Multifunctional effects of bradykinin on glial cells in relation to potential anti-inflammatory effects
Kinins have been reported to be produced and act at the site of injury and inflammation. Despite many reports that they are likely to initiate a particular cascade of inflammatory events, bradykinin (BK) has anti-inflammatory effects in the brain mediated by glial cells. In the present review, we ha...
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| Veröffentlicht in: | Neurochemistry international 2007-07, Vol.51 (2), p.185-191 |
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| creator | Noda, Mami Sasaki, Kenjiro Ifuku, Masataka Wada, Keiji |
| description | Kinins have been reported to be produced and act at the site of injury and inflammation. Despite many reports that they are likely to initiate a particular cascade of inflammatory events, bradykinin (BK) has anti-inflammatory effects in the brain mediated by glial cells. In the present review, we have attempted to describe the complex responses and immediate reaction of glial cells to BK. Glial cells express BK receptors and induce Ca
2+-dependent signal cascades. Among them, production of prostaglandin E
2 (PGE
2), via B
1 receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-α (TNF-α) via increasing intracellular cyclic adenosine monophosphate (cAMP). In addition, BK up-regulates the production of neurotrophic factors such as nerve growth factor (NGF) via B
2 receptors in astrocytes. These results suggest that BK may have anti-inflammatory and neuroprotective effects in the brain through multiple functions on glial cells. These observations may help to understand the paradox on the role of kinins in the central nervous system and may be useful for therapeutic strategy. |
| doi_str_mv | 10.1016/j.neuint.2007.06.017 |
| format | Article |
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2+-dependent signal cascades. Among them, production of prostaglandin E
2 (PGE
2), via B
1 receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-α (TNF-α) via increasing intracellular cyclic adenosine monophosphate (cAMP). In addition, BK up-regulates the production of neurotrophic factors such as nerve growth factor (NGF) via B
2 receptors in astrocytes. These results suggest that BK may have anti-inflammatory and neuroprotective effects in the brain through multiple functions on glial cells. These observations may help to understand the paradox on the role of kinins in the central nervous system and may be useful for therapeutic strategy.</description><identifier>ISSN: 0197-0186</identifier><identifier>EISSN: 1872-9754</identifier><identifier>DOI: 10.1016/j.neuint.2007.06.017</identifier><identifier>PMID: 17669557</identifier><identifier>CODEN: NEUIDS</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Anti-Inflammatory Agents - metabolism ; Anti-Inflammatory Agents - pharmacology ; Astrocyte ; Biological and medical sciences ; Bradykinin - metabolism ; Bradykinin - pharmacology ; Cytoprotection - drug effects ; Cytoprotection - physiology ; Encephalitis - drug therapy ; Encephalitis - metabolism ; Encephalitis - physiopathology ; Fundamental and applied biological sciences. Psychology ; Gliosis - drug therapy ; Gliosis - metabolism ; Gliosis - physiopathology ; Humans ; Lipopolysaccharide ; Microglia ; Nerve Growth Factors - drug effects ; Nerve Growth Factors - metabolism ; Neuroglia - drug effects ; Neuroglia - metabolism ; Prostaglandin E 2 ; Receptors, Bradykinin - agonists ; Receptors, Bradykinin - metabolism ; TNF-α ; Tumor Necrosis Factor-alpha - drug effects ; Tumor Necrosis Factor-alpha - metabolism ; Vertebrates: nervous system and sense organs</subject><ispartof>Neurochemistry international, 2007-07, Vol.51 (2), p.185-191</ispartof><rights>2007 Elsevier Ltd</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-64736b0e0458f5a0719ffa3ad3e3211f16a88a4cc998e881b0d3186f6d569bc73</citedby><cites>FETCH-LOGICAL-c456t-64736b0e0458f5a0719ffa3ad3e3211f16a88a4cc998e881b0d3186f6d569bc73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neuint.2007.06.017$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,782,786,3552,27931,27932,46002</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18976999$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17669557$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Noda, Mami</creatorcontrib><creatorcontrib>Sasaki, Kenjiro</creatorcontrib><creatorcontrib>Ifuku, Masataka</creatorcontrib><creatorcontrib>Wada, Keiji</creatorcontrib><title>Multifunctional effects of bradykinin on glial cells in relation to potential anti-inflammatory effects</title><title>Neurochemistry international</title><addtitle>Neurochem Int</addtitle><description>Kinins have been reported to be produced and act at the site of injury and inflammation. Despite many reports that they are likely to initiate a particular cascade of inflammatory events, bradykinin (BK) has anti-inflammatory effects in the brain mediated by glial cells. In the present review, we have attempted to describe the complex responses and immediate reaction of glial cells to BK. Glial cells express BK receptors and induce Ca
2+-dependent signal cascades. Among them, production of prostaglandin E
2 (PGE
2), via B
1 receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-α (TNF-α) via increasing intracellular cyclic adenosine monophosphate (cAMP). In addition, BK up-regulates the production of neurotrophic factors such as nerve growth factor (NGF) via B
2 receptors in astrocytes. These results suggest that BK may have anti-inflammatory and neuroprotective effects in the brain through multiple functions on glial cells. These observations may help to understand the paradox on the role of kinins in the central nervous system and may be useful for therapeutic strategy.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - metabolism</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Astrocyte</subject><subject>Biological and medical sciences</subject><subject>Bradykinin - metabolism</subject><subject>Bradykinin - pharmacology</subject><subject>Cytoprotection - drug effects</subject><subject>Cytoprotection - physiology</subject><subject>Encephalitis - drug therapy</subject><subject>Encephalitis - metabolism</subject><subject>Encephalitis - physiopathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gliosis - drug therapy</subject><subject>Gliosis - metabolism</subject><subject>Gliosis - physiopathology</subject><subject>Humans</subject><subject>Lipopolysaccharide</subject><subject>Microglia</subject><subject>Nerve Growth Factors - drug effects</subject><subject>Nerve Growth Factors - metabolism</subject><subject>Neuroglia - drug effects</subject><subject>Neuroglia - metabolism</subject><subject>Prostaglandin E 2</subject><subject>Receptors, Bradykinin - agonists</subject><subject>Receptors, Bradykinin - metabolism</subject><subject>TNF-α</subject><subject>Tumor Necrosis Factor-alpha - drug effects</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0197-0186</issn><issn>1872-9754</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1q3DAURkVJaSZJ36AUb9KdXWls_W0CIbRpIaWbZi1k-SpoKksTSQ7M21dmpmSX1QXd831cHYQ-EdwRTNjXXRdgcaF0W4x5h1mHCX-HNkTwbSs5Hc7QBhPJW0wEO0cXOe9wBSWmH9A54YxJSvkGPf1afHF2Caa4GLRvwFowJTfRNmPS0-GvCy40MTRP3tW1Ae9zU18SeL1GmhKbfSwQyrrWdbQuWK_nWZeYDv_7rtB7q32Gj6d5iR6_f_tz96N9-H3_8-72oTUDZaVlA-_ZiAEPVFiqMSfSWt3rqYd-S4glTAuhB2OkFCAEGfHU1_9ZNlEmR8P7S_Tl2LtP8XmBXNTs8nq0DhCXrJggW0rwCg5H0KSYcwKr9snNOh0UwWoVrHbqKFitghVmqgqusc-n_mWcYXoNnYxW4PoE6Gy0t0kH4_IrJyRnUsrK3Rw5qDZeHCSVjYNgYHKpClNTdG9f8g97eJ0b</recordid><startdate>20070701</startdate><enddate>20070701</enddate><creator>Noda, Mami</creator><creator>Sasaki, Kenjiro</creator><creator>Ifuku, Masataka</creator><creator>Wada, Keiji</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</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>7X8</scope></search><sort><creationdate>20070701</creationdate><title>Multifunctional effects of bradykinin on glial cells in relation to potential anti-inflammatory effects</title><author>Noda, Mami ; Sasaki, Kenjiro ; Ifuku, Masataka ; Wada, Keiji</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-64736b0e0458f5a0719ffa3ad3e3211f16a88a4cc998e881b0d3186f6d569bc73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - metabolism</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Astrocyte</topic><topic>Biological and medical sciences</topic><topic>Bradykinin - metabolism</topic><topic>Bradykinin - pharmacology</topic><topic>Cytoprotection - drug effects</topic><topic>Cytoprotection - physiology</topic><topic>Encephalitis - drug therapy</topic><topic>Encephalitis - metabolism</topic><topic>Encephalitis - physiopathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gliosis - drug therapy</topic><topic>Gliosis - metabolism</topic><topic>Gliosis - physiopathology</topic><topic>Humans</topic><topic>Lipopolysaccharide</topic><topic>Microglia</topic><topic>Nerve Growth Factors - drug effects</topic><topic>Nerve Growth Factors - metabolism</topic><topic>Neuroglia - drug effects</topic><topic>Neuroglia - metabolism</topic><topic>Prostaglandin E 2</topic><topic>Receptors, Bradykinin - agonists</topic><topic>Receptors, Bradykinin - metabolism</topic><topic>TNF-α</topic><topic>Tumor Necrosis Factor-alpha - drug effects</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Noda, Mami</creatorcontrib><creatorcontrib>Sasaki, Kenjiro</creatorcontrib><creatorcontrib>Ifuku, Masataka</creatorcontrib><creatorcontrib>Wada, Keiji</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemistry international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Noda, Mami</au><au>Sasaki, Kenjiro</au><au>Ifuku, Masataka</au><au>Wada, Keiji</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Multifunctional effects of bradykinin on glial cells in relation to potential anti-inflammatory effects</atitle><jtitle>Neurochemistry international</jtitle><addtitle>Neurochem Int</addtitle><date>2007-07-01</date><risdate>2007</risdate><volume>51</volume><issue>2</issue><spage>185</spage><epage>191</epage><pages>185-191</pages><issn>0197-0186</issn><eissn>1872-9754</eissn><coden>NEUIDS</coden><abstract>Kinins have been reported to be produced and act at the site of injury and inflammation. Despite many reports that they are likely to initiate a particular cascade of inflammatory events, bradykinin (BK) has anti-inflammatory effects in the brain mediated by glial cells. In the present review, we have attempted to describe the complex responses and immediate reaction of glial cells to BK. Glial cells express BK receptors and induce Ca
2+-dependent signal cascades. Among them, production of prostaglandin E
2 (PGE
2), via B
1 receptors in primary cultured microglia, has a negative feedback effect on lipopolysaccharide (LPS)-induced release of tumor necrosis factor-α (TNF-α) via increasing intracellular cyclic adenosine monophosphate (cAMP). In addition, BK up-regulates the production of neurotrophic factors such as nerve growth factor (NGF) via B
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| subjects | Animals Anti-Inflammatory Agents - metabolism Anti-Inflammatory Agents - pharmacology Astrocyte Biological and medical sciences Bradykinin - metabolism Bradykinin - pharmacology Cytoprotection - drug effects Cytoprotection - physiology Encephalitis - drug therapy Encephalitis - metabolism Encephalitis - physiopathology Fundamental and applied biological sciences. Psychology Gliosis - drug therapy Gliosis - metabolism Gliosis - physiopathology Humans Lipopolysaccharide Microglia Nerve Growth Factors - drug effects Nerve Growth Factors - metabolism Neuroglia - drug effects Neuroglia - metabolism Prostaglandin E 2 Receptors, Bradykinin - agonists Receptors, Bradykinin - metabolism TNF-α Tumor Necrosis Factor-alpha - drug effects Tumor Necrosis Factor-alpha - metabolism Vertebrates: nervous system and sense organs |
| title | Multifunctional effects of bradykinin on glial cells in relation to potential anti-inflammatory effects |
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