Differential Mechanisms of Inflammation and Endothelial Dysfunction by HIV-1 Subtype-B and Recombinant CRF02_AG Tat Proteins on Human Brain Microvascular Endothelial Cells: Implications for Viral Neuropathogenesis
The recombinant HIV-1 CRF02_AG is prevalent in West-Central Africa but its effects on the blood-brain barrier (BBB) and HIV-associated neurocognitive disorders (HAND) are not known. We analyzed the effects of Tat from HIV-1 subtype-B (Tat.B) and CRF02_AG (Tat.AG) on primary human brain microvascular...
Gespeichert in:
| Veröffentlicht in: | Molecular neurobiology 2018-02, Vol.55 (2), p.1352-1363 |
|---|---|
| Hauptverfasser: | , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1363 |
|---|---|
| container_issue | 2 |
| container_start_page | 1352 |
| container_title | Molecular neurobiology |
| container_volume | 55 |
| creator | Bhargavan, Biju Kanmogne, Georgette D. |
| description | The recombinant HIV-1 CRF02_AG is prevalent in West-Central Africa but its effects on the blood-brain barrier (BBB) and HIV-associated neurocognitive disorders (HAND) are not known. We analyzed the effects of Tat from HIV-1 subtype-B (Tat.B) and CRF02_AG (Tat.AG) on primary human brain microvascular endothelial cells (HBMEC), the major BBB component. Exposure of HBMEC to Tat.B increased IL-6 expression and transcription by 9- (
P
|
| doi_str_mv | 10.1007/s12035-017-0382-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6507400</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1862766747</sourcerecordid><originalsourceid>FETCH-LOGICAL-c470t-414a2756016c6dfff562b137d7944f16c63212a1ed5927a19b7aa6c93a4482a63</originalsourceid><addsrcrecordid>eNp1ks1u1DAUhSMEokPhAdggS2zYBGzHsRMWSO30Z0ZqAZXSrXXj2DOuEnuwk0rzoLwPzkwpFImVJd_P5557fbLsNcHvCcbiQyQUF2WOichxUdEcP8lmpCzrnJCKPs1muKqLXHBWHWQvYrzFmFKCxfPsgFaECl6LWfbzxBqjg3aDhQ5darUGZ2MfkTdo6UwHfQ-D9Q6Ba9Gpa_2w1t2EnmyjGZ3a1ZotWixvcoK-jc2w3ej8eIdfaeX7xjpwA5pfnWEqj87RNQzoa_CDti41cWgx9uDQcQDr0KVVwd9BVGMH4VG3ue66-BEt-01n1c5QRMYHdGNDqn7WY_AbGNZ-pZ2ONr7Mnhnoon51fx5m389Or-eL_OLL-XJ-dJErJvCQM8KAipJjwhVvjTElpw0pRCtqxsx0WVBCgei2rKkAUjcCgKu6AMYqCrw4zD7tdTdj0-tWpTUmP3ITbA9hKz1Y-bji7Fqu_J3kJRYM4yTw7l4g-B-jjoPsbVRpWHDaj1GSiqeP4oKJhL79B731Y3BpPEkxnhBalIkieyptMsagzYMZguUUGrkPjUyhkVNo5GTizd9TPLz4nZIE0D0QU8mtdPjT-v-qvwBfYNAK</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2006747235</pqid></control><display><type>article</type><title>Differential Mechanisms of Inflammation and Endothelial Dysfunction by HIV-1 Subtype-B and Recombinant CRF02_AG Tat Proteins on Human Brain Microvascular Endothelial Cells: Implications for Viral Neuropathogenesis</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Bhargavan, Biju ; Kanmogne, Georgette D.</creator><creatorcontrib>Bhargavan, Biju ; Kanmogne, Georgette D.</creatorcontrib><description>The recombinant HIV-1 CRF02_AG is prevalent in West-Central Africa but its effects on the blood-brain barrier (BBB) and HIV-associated neurocognitive disorders (HAND) are not known. We analyzed the effects of Tat from HIV-1 subtype-B (Tat.B) and CRF02_AG (Tat.AG) on primary human brain microvascular endothelial cells (HBMEC), the major BBB component. Exposure of HBMEC to Tat.B increased IL-6 expression and transcription by 9- (
P
< 0.001) and 113-fold (
P
< 0.001), respectively, whereas Tat.AG increased IL-6 expression and transcription by 2.7–3.8-fold and 35.7-fold (
P
< 0.001), respectively. Tat.B induced IL-6 through the interleukin-1 receptor-associated kinase (IRAK)-1/4/mitogen-activated protein kinase kinase(MKK)/C-jun N-terminal kinase(JNK) pathways, in an activator protein-1(AP1)- and nuclear factor-kappaB (NFκB)-independent manner, whereas Tat.AG effects occurred via MKK/JNK/AP1/NFκB pathways. Tat-induced effects were associated with activation of c-jun (serine-63) and SAPK/JNK (Thr183/Tyr185). We demonstrated increased expression of transcription factors associated with these pathways (Jun, RELB, CEBPA), with higher levels in Tat.B-treated cells compared to Tat.AG. Functional studies showed that Tat.B and Tat.AG decreased the expression of tight junction proteins claudin-5 and ZO-1 and decreased the trans-endothelial electric resistance (TEER); Tat.B induced greater reduction in TEER, claudin-5, and ZO-1, compared to Tat.AG. Overall, our data showed increased inflammation and BBB dysfunction with Tat.B, compared to Tat.AG. This suggests these two HIV-1 subtypes differentially affect the BBB and central nervous system; our data provides novel insights into the molecular basis of these differential Tat-mediated effects.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-017-0382-0</identifier><identifier>PMID: 28127697</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Activator protein 1 ; Biomedical and Life Sciences ; Biomedicine ; Blood-brain barrier ; Blood-Brain Barrier - cytology ; Blood-Brain Barrier - metabolism ; Blood-Brain Barrier - virology ; Brain ; Brain - cytology ; Brain - metabolism ; Brain - virology ; c-Jun protein ; Cell Adhesion ; Cell Biology ; Cell Movement - physiology ; Central nervous system ; Cognition ; Endothelial cells ; Endothelial Cells - cytology ; Endothelial Cells - metabolism ; Endothelial Cells - virology ; Endothelium, Vascular - cytology ; Endothelium, Vascular - metabolism ; Endothelium, Vascular - virology ; HIV Infections - metabolism ; Humans ; Inflammation - metabolism ; Inflammation - virology ; Interleukin 1 ; Interleukin 6 ; Interleukin-6 - metabolism ; JNK protein ; Kinases ; MAP kinase ; Microvasculature ; Monocytes - cytology ; Monocytes - metabolism ; Monocytes - virology ; Neurobiology ; Neurology ; Neuropathogenesis ; Neurosciences ; NF-κB protein ; Protein kinase ; Proteins ; RelB protein ; Serine ; tat Gene Products, Human Immunodeficiency Virus - metabolism ; Tat protein ; Transcription factors ; Zonula occludens-1 protein</subject><ispartof>Molecular neurobiology, 2018-02, Vol.55 (2), p.1352-1363</ispartof><rights>Springer Science+Business Media New York 2017</rights><rights>Molecular Neurobiology is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-414a2756016c6dfff562b137d7944f16c63212a1ed5927a19b7aa6c93a4482a63</citedby><cites>FETCH-LOGICAL-c470t-414a2756016c6dfff562b137d7944f16c63212a1ed5927a19b7aa6c93a4482a63</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/s12035-017-0382-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-017-0382-0$$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/28127697$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bhargavan, Biju</creatorcontrib><creatorcontrib>Kanmogne, Georgette D.</creatorcontrib><title>Differential Mechanisms of Inflammation and Endothelial Dysfunction by HIV-1 Subtype-B and Recombinant CRF02_AG Tat Proteins on Human Brain Microvascular Endothelial Cells: Implications for Viral Neuropathogenesis</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><addtitle>Mol Neurobiol</addtitle><description>The recombinant HIV-1 CRF02_AG is prevalent in West-Central Africa but its effects on the blood-brain barrier (BBB) and HIV-associated neurocognitive disorders (HAND) are not known. We analyzed the effects of Tat from HIV-1 subtype-B (Tat.B) and CRF02_AG (Tat.AG) on primary human brain microvascular endothelial cells (HBMEC), the major BBB component. Exposure of HBMEC to Tat.B increased IL-6 expression and transcription by 9- (
P
< 0.001) and 113-fold (
P
< 0.001), respectively, whereas Tat.AG increased IL-6 expression and transcription by 2.7–3.8-fold and 35.7-fold (
P
< 0.001), respectively. Tat.B induced IL-6 through the interleukin-1 receptor-associated kinase (IRAK)-1/4/mitogen-activated protein kinase kinase(MKK)/C-jun N-terminal kinase(JNK) pathways, in an activator protein-1(AP1)- and nuclear factor-kappaB (NFκB)-independent manner, whereas Tat.AG effects occurred via MKK/JNK/AP1/NFκB pathways. Tat-induced effects were associated with activation of c-jun (serine-63) and SAPK/JNK (Thr183/Tyr185). We demonstrated increased expression of transcription factors associated with these pathways (Jun, RELB, CEBPA), with higher levels in Tat.B-treated cells compared to Tat.AG. Functional studies showed that Tat.B and Tat.AG decreased the expression of tight junction proteins claudin-5 and ZO-1 and decreased the trans-endothelial electric resistance (TEER); Tat.B induced greater reduction in TEER, claudin-5, and ZO-1, compared to Tat.AG. Overall, our data showed increased inflammation and BBB dysfunction with Tat.B, compared to Tat.AG. This suggests these two HIV-1 subtypes differentially affect the BBB and central nervous system; our data provides novel insights into the molecular basis of these differential Tat-mediated effects.</description><subject>Activator protein 1</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood-brain barrier</subject><subject>Blood-Brain Barrier - cytology</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>Blood-Brain Barrier - virology</subject><subject>Brain</subject><subject>Brain - cytology</subject><subject>Brain - metabolism</subject><subject>Brain - virology</subject><subject>c-Jun protein</subject><subject>Cell Adhesion</subject><subject>Cell Biology</subject><subject>Cell Movement - physiology</subject><subject>Central nervous system</subject><subject>Cognition</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - cytology</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - virology</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Endothelium, Vascular - virology</subject><subject>HIV Infections - metabolism</subject><subject>Humans</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - virology</subject><subject>Interleukin 1</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - metabolism</subject><subject>JNK protein</subject><subject>Kinases</subject><subject>MAP kinase</subject><subject>Microvasculature</subject><subject>Monocytes - cytology</subject><subject>Monocytes - metabolism</subject><subject>Monocytes - virology</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neuropathogenesis</subject><subject>Neurosciences</subject><subject>NF-κB protein</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>RelB protein</subject><subject>Serine</subject><subject>tat Gene Products, Human Immunodeficiency Virus - metabolism</subject><subject>Tat protein</subject><subject>Transcription factors</subject><subject>Zonula occludens-1 protein</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1ks1u1DAUhSMEokPhAdggS2zYBGzHsRMWSO30Z0ZqAZXSrXXj2DOuEnuwk0rzoLwPzkwpFImVJd_P5557fbLsNcHvCcbiQyQUF2WOichxUdEcP8lmpCzrnJCKPs1muKqLXHBWHWQvYrzFmFKCxfPsgFaECl6LWfbzxBqjg3aDhQ5darUGZ2MfkTdo6UwHfQ-D9Q6Ba9Gpa_2w1t2EnmyjGZ3a1ZotWixvcoK-jc2w3ej8eIdfaeX7xjpwA5pfnWEqj87RNQzoa_CDti41cWgx9uDQcQDr0KVVwd9BVGMH4VG3ue66-BEt-01n1c5QRMYHdGNDqn7WY_AbGNZ-pZ2ONr7Mnhnoon51fx5m389Or-eL_OLL-XJ-dJErJvCQM8KAipJjwhVvjTElpw0pRCtqxsx0WVBCgei2rKkAUjcCgKu6AMYqCrw4zD7tdTdj0-tWpTUmP3ITbA9hKz1Y-bji7Fqu_J3kJRYM4yTw7l4g-B-jjoPsbVRpWHDaj1GSiqeP4oKJhL79B731Y3BpPEkxnhBalIkieyptMsagzYMZguUUGrkPjUyhkVNo5GTizd9TPLz4nZIE0D0QU8mtdPjT-v-qvwBfYNAK</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Bhargavan, Biju</creator><creator>Kanmogne, Georgette D.</creator><general>Springer US</general><general>Springer Nature B.V</general><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>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180201</creationdate><title>Differential Mechanisms of Inflammation and Endothelial Dysfunction by HIV-1 Subtype-B and Recombinant CRF02_AG Tat Proteins on Human Brain Microvascular Endothelial Cells: Implications for Viral Neuropathogenesis</title><author>Bhargavan, Biju ; Kanmogne, Georgette D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-414a2756016c6dfff562b137d7944f16c63212a1ed5927a19b7aa6c93a4482a63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Activator protein 1</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Blood-brain barrier</topic><topic>Blood-Brain Barrier - cytology</topic><topic>Blood-Brain Barrier - metabolism</topic><topic>Blood-Brain Barrier - virology</topic><topic>Brain</topic><topic>Brain - cytology</topic><topic>Brain - metabolism</topic><topic>Brain - virology</topic><topic>c-Jun protein</topic><topic>Cell Adhesion</topic><topic>Cell Biology</topic><topic>Cell Movement - physiology</topic><topic>Central nervous system</topic><topic>Cognition</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - cytology</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - virology</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Endothelium, Vascular - virology</topic><topic>HIV Infections - metabolism</topic><topic>Humans</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - virology</topic><topic>Interleukin 1</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - metabolism</topic><topic>JNK protein</topic><topic>Kinases</topic><topic>MAP kinase</topic><topic>Microvasculature</topic><topic>Monocytes - cytology</topic><topic>Monocytes - metabolism</topic><topic>Monocytes - virology</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neuropathogenesis</topic><topic>Neurosciences</topic><topic>NF-κB protein</topic><topic>Protein kinase</topic><topic>Proteins</topic><topic>RelB protein</topic><topic>Serine</topic><topic>tat Gene Products, Human Immunodeficiency Virus - metabolism</topic><topic>Tat protein</topic><topic>Transcription factors</topic><topic>Zonula occludens-1 protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bhargavan, Biju</creatorcontrib><creatorcontrib>Kanmogne, Georgette D.</creatorcontrib><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>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</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>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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 Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</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>Psychology Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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 China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bhargavan, Biju</au><au>Kanmogne, Georgette D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential Mechanisms of Inflammation and Endothelial Dysfunction by HIV-1 Subtype-B and Recombinant CRF02_AG Tat Proteins on Human Brain Microvascular Endothelial Cells: Implications for Viral Neuropathogenesis</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><addtitle>Mol Neurobiol</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>55</volume><issue>2</issue><spage>1352</spage><epage>1363</epage><pages>1352-1363</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>The recombinant HIV-1 CRF02_AG is prevalent in West-Central Africa but its effects on the blood-brain barrier (BBB) and HIV-associated neurocognitive disorders (HAND) are not known. We analyzed the effects of Tat from HIV-1 subtype-B (Tat.B) and CRF02_AG (Tat.AG) on primary human brain microvascular endothelial cells (HBMEC), the major BBB component. Exposure of HBMEC to Tat.B increased IL-6 expression and transcription by 9- (
P
< 0.001) and 113-fold (
P
< 0.001), respectively, whereas Tat.AG increased IL-6 expression and transcription by 2.7–3.8-fold and 35.7-fold (
P
< 0.001), respectively. Tat.B induced IL-6 through the interleukin-1 receptor-associated kinase (IRAK)-1/4/mitogen-activated protein kinase kinase(MKK)/C-jun N-terminal kinase(JNK) pathways, in an activator protein-1(AP1)- and nuclear factor-kappaB (NFκB)-independent manner, whereas Tat.AG effects occurred via MKK/JNK/AP1/NFκB pathways. Tat-induced effects were associated with activation of c-jun (serine-63) and SAPK/JNK (Thr183/Tyr185). We demonstrated increased expression of transcription factors associated with these pathways (Jun, RELB, CEBPA), with higher levels in Tat.B-treated cells compared to Tat.AG. Functional studies showed that Tat.B and Tat.AG decreased the expression of tight junction proteins claudin-5 and ZO-1 and decreased the trans-endothelial electric resistance (TEER); Tat.B induced greater reduction in TEER, claudin-5, and ZO-1, compared to Tat.AG. Overall, our data showed increased inflammation and BBB dysfunction with Tat.B, compared to Tat.AG. This suggests these two HIV-1 subtypes differentially affect the BBB and central nervous system; our data provides novel insights into the molecular basis of these differential Tat-mediated effects.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28127697</pmid><doi>10.1007/s12035-017-0382-0</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0893-7648 |
| ispartof | Molecular neurobiology, 2018-02, Vol.55 (2), p.1352-1363 |
| issn | 0893-7648 1559-1182 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6507400 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Activator protein 1 Biomedical and Life Sciences Biomedicine Blood-brain barrier Blood-Brain Barrier - cytology Blood-Brain Barrier - metabolism Blood-Brain Barrier - virology Brain Brain - cytology Brain - metabolism Brain - virology c-Jun protein Cell Adhesion Cell Biology Cell Movement - physiology Central nervous system Cognition Endothelial cells Endothelial Cells - cytology Endothelial Cells - metabolism Endothelial Cells - virology Endothelium, Vascular - cytology Endothelium, Vascular - metabolism Endothelium, Vascular - virology HIV Infections - metabolism Humans Inflammation - metabolism Inflammation - virology Interleukin 1 Interleukin 6 Interleukin-6 - metabolism JNK protein Kinases MAP kinase Microvasculature Monocytes - cytology Monocytes - metabolism Monocytes - virology Neurobiology Neurology Neuropathogenesis Neurosciences NF-κB protein Protein kinase Proteins RelB protein Serine tat Gene Products, Human Immunodeficiency Virus - metabolism Tat protein Transcription factors Zonula occludens-1 protein |
| title | Differential Mechanisms of Inflammation and Endothelial Dysfunction by HIV-1 Subtype-B and Recombinant CRF02_AG Tat Proteins on Human Brain Microvascular Endothelial Cells: Implications for Viral Neuropathogenesis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-10T20%3A07%3A29IST&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=Differential%20Mechanisms%20of%20Inflammation%20and%20Endothelial%20Dysfunction%20by%20HIV-1%20Subtype-B%20and%20Recombinant%20CRF02_AG%20Tat%20Proteins%20on%20Human%20Brain%20Microvascular%20Endothelial%20Cells:%20Implications%20for%20Viral%20Neuropathogenesis&rft.jtitle=Molecular%20neurobiology&rft.au=Bhargavan,%20Biju&rft.date=2018-02-01&rft.volume=55&rft.issue=2&rft.spage=1352&rft.epage=1363&rft.pages=1352-1363&rft.issn=0893-7648&rft.eissn=1559-1182&rft_id=info:doi/10.1007/s12035-017-0382-0&rft_dat=%3Cproquest_pubme%3E1862766747%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=2006747235&rft_id=info:pmid/28127697&rfr_iscdi=true |