Alpha7 nicotinic acetylcholine receptor is required for amyloid pathology in brain endothelial cells induced by Glycoprotein 120, methamphetamine and nicotine
One of the most challenging issues in HIV-associated neurocognitive disorders (HAND) caused by HIV-1 virotoxins and drug abuse is the lack of understanding the underlying mechanisms that are commonly associated with disorders of the blood-brain barrier (BBB), which mainly consists of brain microvasc...
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| Veröffentlicht in: | Scientific reports 2017-01, Vol.7 (1), p.40467-40467, Article 40467 |
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| creator | Liu, Liqun Yu, Jingyi Li, Li Zhang, Bao Liu, Lingjuan Wu, Chun-Hua Jong, Ambrose Mao, Ding-An Huang, Sheng-He |
| description | One of the most challenging issues in HIV-associated neurocognitive disorders (HAND) caused by HIV-1 virotoxins and drug abuse is the lack of understanding the underlying mechanisms that are commonly associated with disorders of the blood-brain barrier (BBB), which mainly consists of brain microvascular endothelial cells (BMEC). Here, we hypothesized that Glycoprotein 120 (gp120), methamphetamine (METH) and nicotine (NT) can enhance amyloid-beta (Aβ) accumulation in BMEC through Alpha7 nicotinic acetylcholine receptor (α7 nAChR). Both
in vitro
(human BMEC) (HBMEC) and
in vivo
(mice) models of BBB were used to dissect the role of α7 nAChR in up-regulation of Aβ induced by gp120, METH and NT. Aβ release from and transport across HBMEC were significantly increased by these factors. Methyllycaconitine (MLA), an antagonist of α7 nAChR, could efficiently block these pathogenic effects. Furthermore, our animal data showed that these factors could significantly increase the levels of Aβ, Tau and Ubiquitin C-Terminal Hydrolase L1 (UCHL1) in mouse cerebrospinal fluid (CSF) and Aβ in the mouse brains. These pathogenicities were significantly reduced by MLA, suggesting that α7 nAChR may play an important role in neuropathology caused by gp120, METH and NT, which are the major pathogenic factors contributing to the pathogenesis of HAND. |
| doi_str_mv | 10.1038/srep40467 |
| format | Article |
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in vitro
(human BMEC) (HBMEC) and
in vivo
(mice) models of BBB were used to dissect the role of α7 nAChR in up-regulation of Aβ induced by gp120, METH and NT. Aβ release from and transport across HBMEC were significantly increased by these factors. Methyllycaconitine (MLA), an antagonist of α7 nAChR, could efficiently block these pathogenic effects. Furthermore, our animal data showed that these factors could significantly increase the levels of Aβ, Tau and Ubiquitin C-Terminal Hydrolase L1 (UCHL1) in mouse cerebrospinal fluid (CSF) and Aβ in the mouse brains. These pathogenicities were significantly reduced by MLA, suggesting that α7 nAChR may play an important role in neuropathology caused by gp120, METH and NT, which are the major pathogenic factors contributing to the pathogenesis of HAND.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep40467</identifier><identifier>PMID: 28074940</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>14/34 ; 14/63 ; 631/378 ; 64/60 ; 692/4017 ; 82/51 ; 82/80 ; Acetylcholine receptors (nicotinic) ; Aconitine - analogs & derivatives ; Aconitine - pharmacology ; alpha7 Nicotinic Acetylcholine Receptor - antagonists & inhibitors ; alpha7 Nicotinic Acetylcholine Receptor - metabolism ; Alzheimer Disease - blood ; Alzheimer Disease - cerebrospinal fluid ; Alzheimer Disease - pathology ; Amyloid - metabolism ; Amyloid beta-Peptides - metabolism ; Animal models ; Animals ; Biomarkers - metabolism ; Blood-brain barrier ; Blood-Brain Barrier - drug effects ; Blood-Brain Barrier - injuries ; Blood-Brain Barrier - metabolism ; Blood-Brain Barrier - pathology ; Brain ; Brain - pathology ; Cell Movement - drug effects ; Cellular Senescence - drug effects ; Cerebrospinal fluid ; Cognition ; Drug abuse ; Endothelial cells ; Endothelial Cells - drug effects ; Endothelial Cells - metabolism ; Glycoprotein gp120 ; Glycoproteins ; HIV Envelope Protein gp120 - pharmacology ; HL-60 Cells ; Humanities and Social Sciences ; Humans ; Hydrolase ; Methamphetamine ; Methamphetamine - pharmacology ; Methyllycaconitine ; Mice, Inbred C57BL ; Microvasculature ; Monocytes - drug effects ; Monocytes - metabolism ; multidisciplinary ; Nicotine ; Nicotine - pharmacology ; Protein Transport - drug effects ; Receptor for Advanced Glycation End Products - metabolism ; S100 Proteins - metabolism ; Science ; Science (multidisciplinary) ; Tau protein ; Time Factors ; Ubiquitin ; Ubiquitin thiolesterase ; β-Amyloid</subject><ispartof>Scientific reports, 2017-01, Vol.7 (1), p.40467-40467, Article 40467</ispartof><rights>The Author(s) 2017</rights><rights>Copyright Nature Publishing Group Jan 2017</rights><rights>Copyright © 2017, The Author(s) 2017 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-8414d1d48fbaec73a2c370c36abad20b3178be049d4a1567c4c5f096a7856f513</citedby><cites>FETCH-LOGICAL-c504t-8414d1d48fbaec73a2c370c36abad20b3178be049d4a1567c4c5f096a7856f513</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5225415/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5225415/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,41099,42168,51554,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28074940$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Liqun</creatorcontrib><creatorcontrib>Yu, Jingyi</creatorcontrib><creatorcontrib>Li, Li</creatorcontrib><creatorcontrib>Zhang, Bao</creatorcontrib><creatorcontrib>Liu, Lingjuan</creatorcontrib><creatorcontrib>Wu, Chun-Hua</creatorcontrib><creatorcontrib>Jong, Ambrose</creatorcontrib><creatorcontrib>Mao, Ding-An</creatorcontrib><creatorcontrib>Huang, Sheng-He</creatorcontrib><title>Alpha7 nicotinic acetylcholine receptor is required for amyloid pathology in brain endothelial cells induced by Glycoprotein 120, methamphetamine and nicotine</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>One of the most challenging issues in HIV-associated neurocognitive disorders (HAND) caused by HIV-1 virotoxins and drug abuse is the lack of understanding the underlying mechanisms that are commonly associated with disorders of the blood-brain barrier (BBB), which mainly consists of brain microvascular endothelial cells (BMEC). Here, we hypothesized that Glycoprotein 120 (gp120), methamphetamine (METH) and nicotine (NT) can enhance amyloid-beta (Aβ) accumulation in BMEC through Alpha7 nicotinic acetylcholine receptor (α7 nAChR). Both
in vitro
(human BMEC) (HBMEC) and
in vivo
(mice) models of BBB were used to dissect the role of α7 nAChR in up-regulation of Aβ induced by gp120, METH and NT. Aβ release from and transport across HBMEC were significantly increased by these factors. Methyllycaconitine (MLA), an antagonist of α7 nAChR, could efficiently block these pathogenic effects. Furthermore, our animal data showed that these factors could significantly increase the levels of Aβ, Tau and Ubiquitin C-Terminal Hydrolase L1 (UCHL1) in mouse cerebrospinal fluid (CSF) and Aβ in the mouse brains. These pathogenicities were significantly reduced by MLA, suggesting that α7 nAChR may play an important role in neuropathology caused by gp120, METH and NT, which are the major pathogenic factors contributing to the pathogenesis of HAND.</description><subject>14/34</subject><subject>14/63</subject><subject>631/378</subject><subject>64/60</subject><subject>692/4017</subject><subject>82/51</subject><subject>82/80</subject><subject>Acetylcholine receptors (nicotinic)</subject><subject>Aconitine - analogs & derivatives</subject><subject>Aconitine - pharmacology</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - antagonists & inhibitors</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>Alzheimer Disease - blood</subject><subject>Alzheimer Disease - cerebrospinal fluid</subject><subject>Alzheimer Disease - pathology</subject><subject>Amyloid - metabolism</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>Animal models</subject><subject>Animals</subject><subject>Biomarkers - metabolism</subject><subject>Blood-brain barrier</subject><subject>Blood-Brain Barrier - drug effects</subject><subject>Blood-Brain Barrier - injuries</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>Blood-Brain Barrier - pathology</subject><subject>Brain</subject><subject>Brain - pathology</subject><subject>Cell Movement - drug effects</subject><subject>Cellular Senescence - drug effects</subject><subject>Cerebrospinal fluid</subject><subject>Cognition</subject><subject>Drug abuse</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - metabolism</subject><subject>Glycoprotein gp120</subject><subject>Glycoproteins</subject><subject>HIV Envelope Protein gp120 - pharmacology</subject><subject>HL-60 Cells</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Hydrolase</subject><subject>Methamphetamine</subject><subject>Methamphetamine - pharmacology</subject><subject>Methyllycaconitine</subject><subject>Mice, Inbred C57BL</subject><subject>Microvasculature</subject><subject>Monocytes - drug effects</subject><subject>Monocytes - metabolism</subject><subject>multidisciplinary</subject><subject>Nicotine</subject><subject>Nicotine - pharmacology</subject><subject>Protein Transport - drug effects</subject><subject>Receptor for Advanced Glycation End Products - metabolism</subject><subject>S100 Proteins - metabolism</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Tau protein</subject><subject>Time Factors</subject><subject>Ubiquitin</subject><subject>Ubiquitin thiolesterase</subject><subject>β-Amyloid</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkcFu1DAQhiMEolXpgRdAlrgAYsF27Di5IFVVKUiVuMA5mjiTjSvHTm2nUl6GZ8XbbVcL-DAeaz7_M6O_KF4z-onRsv4cA86Ciko9K045FXLDS86fH-UnxXmMtzQfyRvBmpfFCa-pEo2gp8XvCzuPoIgz2ieTIwGNabV69NY4JAE1zskHYmLO7xYTsCdDfsO0Wm96MkPKqN-uxDjSBcgRXe_TiNaAJRqtjbnULzp_7FZybVft5-ATZpJx-pFMmEaY5hETTLuW4PqncfBV8WIAG_H88T4rfn29-nn5bXPz4_r75cXNRksq0qYWTPSsF_XQAWpVAtelorqsoIOe065kqu6QiqYXwGSltNByoE0FqpbVIFl5VnzZ685LN2Gv0aUAtp2DmSCsrQfT_l1xZmy3_r6VnEvBZBZ49ygQ_N2CMbWTibvlwaFfYstqqZTkiu96vf0HvfVLcHm9TDWNZFQ-CL7fUzr4mD0eDsMw2u6Mbw_GZ_bN8fQH8snmDHzYAzGX3BbDUcv_1P4A5S669A</recordid><startdate>20170111</startdate><enddate>20170111</enddate><creator>Liu, Liqun</creator><creator>Yu, Jingyi</creator><creator>Li, Li</creator><creator>Zhang, Bao</creator><creator>Liu, Lingjuan</creator><creator>Wu, Chun-Hua</creator><creator>Jong, Ambrose</creator><creator>Mao, Ding-An</creator><creator>Huang, Sheng-He</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20170111</creationdate><title>Alpha7 nicotinic acetylcholine receptor is required for amyloid pathology in brain endothelial cells induced by Glycoprotein 120, methamphetamine and nicotine</title><author>Liu, Liqun ; Yu, Jingyi ; Li, Li ; Zhang, Bao ; Liu, Lingjuan ; Wu, Chun-Hua ; Jong, Ambrose ; Mao, Ding-An ; Huang, Sheng-He</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-8414d1d48fbaec73a2c370c36abad20b3178be049d4a1567c4c5f096a7856f513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>14/34</topic><topic>14/63</topic><topic>631/378</topic><topic>64/60</topic><topic>692/4017</topic><topic>82/51</topic><topic>82/80</topic><topic>Acetylcholine receptors (nicotinic)</topic><topic>Aconitine - analogs & derivatives</topic><topic>Aconitine - pharmacology</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - antagonists & inhibitors</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - metabolism</topic><topic>Alzheimer Disease - blood</topic><topic>Alzheimer Disease - cerebrospinal fluid</topic><topic>Alzheimer Disease - pathology</topic><topic>Amyloid - metabolism</topic><topic>Amyloid beta-Peptides - metabolism</topic><topic>Animal models</topic><topic>Animals</topic><topic>Biomarkers - metabolism</topic><topic>Blood-brain barrier</topic><topic>Blood-Brain Barrier - drug effects</topic><topic>Blood-Brain Barrier - injuries</topic><topic>Blood-Brain Barrier - metabolism</topic><topic>Blood-Brain Barrier - pathology</topic><topic>Brain</topic><topic>Brain - pathology</topic><topic>Cell Movement - drug effects</topic><topic>Cellular Senescence - drug effects</topic><topic>Cerebrospinal fluid</topic><topic>Cognition</topic><topic>Drug abuse</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - metabolism</topic><topic>Glycoprotein gp120</topic><topic>Glycoproteins</topic><topic>HIV Envelope Protein gp120 - pharmacology</topic><topic>HL-60 Cells</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Hydrolase</topic><topic>Methamphetamine</topic><topic>Methamphetamine - pharmacology</topic><topic>Methyllycaconitine</topic><topic>Mice, Inbred C57BL</topic><topic>Microvasculature</topic><topic>Monocytes - drug effects</topic><topic>Monocytes - metabolism</topic><topic>multidisciplinary</topic><topic>Nicotine</topic><topic>Nicotine - pharmacology</topic><topic>Protein Transport - drug effects</topic><topic>Receptor for Advanced Glycation End Products - metabolism</topic><topic>S100 Proteins - metabolism</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Tau protein</topic><topic>Time Factors</topic><topic>Ubiquitin</topic><topic>Ubiquitin thiolesterase</topic><topic>β-Amyloid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Liqun</creatorcontrib><creatorcontrib>Yu, Jingyi</creatorcontrib><creatorcontrib>Li, Li</creatorcontrib><creatorcontrib>Zhang, Bao</creatorcontrib><creatorcontrib>Liu, Lingjuan</creatorcontrib><creatorcontrib>Wu, Chun-Hua</creatorcontrib><creatorcontrib>Jong, Ambrose</creatorcontrib><creatorcontrib>Mao, Ding-An</creatorcontrib><creatorcontrib>Huang, Sheng-He</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Liqun</au><au>Yu, Jingyi</au><au>Li, Li</au><au>Zhang, Bao</au><au>Liu, Lingjuan</au><au>Wu, Chun-Hua</au><au>Jong, Ambrose</au><au>Mao, Ding-An</au><au>Huang, Sheng-He</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alpha7 nicotinic acetylcholine receptor is required for amyloid pathology in brain endothelial cells induced by Glycoprotein 120, methamphetamine and nicotine</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2017-01-11</date><risdate>2017</risdate><volume>7</volume><issue>1</issue><spage>40467</spage><epage>40467</epage><pages>40467-40467</pages><artnum>40467</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>One of the most challenging issues in HIV-associated neurocognitive disorders (HAND) caused by HIV-1 virotoxins and drug abuse is the lack of understanding the underlying mechanisms that are commonly associated with disorders of the blood-brain barrier (BBB), which mainly consists of brain microvascular endothelial cells (BMEC). Here, we hypothesized that Glycoprotein 120 (gp120), methamphetamine (METH) and nicotine (NT) can enhance amyloid-beta (Aβ) accumulation in BMEC through Alpha7 nicotinic acetylcholine receptor (α7 nAChR). Both
in vitro
(human BMEC) (HBMEC) and
in vivo
(mice) models of BBB were used to dissect the role of α7 nAChR in up-regulation of Aβ induced by gp120, METH and NT. Aβ release from and transport across HBMEC were significantly increased by these factors. Methyllycaconitine (MLA), an antagonist of α7 nAChR, could efficiently block these pathogenic effects. Furthermore, our animal data showed that these factors could significantly increase the levels of Aβ, Tau and Ubiquitin C-Terminal Hydrolase L1 (UCHL1) in mouse cerebrospinal fluid (CSF) and Aβ in the mouse brains. These pathogenicities were significantly reduced by MLA, suggesting that α7 nAChR may play an important role in neuropathology caused by gp120, METH and NT, which are the major pathogenic factors contributing to the pathogenesis of HAND.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>28074940</pmid><doi>10.1038/srep40467</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Scientific reports, 2017-01, Vol.7 (1), p.40467-40467, Article 40467 |
| issn | 2045-2322 2045-2322 |
| language | eng |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Springer Nature OA Free Journals; Nature Free; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | 14/34 14/63 631/378 64/60 692/4017 82/51 82/80 Acetylcholine receptors (nicotinic) Aconitine - analogs & derivatives Aconitine - pharmacology alpha7 Nicotinic Acetylcholine Receptor - antagonists & inhibitors alpha7 Nicotinic Acetylcholine Receptor - metabolism Alzheimer Disease - blood Alzheimer Disease - cerebrospinal fluid Alzheimer Disease - pathology Amyloid - metabolism Amyloid beta-Peptides - metabolism Animal models Animals Biomarkers - metabolism Blood-brain barrier Blood-Brain Barrier - drug effects Blood-Brain Barrier - injuries Blood-Brain Barrier - metabolism Blood-Brain Barrier - pathology Brain Brain - pathology Cell Movement - drug effects Cellular Senescence - drug effects Cerebrospinal fluid Cognition Drug abuse Endothelial cells Endothelial Cells - drug effects Endothelial Cells - metabolism Glycoprotein gp120 Glycoproteins HIV Envelope Protein gp120 - pharmacology HL-60 Cells Humanities and Social Sciences Humans Hydrolase Methamphetamine Methamphetamine - pharmacology Methyllycaconitine Mice, Inbred C57BL Microvasculature Monocytes - drug effects Monocytes - metabolism multidisciplinary Nicotine Nicotine - pharmacology Protein Transport - drug effects Receptor for Advanced Glycation End Products - metabolism S100 Proteins - metabolism Science Science (multidisciplinary) Tau protein Time Factors Ubiquitin Ubiquitin thiolesterase β-Amyloid |
| title | Alpha7 nicotinic acetylcholine receptor is required for amyloid pathology in brain endothelial cells induced by Glycoprotein 120, methamphetamine and nicotine |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-24T08%3A38%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Alpha7%20nicotinic%20acetylcholine%20receptor%20is%20required%20for%20amyloid%20pathology%20in%20brain%20endothelial%20cells%20induced%20by%20Glycoprotein%20120,%20methamphetamine%20and%20nicotine&rft.jtitle=Scientific%20reports&rft.au=Liu,%20Liqun&rft.date=2017-01-11&rft.volume=7&rft.issue=1&rft.spage=40467&rft.epage=40467&rft.pages=40467-40467&rft.artnum=40467&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/srep40467&rft_dat=%3Cproquest_pubme%3E1899510515%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1899510515&rft_id=info:pmid/28074940&rfr_iscdi=true |