
@article{fa96fa73-ec97-4ce6-92cc-c08c236ee883, abstract = {{<p>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 β-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.</p>}}, author = {{Cheng, Xiaowen and Boza-Serrano, Antonio and Turesson, Michelle Foldschak and Deierborg, Tomas and Ekblad, Eva and Voss, Ulrikke}}, issn = {{2045-2322}}, language = {{eng}}, month = {{09}}, publisher = {{Nature Publishing Group}}, series = {{Scientific Reports}}, title = {{Galectin-3 causes enteric neuronal loss in mice after left sided permanent middle cerebral artery occlusion, a model of stroke}}, url = {{http://dx.doi.org/10.1038/srep32893}}, doi = {{10.1038/srep32893}}, volume = {{6}}, year = {{2016}}, }