α7-Nicotinic Acetylcholine Receptor Activation Modulates BV2 Microglial Plasticity via miR-21/TNF-α/NFκB in Oxygen–Glucose Deprivation/Reoxygenation
Elevated inflammatory reactions are a significant component in cerebral ischemia–reperfusion injury (CIRI). Activation of α7-Nicotinic Acetylcholine Receptor (α7nAChR) reduces stroke-induced inflammation in rats, but the anti-inflammatory pathway in microglia under CIRI condition remains unclear. Th...
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| Veröffentlicht in: | Journal of molecular neuroscience 2024-12, Vol.75 (1), p.2, Article 2 |
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| creator | Hasan, Mohammad Yusuf Roslan, Azim Haikal Md Azmi, Norazrina Ibrahim, Norlinah Mohamed Arulsamy, Alina Lee, Vanessa Lin Lin Siran, Rosfaiizah Vidyadaran, Sharmili Chua, Eng Wee Mahadi, Mohd Kaisan |
| description | Elevated inflammatory reactions are a significant component in cerebral ischemia–reperfusion injury (CIRI). Activation of α7-Nicotinic Acetylcholine Receptor (α7nAChR) reduces stroke-induced inflammation in rats, but the anti-inflammatory pathway in microglia under CIRI condition remains unclear. This study employed qRT-PCR, protein assays, NanoString analysis, and bioinformatics to examine the effects of PNU282987 treatment (α7nAChR agonist) on BV2 microglial functional differentiation in oxygen–glucose deprivation/reoxygenation (OGDR) condition. OGDR significantly increased the gene expression of pro-inflammatory markers such as TNF-α, IL-6, and IL1β, while α7nAChR agonists reduced these markers. The anti-inflammatory gene marker IL-10 was upregulated by α7nAChR agonist treatment. Downstream pathway marker analysis showed that both gene and protein expression of NFκB was associated with anti-inflammatory effects. Blocking microRNA-21 with antagomir reversed the anti-inflammatory effects. NanoString analysis revealed that microRNA-21 inhibition significantly affected inflammation-related genes, including
AL1RAP
,
TLR9
,
FLT1
,
PTGIR
,
NFκB
,
TREM2
,
TNF
,
SMAD7
,
FOS
,
CCL5
,
IFIT1
,
CFB
,
CXCL10
,
IFI44
,
DDIT3
,
IRF7
,
OASL1
,
IL1A
,
IFIT2
,
C3
,
CD40
,
STAT2
,
IFIT3
,
IL1RN
,
OAS1A
,
CSF1
,
CCL4
,
CCL2
,
CCL3
,
BCL2L1
, and
ITGB2
. Enrichment analysis of upregulated genes identified Gene Ontology Biological Processes related to cytokine responses and TNF-associated pathways. This study highlights α7nAChR activation as a key regulator of anti-inflammatory responses in BV2 microglia under OGDR conditions, with micro-RNA21 identified as a crucial mediator of receptor-driven neuroprotection via the TNF-α/NF
κ
B signalling pathway. |
| doi_str_mv | 10.1007/s12031-024-02300-9 |
| format | Article |
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AL1RAP
,
TLR9
,
FLT1
,
PTGIR
,
NFκB
,
TREM2
,
TNF
,
SMAD7
,
FOS
,
CCL5
,
IFIT1
,
CFB
,
CXCL10
,
IFI44
,
DDIT3
,
IRF7
,
OASL1
,
IL1A
,
IFIT2
,
C3
,
CD40
,
STAT2
,
IFIT3
,
IL1RN
,
OAS1A
,
CSF1
,
CCL4
,
CCL2
,
CCL3
,
BCL2L1
, and
ITGB2
. Enrichment analysis of upregulated genes identified Gene Ontology Biological Processes related to cytokine responses and TNF-associated pathways. This study highlights α7nAChR activation as a key regulator of anti-inflammatory responses in BV2 microglia under OGDR conditions, with micro-RNA21 identified as a crucial mediator of receptor-driven neuroprotection via the TNF-α/NF
κ
B signalling pathway.</description><identifier>ISSN: 1559-1166</identifier><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-024-02300-9</identifier><identifier>PMID: 39718716</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acetylcholine receptors (nicotinic) ; Agonists ; alpha7 Nicotinic Acetylcholine Receptor - genetics ; alpha7 Nicotinic Acetylcholine Receptor - metabolism ; Animals ; Benzamides - pharmacology ; Bioinformatics ; Biological activity ; Biomarkers ; Biomedical and Life Sciences ; Biomedicine ; Bridged Bicyclo Compounds - pharmacology ; CD40 antigen ; Cell Biology ; Cell Hypoxia ; Cell Line ; Cerebrum ; CXCL10 protein ; Deprivation ; Gene expression ; Genes ; Glucose ; Glucose - metabolism ; Inflammation ; Interferon regulatory factor 7 ; Ischemia ; Mice ; Microglia ; Microglia - drug effects ; Microglia - metabolism ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Monocyte chemoattractant protein 1 ; Neurochemistry ; Neurology ; Neuroprotection ; Neurosciences ; NF-kappa B - metabolism ; NF-κB protein ; Nicotinic Agonists - pharmacology ; Oxygen ; Oxygen - metabolism ; Proteins ; Proteomics ; Receptor mechanisms ; Receptors ; Reperfusion ; Ribonucleic acid ; RNA ; Signal Transduction ; Smad7 protein ; Stat2 protein ; TLR9 protein ; Toll-like receptors ; Transcription activation ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Tumor Necrosis Factor-alpha - pharmacology ; Tumor necrosis factor-α</subject><ispartof>Journal of molecular neuroscience, 2024-12, Vol.75 (1), p.2, Article 2</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024 Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>Copyright Springer Nature B.V. Mar 2025</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c256t-7bee978bde34d1325bc89a19c7b215098a2293c4effaeb7aa0889734644baf8b3</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/s12031-024-02300-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-024-02300-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,41471,42540,51302</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39718716$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hasan, Mohammad Yusuf</creatorcontrib><creatorcontrib>Roslan, Azim Haikal Md</creatorcontrib><creatorcontrib>Azmi, Norazrina</creatorcontrib><creatorcontrib>Ibrahim, Norlinah Mohamed</creatorcontrib><creatorcontrib>Arulsamy, Alina</creatorcontrib><creatorcontrib>Lee, Vanessa Lin Lin</creatorcontrib><creatorcontrib>Siran, Rosfaiizah</creatorcontrib><creatorcontrib>Vidyadaran, Sharmili</creatorcontrib><creatorcontrib>Chua, Eng Wee</creatorcontrib><creatorcontrib>Mahadi, Mohd Kaisan</creatorcontrib><title>α7-Nicotinic Acetylcholine Receptor Activation Modulates BV2 Microglial Plasticity via miR-21/TNF-α/NFκB in Oxygen–Glucose Deprivation/Reoxygenation</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>Elevated inflammatory reactions are a significant component in cerebral ischemia–reperfusion injury (CIRI). Activation of α7-Nicotinic Acetylcholine Receptor (α7nAChR) reduces stroke-induced inflammation in rats, but the anti-inflammatory pathway in microglia under CIRI condition remains unclear. This study employed qRT-PCR, protein assays, NanoString analysis, and bioinformatics to examine the effects of PNU282987 treatment (α7nAChR agonist) on BV2 microglial functional differentiation in oxygen–glucose deprivation/reoxygenation (OGDR) condition. OGDR significantly increased the gene expression of pro-inflammatory markers such as TNF-α, IL-6, and IL1β, while α7nAChR agonists reduced these markers. The anti-inflammatory gene marker IL-10 was upregulated by α7nAChR agonist treatment. Downstream pathway marker analysis showed that both gene and protein expression of NFκB was associated with anti-inflammatory effects. Blocking microRNA-21 with antagomir reversed the anti-inflammatory effects. NanoString analysis revealed that microRNA-21 inhibition significantly affected inflammation-related genes, including
AL1RAP
,
TLR9
,
FLT1
,
PTGIR
,
NFκB
,
TREM2
,
TNF
,
SMAD7
,
FOS
,
CCL5
,
IFIT1
,
CFB
,
CXCL10
,
IFI44
,
DDIT3
,
IRF7
,
OASL1
,
IL1A
,
IFIT2
,
C3
,
CD40
,
STAT2
,
IFIT3
,
IL1RN
,
OAS1A
,
CSF1
,
CCL4
,
CCL2
,
CCL3
,
BCL2L1
, and
ITGB2
. Enrichment analysis of upregulated genes identified Gene Ontology Biological Processes related to cytokine responses and TNF-associated pathways. This study highlights α7nAChR activation as a key regulator of anti-inflammatory responses in BV2 microglia under OGDR conditions, with micro-RNA21 identified as a crucial mediator of receptor-driven neuroprotection via the TNF-α/NF
κ
B signalling pathway.</description><subject>Acetylcholine receptors (nicotinic)</subject><subject>Agonists</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - genetics</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>Animals</subject><subject>Benzamides - pharmacology</subject><subject>Bioinformatics</subject><subject>Biological activity</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bridged Bicyclo Compounds - pharmacology</subject><subject>CD40 antigen</subject><subject>Cell Biology</subject><subject>Cell Hypoxia</subject><subject>Cell Line</subject><subject>Cerebrum</subject><subject>CXCL10 protein</subject><subject>Deprivation</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Inflammation</subject><subject>Interferon regulatory factor 7</subject><subject>Ischemia</subject><subject>Mice</subject><subject>Microglia</subject><subject>Microglia - drug effects</subject><subject>Microglia - metabolism</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neuroprotection</subject><subject>Neurosciences</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Nicotinic Agonists - pharmacology</subject><subject>Oxygen</subject><subject>Oxygen - metabolism</subject><subject>Proteins</subject><subject>Proteomics</subject><subject>Receptor mechanisms</subject><subject>Receptors</subject><subject>Reperfusion</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signal Transduction</subject><subject>Smad7 protein</subject><subject>Stat2 protein</subject><subject>TLR9 protein</subject><subject>Toll-like receptors</subject><subject>Transcription activation</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumor necrosis factor-α</subject><issn>1559-1166</issn><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc9uEzEQxlcIREvhBTggS1y4uPG_XdvHtpAWqU1RVLiuvM5scOWs07W3IjfegROP0SsPkYfgSTBJShEHDpY9nt989sxXFC8pOaSEyFGkjHCKCRN5cUKwflTs07LUmNKqevzXea94FuM1IYwKqp4We1xLqiSt9ovv6zuJJ86G5Dpn0ZGFtPL2c_CuAzQFC8sU-nyd3K1JLnToIswGbxJEdPyJoQtn-zD3znj0wZuYnHVphW6dQQs3xYyOriZjvL4bTcbrH8fIdejyy2oO3c-v3079YEME9BaW_U57NIWwSW-i58WT1vgIL3b7QfFx_O7q5AyfX56-Pzk6x5aVVcKyAdBSNTPgYkY5KxurtKHayobRkmhlGNPcCmhbA400hiilJReVEI1pVcMPijdb3WUfbgaIqV64aMF700EYYs2pUEoQXsqMvv4HvQ5D3-XfbShdCSnLTLEtlUcTYw9tnTtcmH5VU1L_Nq7eGldn4-qNcbXORa920kOzgNmfknunMsC3QMypbg79w9v_kf0FKuWnjw</recordid><startdate>20241224</startdate><enddate>20241224</enddate><creator>Hasan, Mohammad Yusuf</creator><creator>Roslan, Azim Haikal Md</creator><creator>Azmi, Norazrina</creator><creator>Ibrahim, Norlinah Mohamed</creator><creator>Arulsamy, Alina</creator><creator>Lee, Vanessa Lin Lin</creator><creator>Siran, Rosfaiizah</creator><creator>Vidyadaran, Sharmili</creator><creator>Chua, Eng Wee</creator><creator>Mahadi, Mohd Kaisan</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>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20241224</creationdate><title>α7-Nicotinic Acetylcholine Receptor Activation Modulates BV2 Microglial Plasticity via miR-21/TNF-α/NFκB in Oxygen–Glucose Deprivation/Reoxygenation</title><author>Hasan, Mohammad Yusuf ; Roslan, Azim Haikal Md ; Azmi, Norazrina ; Ibrahim, Norlinah Mohamed ; Arulsamy, Alina ; Lee, Vanessa Lin Lin ; Siran, Rosfaiizah ; Vidyadaran, Sharmili ; Chua, Eng Wee ; Mahadi, Mohd Kaisan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c256t-7bee978bde34d1325bc89a19c7b215098a2293c4effaeb7aa0889734644baf8b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acetylcholine receptors (nicotinic)</topic><topic>Agonists</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - genetics</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - metabolism</topic><topic>Animals</topic><topic>Benzamides - pharmacology</topic><topic>Bioinformatics</topic><topic>Biological activity</topic><topic>Biomarkers</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bridged Bicyclo Compounds - pharmacology</topic><topic>CD40 antigen</topic><topic>Cell Biology</topic><topic>Cell Hypoxia</topic><topic>Cell Line</topic><topic>Cerebrum</topic><topic>CXCL10 protein</topic><topic>Deprivation</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Inflammation</topic><topic>Interferon regulatory factor 7</topic><topic>Ischemia</topic><topic>Mice</topic><topic>Microglia</topic><topic>Microglia - drug effects</topic><topic>Microglia - metabolism</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Monocyte chemoattractant protein 1</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neuroprotection</topic><topic>Neurosciences</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>Nicotinic Agonists - pharmacology</topic><topic>Oxygen</topic><topic>Oxygen - metabolism</topic><topic>Proteins</topic><topic>Proteomics</topic><topic>Receptor mechanisms</topic><topic>Receptors</topic><topic>Reperfusion</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Signal Transduction</topic><topic>Smad7 protein</topic><topic>Stat2 protein</topic><topic>TLR9 protein</topic><topic>Toll-like receptors</topic><topic>Transcription activation</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor Necrosis Factor-alpha - pharmacology</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hasan, Mohammad Yusuf</creatorcontrib><creatorcontrib>Roslan, Azim Haikal Md</creatorcontrib><creatorcontrib>Azmi, Norazrina</creatorcontrib><creatorcontrib>Ibrahim, Norlinah Mohamed</creatorcontrib><creatorcontrib>Arulsamy, Alina</creatorcontrib><creatorcontrib>Lee, Vanessa Lin Lin</creatorcontrib><creatorcontrib>Siran, Rosfaiizah</creatorcontrib><creatorcontrib>Vidyadaran, Sharmili</creatorcontrib><creatorcontrib>Chua, Eng Wee</creatorcontrib><creatorcontrib>Mahadi, Mohd Kaisan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hasan, Mohammad Yusuf</au><au>Roslan, Azim Haikal Md</au><au>Azmi, Norazrina</au><au>Ibrahim, Norlinah Mohamed</au><au>Arulsamy, Alina</au><au>Lee, Vanessa Lin Lin</au><au>Siran, Rosfaiizah</au><au>Vidyadaran, Sharmili</au><au>Chua, Eng Wee</au><au>Mahadi, Mohd Kaisan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>α7-Nicotinic Acetylcholine Receptor Activation Modulates BV2 Microglial Plasticity via miR-21/TNF-α/NFκB in Oxygen–Glucose Deprivation/Reoxygenation</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2024-12-24</date><risdate>2024</risdate><volume>75</volume><issue>1</issue><spage>2</spage><pages>2-</pages><artnum>2</artnum><issn>1559-1166</issn><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>Elevated inflammatory reactions are a significant component in cerebral ischemia–reperfusion injury (CIRI). Activation of α7-Nicotinic Acetylcholine Receptor (α7nAChR) reduces stroke-induced inflammation in rats, but the anti-inflammatory pathway in microglia under CIRI condition remains unclear. This study employed qRT-PCR, protein assays, NanoString analysis, and bioinformatics to examine the effects of PNU282987 treatment (α7nAChR agonist) on BV2 microglial functional differentiation in oxygen–glucose deprivation/reoxygenation (OGDR) condition. OGDR significantly increased the gene expression of pro-inflammatory markers such as TNF-α, IL-6, and IL1β, while α7nAChR agonists reduced these markers. The anti-inflammatory gene marker IL-10 was upregulated by α7nAChR agonist treatment. Downstream pathway marker analysis showed that both gene and protein expression of NFκB was associated with anti-inflammatory effects. Blocking microRNA-21 with antagomir reversed the anti-inflammatory effects. NanoString analysis revealed that microRNA-21 inhibition significantly affected inflammation-related genes, including
AL1RAP
,
TLR9
,
FLT1
,
PTGIR
,
NFκB
,
TREM2
,
TNF
,
SMAD7
,
FOS
,
CCL5
,
IFIT1
,
CFB
,
CXCL10
,
IFI44
,
DDIT3
,
IRF7
,
OASL1
,
IL1A
,
IFIT2
,
C3
,
CD40
,
STAT2
,
IFIT3
,
IL1RN
,
OAS1A
,
CSF1
,
CCL4
,
CCL2
,
CCL3
,
BCL2L1
, and
ITGB2
. Enrichment analysis of upregulated genes identified Gene Ontology Biological Processes related to cytokine responses and TNF-associated pathways. This study highlights α7nAChR activation as a key regulator of anti-inflammatory responses in BV2 microglia under OGDR conditions, with micro-RNA21 identified as a crucial mediator of receptor-driven neuroprotection via the TNF-α/NF
κ
B signalling pathway.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>39718716</pmid><doi>10.1007/s12031-024-02300-9</doi></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1559-1166 |
| ispartof | Journal of molecular neuroscience, 2024-12, Vol.75 (1), p.2, Article 2 |
| issn | 1559-1166 0895-8696 1559-1166 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_3148840357 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Acetylcholine receptors (nicotinic) Agonists alpha7 Nicotinic Acetylcholine Receptor - genetics alpha7 Nicotinic Acetylcholine Receptor - metabolism Animals Benzamides - pharmacology Bioinformatics Biological activity Biomarkers Biomedical and Life Sciences Biomedicine Bridged Bicyclo Compounds - pharmacology CD40 antigen Cell Biology Cell Hypoxia Cell Line Cerebrum CXCL10 protein Deprivation Gene expression Genes Glucose Glucose - metabolism Inflammation Interferon regulatory factor 7 Ischemia Mice Microglia Microglia - drug effects Microglia - metabolism MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Monocyte chemoattractant protein 1 Neurochemistry Neurology Neuroprotection Neurosciences NF-kappa B - metabolism NF-κB protein Nicotinic Agonists - pharmacology Oxygen Oxygen - metabolism Proteins Proteomics Receptor mechanisms Receptors Reperfusion Ribonucleic acid RNA Signal Transduction Smad7 protein Stat2 protein TLR9 protein Toll-like receptors Transcription activation Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Tumor Necrosis Factor-alpha - pharmacology Tumor necrosis factor-α |
| title | α7-Nicotinic Acetylcholine Receptor Activation Modulates BV2 Microglial Plasticity via miR-21/TNF-α/NFκB in Oxygen–Glucose Deprivation/Reoxygenation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T14%3A14%3A52IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=%CE%B17-Nicotinic%20Acetylcholine%20Receptor%20Activation%20Modulates%20BV2%20Microglial%20Plasticity%20via%20miR-21/TNF-%CE%B1/NF%CE%BAB%20in%20Oxygen%E2%80%93Glucose%20Deprivation/Reoxygenation&rft.jtitle=Journal%20of%20molecular%20neuroscience&rft.au=Hasan,%20Mohammad%20Yusuf&rft.date=2024-12-24&rft.volume=75&rft.issue=1&rft.spage=2&rft.pages=2-&rft.artnum=2&rft.issn=1559-1166&rft.eissn=1559-1166&rft_id=info:doi/10.1007/s12031-024-02300-9&rft_dat=%3Cproquest_cross%3E3148840357%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3148964775&rft_id=info:pmid/39718716&rfr_iscdi=true |