Activation of Alpha-7 Nicotinic Acetylcholine Receptor Reduces Brain Edema in Mice with Ischemic Stroke and Bone Fracture

Stroke is an important risk factor for bone fracture. We showed previously that bone fracture at the acute stage of ischemic stroke worsens, and activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) improves, stroke recovery by attenuating inflammation. We hypothesized that activation of α-...

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Veröffentlicht in:Molecular neurobiology 2017-12, Vol.54 (10), p.8278-8286
Hauptverfasser: Zou, Dingquan, Luo, Man, Han, Zhenying, Zhan, Lei, Zhu, Wan, Kang, Shuai, Bao, Chen, Li, Zhao, Nelson, Jeffrey, Zhang, Rui, Su, Hua
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container_end_page 8286
container_issue 10
container_start_page 8278
container_title Molecular neurobiology
container_volume 54
creator Zou, Dingquan
Luo, Man
Han, Zhenying
Zhan, Lei
Zhu, Wan
Kang, Shuai
Bao, Chen
Li, Zhao
Nelson, Jeffrey
Zhang, Rui
Su, Hua
description Stroke is an important risk factor for bone fracture. We showed previously that bone fracture at the acute stage of ischemic stroke worsens, and activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) improves, stroke recovery by attenuating inflammation. We hypothesized that activation of α-7 nAchR also improves the blood-brain barrier (BBB) integrity. Permanent distal middle cerebral artery occlusion (pMCAO) was performed on C57BL/6J mice followed by tibia fracture 1 day later. Mice were treated with 0.8 mg/kg PHA 568487 (PHA, α-7 nAchR-specific agonist), 6 mg/kg methyllycaconitine (MLA, α-7 nAchR antagonist), or saline 1 and 2 days after pMCAO. Brain water content, the expression of monoamine oxidase B (MAO-B), and tight junction protein (claudin-5) were assessed. We found that tibia fracture increased water content in the ischemic stroke brain ( p  = 0.006) and MAO-B-positive astrocytes ( p  
doi_str_mv 10.1007/s12035-016-0310-8
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We showed previously that bone fracture at the acute stage of ischemic stroke worsens, and activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) improves, stroke recovery by attenuating inflammation. We hypothesized that activation of α-7 nAchR also improves the blood-brain barrier (BBB) integrity. Permanent distal middle cerebral artery occlusion (pMCAO) was performed on C57BL/6J mice followed by tibia fracture 1 day later. Mice were treated with 0.8 mg/kg PHA 568487 (PHA, α-7 nAchR-specific agonist), 6 mg/kg methyllycaconitine (MLA, α-7 nAchR antagonist), or saline 1 and 2 days after pMCAO. Brain water content, the expression of monoamine oxidase B (MAO-B), and tight junction protein (claudin-5) were assessed. We found that tibia fracture increased water content in the ischemic stroke brain ( p  = 0.006) and MAO-B-positive astrocytes ( p  &lt; 0.001). PHA treatment reduced water content and MAO-B-positive astrocytes and increased claudin-5 expression in stroke and stroke + tibia fracture mice ( p  &lt; 0.05), while MLA had the opposite effect. Our findings suggest that in addition to inhibiting inflammation, activation of α-7 nAchR also reduces brain edema, possibly through diminished astrocyte oxidative stress and improved BBB integrity. 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All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-f9a6b6c8cdbdb6cd967f14b7b8ffafb2cf89d243af0ca388baa4a83c556edfd83</citedby><cites>FETCH-LOGICAL-c470t-f9a6b6c8cdbdb6cd967f14b7b8ffafb2cf89d243af0ca388baa4a83c556edfd83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-016-0310-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-016-0310-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27914011$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zou, Dingquan</creatorcontrib><creatorcontrib>Luo, Man</creatorcontrib><creatorcontrib>Han, Zhenying</creatorcontrib><creatorcontrib>Zhan, Lei</creatorcontrib><creatorcontrib>Zhu, Wan</creatorcontrib><creatorcontrib>Kang, Shuai</creatorcontrib><creatorcontrib>Bao, Chen</creatorcontrib><creatorcontrib>Li, Zhao</creatorcontrib><creatorcontrib>Nelson, Jeffrey</creatorcontrib><creatorcontrib>Zhang, Rui</creatorcontrib><creatorcontrib>Su, Hua</creatorcontrib><title>Activation of Alpha-7 Nicotinic Acetylcholine Receptor Reduces Brain Edema in Mice with Ischemic Stroke and Bone Fracture</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>Stroke is an important risk factor for bone fracture. We showed previously that bone fracture at the acute stage of ischemic stroke worsens, and activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) improves, stroke recovery by attenuating inflammation. We hypothesized that activation of α-7 nAchR also improves the blood-brain barrier (BBB) integrity. Permanent distal middle cerebral artery occlusion (pMCAO) was performed on C57BL/6J mice followed by tibia fracture 1 day later. Mice were treated with 0.8 mg/kg PHA 568487 (PHA, α-7 nAchR-specific agonist), 6 mg/kg methyllycaconitine (MLA, α-7 nAchR antagonist), or saline 1 and 2 days after pMCAO. Brain water content, the expression of monoamine oxidase B (MAO-B), and tight junction protein (claudin-5) were assessed. We found that tibia fracture increased water content in the ischemic stroke brain ( p  = 0.006) and MAO-B-positive astrocytes ( p  &lt; 0.001). PHA treatment reduced water content and MAO-B-positive astrocytes and increased claudin-5 expression in stroke and stroke + tibia fracture mice ( p  &lt; 0.05), while MLA had the opposite effect. Our findings suggest that in addition to inhibiting inflammation, activation of α-7 nAchR also reduces brain edema, possibly through diminished astrocyte oxidative stress and improved BBB integrity. Thus, the α-7 nAchR-specific agonist could be developed into a new therapy for improving recovery of patients with stroke or stroke + bone fracture.</description><subject>Acetylcholine</subject><subject>Acetylcholine receptors (nicotinic)</subject><subject>Activation</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>Amine oxidase (flavin-containing)</subject><subject>Animals</subject><subject>Astrocytes</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood-brain barrier</subject><subject>Brain Edema - metabolism</subject><subject>Brain Edema - pathology</subject><subject>Brain Edema - prevention &amp; control</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Brain Ischemia - prevention &amp; control</subject><subject>Cell Biology</subject><subject>Cerebral blood flow</subject><subject>Edema</subject><subject>Fractures</subject><subject>Fractures, Bone - metabolism</subject><subject>Fractures, Bone - pathology</subject><subject>Fractures, Bone - prevention &amp; 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We showed previously that bone fracture at the acute stage of ischemic stroke worsens, and activation of α-7 nicotinic acetylcholine receptor (α-7 nAchR) improves, stroke recovery by attenuating inflammation. We hypothesized that activation of α-7 nAchR also improves the blood-brain barrier (BBB) integrity. Permanent distal middle cerebral artery occlusion (pMCAO) was performed on C57BL/6J mice followed by tibia fracture 1 day later. Mice were treated with 0.8 mg/kg PHA 568487 (PHA, α-7 nAchR-specific agonist), 6 mg/kg methyllycaconitine (MLA, α-7 nAchR antagonist), or saline 1 and 2 days after pMCAO. Brain water content, the expression of monoamine oxidase B (MAO-B), and tight junction protein (claudin-5) were assessed. We found that tibia fracture increased water content in the ischemic stroke brain ( p  = 0.006) and MAO-B-positive astrocytes ( p  &lt; 0.001). PHA treatment reduced water content and MAO-B-positive astrocytes and increased claudin-5 expression in stroke and stroke + tibia fracture mice ( p  &lt; 0.05), while MLA had the opposite effect. Our findings suggest that in addition to inhibiting inflammation, activation of α-7 nAchR also reduces brain edema, possibly through diminished astrocyte oxidative stress and improved BBB integrity. Thus, the α-7 nAchR-specific agonist could be developed into a new therapy for improving recovery of patients with stroke or stroke + bone fracture.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>27914011</pmid><doi>10.1007/s12035-016-0310-8</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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subjects Acetylcholine
Acetylcholine receptors (nicotinic)
Activation
alpha7 Nicotinic Acetylcholine Receptor - metabolism
Amine oxidase (flavin-containing)
Animals
Astrocytes
Biomedical and Life Sciences
Biomedicine
Blood-brain barrier
Brain Edema - metabolism
Brain Edema - pathology
Brain Edema - prevention & control
Brain Ischemia - metabolism
Brain Ischemia - pathology
Brain Ischemia - prevention & control
Cell Biology
Cerebral blood flow
Edema
Fractures
Fractures, Bone - metabolism
Fractures, Bone - pathology
Fractures, Bone - prevention & control
Ischemia
Male
Methyllycaconitine
Mice
Mice, Inbred C57BL
Moisture content
Neurobiology
Neurology
Neurosciences
Oxidative stress
Random Allocation
Risk factors
Stroke
Stroke - metabolism
Stroke - pathology
Stroke - prevention & control
Tibia
Tibia - injuries
Tibia - metabolism
Water content
Water treatment
title Activation of Alpha-7 Nicotinic Acetylcholine Receptor Reduces Brain Edema in Mice with Ischemic Stroke and Bone Fracture
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