A Synthetic Biotinylated Peptide, BP21, Inhibits the Induction of mRNA Expression of Inflammatory Substances by Oxidized- and Lyso-Phosphatidylcholine
Preclinical Research Oxidized low‐density lipoprotein (ox‐LDL) is implicated in many inflammatory diseases, e.g., type 2 diabetes, obesity, atherosclerosis, and metabolic syndrome. We previously reported that a synthetic biotinylated peptide, BP21, inhibits the bioactivity of ox‐LDL via direct bindi...
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| Veröffentlicht in: | Drug development research 2014-06, Vol.75 (4), p.246-256 |
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| creator | Sato, Akira Kumagai, Takeshi Ebina, Keiichi |
| description | Preclinical Research
Oxidized low‐density lipoprotein (ox‐LDL) is implicated in many inflammatory diseases, e.g., type 2 diabetes, obesity, atherosclerosis, and metabolic syndrome. We previously reported that a synthetic biotinylated peptide, BP21, inhibits the bioactivity of ox‐LDL via direct binding to ox‐LDL. Here, we investigated the effect of BP21 on the mRNA expression of proinflammatory mediators induced by two major components of ox‐LDL, oxidized‐ and lyso‐phosphatidylcholine (ox‐PC and LPC), in monocytes/macrophages (THP‐1 cells) and adipocytes (3T3‐L1 cells). In THP‐1 cells, BP21 markedly reduced the mRNA expression of interleukin (IL)‐6, adipocyte fatty acid‐binding protein (aP2), tumor necrosis factor‐α, and mitogen‐activated protein kinase phosphatase‐1, which are induced by one of the major bioactive components of ox‐PC, 1‐palmitoyl‐2‐(5′‐oxo‐valeroyl)‐sn‐glycero‐3‐phosphocholine (POVPC), and reduced the mRNA expression of IL‐6, the ox‐LDL‐specific scavenger receptor CD36, and aP2 induced by LPC. In adipocytes, the mRNA expression of IL‐1β as an adipokine and aP2 is highly induced by ox‐PC and LPC, and BP21 markedly reduced the mRNA expression of IL‐1β and aP2 induced by POVPC and LPC. Furthermore, BP21 specifically bound to LPC and POVPC in a dose‐dependent manner. These results suggest that BP21 may be useful lead for the potential treatment and prevention of inflammatory diseases caused by ox‐PC and LPC. |
| doi_str_mv | 10.1002/ddr.21178 |
| format | Article |
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Oxidized low‐density lipoprotein (ox‐LDL) is implicated in many inflammatory diseases, e.g., type 2 diabetes, obesity, atherosclerosis, and metabolic syndrome. We previously reported that a synthetic biotinylated peptide, BP21, inhibits the bioactivity of ox‐LDL via direct binding to ox‐LDL. Here, we investigated the effect of BP21 on the mRNA expression of proinflammatory mediators induced by two major components of ox‐LDL, oxidized‐ and lyso‐phosphatidylcholine (ox‐PC and LPC), in monocytes/macrophages (THP‐1 cells) and adipocytes (3T3‐L1 cells). In THP‐1 cells, BP21 markedly reduced the mRNA expression of interleukin (IL)‐6, adipocyte fatty acid‐binding protein (aP2), tumor necrosis factor‐α, and mitogen‐activated protein kinase phosphatase‐1, which are induced by one of the major bioactive components of ox‐PC, 1‐palmitoyl‐2‐(5′‐oxo‐valeroyl)‐sn‐glycero‐3‐phosphocholine (POVPC), and reduced the mRNA expression of IL‐6, the ox‐LDL‐specific scavenger receptor CD36, and aP2 induced by LPC. In adipocytes, the mRNA expression of IL‐1β as an adipokine and aP2 is highly induced by ox‐PC and LPC, and BP21 markedly reduced the mRNA expression of IL‐1β and aP2 induced by POVPC and LPC. Furthermore, BP21 specifically bound to LPC and POVPC in a dose‐dependent manner. These results suggest that BP21 may be useful lead for the potential treatment and prevention of inflammatory diseases caused by ox‐PC and LPC.</description><identifier>ISSN: 0272-4391</identifier><identifier>EISSN: 1098-2299</identifier><identifier>DOI: 10.1002/ddr.21178</identifier><identifier>PMID: 24890951</identifier><identifier>CODEN: DDREDK</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>3T3-L1 Cells ; adipocyte ; Adipocytes ; Adipocytes - drug effects ; Adipocytes - immunology ; Animals ; anti-inflammatory drug ; Biotin - analogs & derivatives ; Biotin - chemistry ; Biotin - pharmacology ; biotinylated peptide ; Biotinylation ; Cell Line, Tumor ; Cytokines ; Gene Expression Regulation - drug effects ; Hemolysin Proteins - chemistry ; Hemolysin Proteins - pharmacology ; Humans ; inflammation ; Kinases ; Lipoproteins, LDL - antagonists & inhibitors ; lysophosphatidylcholine ; Lysophosphatidylcholines - immunology ; Mice ; monocyte/macrophage ; Monocytes - drug effects ; Monocytes - immunology ; oxidized phosphatidylcholine ; Peptide Fragments - chemistry ; Peptide Fragments - pharmacology ; Peptides - chemistry ; Peptides - pharmacology ; Phosphatidylcholines - immunology ; RNA, Messenger - metabolism</subject><ispartof>Drug development research, 2014-06, Vol.75 (4), p.246-256</ispartof><rights>2014 Wiley Periodicals, Inc.</rights><rights>Copyright © 2014 Wiley Periodicals, Inc., A Wiley Company</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fddr.21178$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fddr.21178$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24890951$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sato, Akira</creatorcontrib><creatorcontrib>Kumagai, Takeshi</creatorcontrib><creatorcontrib>Ebina, Keiichi</creatorcontrib><title>A Synthetic Biotinylated Peptide, BP21, Inhibits the Induction of mRNA Expression of Inflammatory Substances by Oxidized- and Lyso-Phosphatidylcholine</title><title>Drug development research</title><addtitle>Drug Dev. Res</addtitle><description>Preclinical Research
Oxidized low‐density lipoprotein (ox‐LDL) is implicated in many inflammatory diseases, e.g., type 2 diabetes, obesity, atherosclerosis, and metabolic syndrome. We previously reported that a synthetic biotinylated peptide, BP21, inhibits the bioactivity of ox‐LDL via direct binding to ox‐LDL. Here, we investigated the effect of BP21 on the mRNA expression of proinflammatory mediators induced by two major components of ox‐LDL, oxidized‐ and lyso‐phosphatidylcholine (ox‐PC and LPC), in monocytes/macrophages (THP‐1 cells) and adipocytes (3T3‐L1 cells). In THP‐1 cells, BP21 markedly reduced the mRNA expression of interleukin (IL)‐6, adipocyte fatty acid‐binding protein (aP2), tumor necrosis factor‐α, and mitogen‐activated protein kinase phosphatase‐1, which are induced by one of the major bioactive components of ox‐PC, 1‐palmitoyl‐2‐(5′‐oxo‐valeroyl)‐sn‐glycero‐3‐phosphocholine (POVPC), and reduced the mRNA expression of IL‐6, the ox‐LDL‐specific scavenger receptor CD36, and aP2 induced by LPC. In adipocytes, the mRNA expression of IL‐1β as an adipokine and aP2 is highly induced by ox‐PC and LPC, and BP21 markedly reduced the mRNA expression of IL‐1β and aP2 induced by POVPC and LPC. Furthermore, BP21 specifically bound to LPC and POVPC in a dose‐dependent manner. These results suggest that BP21 may be useful lead for the potential treatment and prevention of inflammatory diseases caused by ox‐PC and LPC.</description><subject>3T3-L1 Cells</subject><subject>adipocyte</subject><subject>Adipocytes</subject><subject>Adipocytes - drug effects</subject><subject>Adipocytes - immunology</subject><subject>Animals</subject><subject>anti-inflammatory drug</subject><subject>Biotin - analogs & derivatives</subject><subject>Biotin - chemistry</subject><subject>Biotin - pharmacology</subject><subject>biotinylated peptide</subject><subject>Biotinylation</subject><subject>Cell Line, Tumor</subject><subject>Cytokines</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hemolysin Proteins - chemistry</subject><subject>Hemolysin Proteins - pharmacology</subject><subject>Humans</subject><subject>inflammation</subject><subject>Kinases</subject><subject>Lipoproteins, LDL - antagonists & inhibitors</subject><subject>lysophosphatidylcholine</subject><subject>Lysophosphatidylcholines - immunology</subject><subject>Mice</subject><subject>monocyte/macrophage</subject><subject>Monocytes - drug effects</subject><subject>Monocytes - immunology</subject><subject>oxidized phosphatidylcholine</subject><subject>Peptide Fragments - chemistry</subject><subject>Peptide Fragments - pharmacology</subject><subject>Peptides - chemistry</subject><subject>Peptides - pharmacology</subject><subject>Phosphatidylcholines - immunology</subject><subject>RNA, Messenger - metabolism</subject><issn>0272-4391</issn><issn>1098-2299</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc9u3CAQxlHVqtmmPfQFKqReeogTwKyB427-rrRKVkmqSL0gDFgmtY1jsLrug_R5S7LbHHpimPl9M6P5APiM0TFGiJwYMxwTjBl_A2YYCZ4RIsRbMEOEkYzmAh-ADyE8IoQx5fw9OCCUCyTmeAb-LODd1MXaRqfh0vnouqlR0Rq4sX10xh7B5YbgI7jqale6GGBi08eMOjrfQV_B9vZ6Ac-3_WBD2KdWXdWotlXRDxO8G8sQVadtgOUEb7bOuN_WZFB1Bq6n4LNN7UNfqzRtanTtG9fZj-BdpZpgP-3fQ_D94vz-9Cpb31yuThfrzOU855lAOUO6pIpXmmhmBS8x5xqpyhYFQxbTgjBjKBKUFqXgRKuKFdrQyiJMlc0Pwbdd337wT6MNUbYuaNs0qrN-DBLPczYXlBOW0K__oY9-HLq03TNV4IIJUiTqy54ay9Ya2Q-uVcMk_108ASc74Jdr7PRax0g-WymTlfLFSnl2dvsSJEW2U7gQ7fZVoYafsmBpPflwfSmX9_mPi6t5IR_yvxs8oDs</recordid><startdate>201406</startdate><enddate>201406</enddate><creator>Sato, Akira</creator><creator>Kumagai, Takeshi</creator><creator>Ebina, Keiichi</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7QO</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201406</creationdate><title>A Synthetic Biotinylated Peptide, BP21, Inhibits the Induction of mRNA Expression of Inflammatory Substances by Oxidized- and Lyso-Phosphatidylcholine</title><author>Sato, Akira ; Kumagai, Takeshi ; Ebina, Keiichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i3838-90370cb4a8fc2c7e98b188c0afe6670e14627dd409446b982caf76cd4fe014ae3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>3T3-L1 Cells</topic><topic>adipocyte</topic><topic>Adipocytes</topic><topic>Adipocytes - drug effects</topic><topic>Adipocytes - immunology</topic><topic>Animals</topic><topic>anti-inflammatory drug</topic><topic>Biotin - analogs & derivatives</topic><topic>Biotin - chemistry</topic><topic>Biotin - pharmacology</topic><topic>biotinylated peptide</topic><topic>Biotinylation</topic><topic>Cell Line, Tumor</topic><topic>Cytokines</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Hemolysin Proteins - chemistry</topic><topic>Hemolysin Proteins - pharmacology</topic><topic>Humans</topic><topic>inflammation</topic><topic>Kinases</topic><topic>Lipoproteins, LDL - antagonists & inhibitors</topic><topic>lysophosphatidylcholine</topic><topic>Lysophosphatidylcholines - immunology</topic><topic>Mice</topic><topic>monocyte/macrophage</topic><topic>Monocytes - drug effects</topic><topic>Monocytes - immunology</topic><topic>oxidized phosphatidylcholine</topic><topic>Peptide Fragments - chemistry</topic><topic>Peptide Fragments - pharmacology</topic><topic>Peptides - chemistry</topic><topic>Peptides - pharmacology</topic><topic>Phosphatidylcholines - immunology</topic><topic>RNA, Messenger - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sato, Akira</creatorcontrib><creatorcontrib>Kumagai, Takeshi</creatorcontrib><creatorcontrib>Ebina, Keiichi</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Biotechnology Research Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Drug development research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sato, Akira</au><au>Kumagai, Takeshi</au><au>Ebina, Keiichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Synthetic Biotinylated Peptide, BP21, Inhibits the Induction of mRNA Expression of Inflammatory Substances by Oxidized- and Lyso-Phosphatidylcholine</atitle><jtitle>Drug development research</jtitle><addtitle>Drug Dev. Res</addtitle><date>2014-06</date><risdate>2014</risdate><volume>75</volume><issue>4</issue><spage>246</spage><epage>256</epage><pages>246-256</pages><issn>0272-4391</issn><eissn>1098-2299</eissn><coden>DDREDK</coden><abstract>Preclinical Research
Oxidized low‐density lipoprotein (ox‐LDL) is implicated in many inflammatory diseases, e.g., type 2 diabetes, obesity, atherosclerosis, and metabolic syndrome. We previously reported that a synthetic biotinylated peptide, BP21, inhibits the bioactivity of ox‐LDL via direct binding to ox‐LDL. Here, we investigated the effect of BP21 on the mRNA expression of proinflammatory mediators induced by two major components of ox‐LDL, oxidized‐ and lyso‐phosphatidylcholine (ox‐PC and LPC), in monocytes/macrophages (THP‐1 cells) and adipocytes (3T3‐L1 cells). In THP‐1 cells, BP21 markedly reduced the mRNA expression of interleukin (IL)‐6, adipocyte fatty acid‐binding protein (aP2), tumor necrosis factor‐α, and mitogen‐activated protein kinase phosphatase‐1, which are induced by one of the major bioactive components of ox‐PC, 1‐palmitoyl‐2‐(5′‐oxo‐valeroyl)‐sn‐glycero‐3‐phosphocholine (POVPC), and reduced the mRNA expression of IL‐6, the ox‐LDL‐specific scavenger receptor CD36, and aP2 induced by LPC. In adipocytes, the mRNA expression of IL‐1β as an adipokine and aP2 is highly induced by ox‐PC and LPC, and BP21 markedly reduced the mRNA expression of IL‐1β and aP2 induced by POVPC and LPC. Furthermore, BP21 specifically bound to LPC and POVPC in a dose‐dependent manner. These results suggest that BP21 may be useful lead for the potential treatment and prevention of inflammatory diseases caused by ox‐PC and LPC.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>24890951</pmid><doi>10.1002/ddr.21178</doi><tpages>11</tpages></addata></record> |
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| subjects | 3T3-L1 Cells adipocyte Adipocytes Adipocytes - drug effects Adipocytes - immunology Animals anti-inflammatory drug Biotin - analogs & derivatives Biotin - chemistry Biotin - pharmacology biotinylated peptide Biotinylation Cell Line, Tumor Cytokines Gene Expression Regulation - drug effects Hemolysin Proteins - chemistry Hemolysin Proteins - pharmacology Humans inflammation Kinases Lipoproteins, LDL - antagonists & inhibitors lysophosphatidylcholine Lysophosphatidylcholines - immunology Mice monocyte/macrophage Monocytes - drug effects Monocytes - immunology oxidized phosphatidylcholine Peptide Fragments - chemistry Peptide Fragments - pharmacology Peptides - chemistry Peptides - pharmacology Phosphatidylcholines - immunology RNA, Messenger - metabolism |
| title | A Synthetic Biotinylated Peptide, BP21, Inhibits the Induction of mRNA Expression of Inflammatory Substances by Oxidized- and Lyso-Phosphatidylcholine |
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