Increased MCP-1 gene expression in monocytes of severe OSA patients and under intermittent hypoxia
Purpose Obstructive sleep apnea (OSA) is known to be a risk factor of coronary artery disease. Monocyte chemoattractant protein-1 (MCP-1), as a critical factor for monocyte infiltration, is known to play a role in the development of atherosclerosis. This study aimed to investigate the effect of inte...
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| Veröffentlicht in: | Sleep & breathing 2016-03, Vol.20 (1), p.425-433 |
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| creator | Chuang, Li-Pang Chen, Ning-Hung Lin, Yuling Ko, Wen-Shan Pang, Jong-Hwei S. |
| description | Purpose
Obstructive sleep apnea (OSA) is known to be a risk factor of coronary artery disease. Monocyte chemoattractant protein-1 (MCP-1), as a critical factor for monocyte infiltration, is known to play a role in the development of atherosclerosis. This study aimed to investigate the effect of intermittent hypoxia, the hallmark of OSA, on the MCP-1 expression of monocytes.
Methods
Peripheral blood was sampled from 61 adults enrolled for suspected OSA. RNA was prepared from the isolated monocytes for the analysis of MCP-1. The effect of in vitro intermittent hypoxia on the regulation and function of MCP-1 was investigated on THP-1 monocytic cells and human monocytes. The mRNA and secreted protein levels were investigated by RT/real-time PCR and enzyme-linked immunosorbent assay, respectively.
Results
Monocytic MCP-1 gene expression was found to be increased significantly in severe OSA patients. In vitro intermittent hypoxia was demonstrated to increase the mRNA and protein expression levels of MCP-1 dose- and time-dependently in THP-1 monocytic cells. The MCP-1 mRNA expression in monocytes isolated from OSA patient was induced to a much higher level compared to that from normal control. Pre-treatment with inhibitor for p42/44 MAPK or p38 MAPK suppressed the activation of MCP-1 expression by intermittent hypoxia.
Conclusions
This is the first study to demonstrate the increase of MCP-1 gene expression in monocytes of severe OSA patients. In addition, monocytic MCP-1 gene expression can be induced under intermittent hypoxia. |
| doi_str_mv | 10.1007/s11325-015-1252-5 |
| format | Article |
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Obstructive sleep apnea (OSA) is known to be a risk factor of coronary artery disease. Monocyte chemoattractant protein-1 (MCP-1), as a critical factor for monocyte infiltration, is known to play a role in the development of atherosclerosis. This study aimed to investigate the effect of intermittent hypoxia, the hallmark of OSA, on the MCP-1 expression of monocytes.
Methods
Peripheral blood was sampled from 61 adults enrolled for suspected OSA. RNA was prepared from the isolated monocytes for the analysis of MCP-1. The effect of in vitro intermittent hypoxia on the regulation and function of MCP-1 was investigated on THP-1 monocytic cells and human monocytes. The mRNA and secreted protein levels were investigated by RT/real-time PCR and enzyme-linked immunosorbent assay, respectively.
Results
Monocytic MCP-1 gene expression was found to be increased significantly in severe OSA patients. In vitro intermittent hypoxia was demonstrated to increase the mRNA and protein expression levels of MCP-1 dose- and time-dependently in THP-1 monocytic cells. The MCP-1 mRNA expression in monocytes isolated from OSA patient was induced to a much higher level compared to that from normal control. Pre-treatment with inhibitor for p42/44 MAPK or p38 MAPK suppressed the activation of MCP-1 expression by intermittent hypoxia.
Conclusions
This is the first study to demonstrate the increase of MCP-1 gene expression in monocytes of severe OSA patients. In addition, monocytic MCP-1 gene expression can be induced under intermittent hypoxia.</description><identifier>ISSN: 1520-9512</identifier><identifier>EISSN: 1522-1709</identifier><identifier>DOI: 10.1007/s11325-015-1252-5</identifier><identifier>PMID: 26354107</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adult ; Atherosclerosis - diagnosis ; Atherosclerosis - genetics ; Chemokine CCL2 - genetics ; Dentistry ; Female ; Gene expression ; Gene Expression - genetics ; Humans ; Hypoxia ; Hypoxia - diagnosis ; Hypoxia - genetics ; Hypoxia • Original Article ; Internal Medicine ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Monocytes - metabolism ; Neurology ; Otorhinolaryngology ; Pediatrics ; Pneumology/Respiratory System ; Polysomnography ; Reference Values ; Risk Factors ; RNA, Messenger - genetics ; Sleep apnea ; Sleep Apnea, Obstructive - diagnosis ; Sleep Apnea, Obstructive - genetics</subject><ispartof>Sleep & breathing, 2016-03, Vol.20 (1), p.425-433</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c541t-1eb3d5e03f6733f50d56f5647fab6295fd06111b1b1eee7d642e9f86d2b923d53</citedby><cites>FETCH-LOGICAL-c541t-1eb3d5e03f6733f50d56f5647fab6295fd06111b1b1eee7d642e9f86d2b923d53</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/s11325-015-1252-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11325-015-1252-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26354107$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chuang, Li-Pang</creatorcontrib><creatorcontrib>Chen, Ning-Hung</creatorcontrib><creatorcontrib>Lin, Yuling</creatorcontrib><creatorcontrib>Ko, Wen-Shan</creatorcontrib><creatorcontrib>Pang, Jong-Hwei S.</creatorcontrib><title>Increased MCP-1 gene expression in monocytes of severe OSA patients and under intermittent hypoxia</title><title>Sleep & breathing</title><addtitle>Sleep Breath</addtitle><addtitle>Sleep Breath</addtitle><description>Purpose
Obstructive sleep apnea (OSA) is known to be a risk factor of coronary artery disease. Monocyte chemoattractant protein-1 (MCP-1), as a critical factor for monocyte infiltration, is known to play a role in the development of atherosclerosis. This study aimed to investigate the effect of intermittent hypoxia, the hallmark of OSA, on the MCP-1 expression of monocytes.
Methods
Peripheral blood was sampled from 61 adults enrolled for suspected OSA. RNA was prepared from the isolated monocytes for the analysis of MCP-1. The effect of in vitro intermittent hypoxia on the regulation and function of MCP-1 was investigated on THP-1 monocytic cells and human monocytes. The mRNA and secreted protein levels were investigated by RT/real-time PCR and enzyme-linked immunosorbent assay, respectively.
Results
Monocytic MCP-1 gene expression was found to be increased significantly in severe OSA patients. In vitro intermittent hypoxia was demonstrated to increase the mRNA and protein expression levels of MCP-1 dose- and time-dependently in THP-1 monocytic cells. The MCP-1 mRNA expression in monocytes isolated from OSA patient was induced to a much higher level compared to that from normal control. Pre-treatment with inhibitor for p42/44 MAPK or p38 MAPK suppressed the activation of MCP-1 expression by intermittent hypoxia.
Conclusions
This is the first study to demonstrate the increase of MCP-1 gene expression in monocytes of severe OSA patients. In addition, monocytic MCP-1 gene expression can be induced under intermittent hypoxia.</description><subject>Adult</subject><subject>Atherosclerosis - diagnosis</subject><subject>Atherosclerosis - genetics</subject><subject>Chemokine CCL2 - genetics</subject><subject>Dentistry</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression - genetics</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Hypoxia - diagnosis</subject><subject>Hypoxia - genetics</subject><subject>Hypoxia • Original Article</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Monocytes - metabolism</subject><subject>Neurology</subject><subject>Otorhinolaryngology</subject><subject>Pediatrics</subject><subject>Pneumology/Respiratory System</subject><subject>Polysomnography</subject><subject>Reference Values</subject><subject>Risk Factors</subject><subject>RNA, Messenger - genetics</subject><subject>Sleep apnea</subject><subject>Sleep Apnea, Obstructive - diagnosis</subject><subject>Sleep Apnea, Obstructive - genetics</subject><issn>1520-9512</issn><issn>1522-1709</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkU1vFSEUhomxsbX6A9wYEjduUA4McFk2N340qWmT1jWZGQ51mjswwkzT--9lvNUYE2NYQOA57znkIeQV8HfAuXlfAKRQjINiIJRg6gk5ASUEA8Pt059nzqwCcUyel3LHOTQbC8_IsdBSNcDNCenOY5-xLejpl-0VA3qLESk-TBlLGVKkQ6Rjiqnfz1hoCrTgPWakl9dndGrnAeNcaBs9XaLHXOkZ8zjMc72n3_ZTehjaF-QotLuCLx_3U_L144eb7Wd2cfnpfHt2wfo6y8wAO-kVchm0kTIo7pUOSjcmtJ0WVgXPNQB0dSGi8boRaMNGe9FZUSvlKXl7yJ1y-r5gmd04lB53uzZiWooDC9YakGbzf9SYBjQ3Wlb0zV_oXVpyrB9ZKSmMtnoNhAPV51RKxuCmPIxt3jvgbnXlDq5cdeVWV26d9_Vj8tKN6H9X_JJTAXEASn2Kt5j_aP3P1B9-T52I</recordid><startdate>20160301</startdate><enddate>20160301</enddate><creator>Chuang, Li-Pang</creator><creator>Chen, Ning-Hung</creator><creator>Lin, Yuling</creator><creator>Ko, Wen-Shan</creator><creator>Pang, Jong-Hwei S.</creator><general>Springer Berlin Heidelberg</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>0-V</scope><scope>3V.</scope><scope>7T5</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>88J</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2R</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20160301</creationdate><title>Increased MCP-1 gene expression in monocytes of severe OSA patients and under intermittent hypoxia</title><author>Chuang, Li-Pang ; Chen, Ning-Hung ; Lin, Yuling ; Ko, Wen-Shan ; Pang, Jong-Hwei S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c541t-1eb3d5e03f6733f50d56f5647fab6295fd06111b1b1eee7d642e9f86d2b923d53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adult</topic><topic>Atherosclerosis - diagnosis</topic><topic>Atherosclerosis - genetics</topic><topic>Chemokine CCL2 - genetics</topic><topic>Dentistry</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression - genetics</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Hypoxia - diagnosis</topic><topic>Hypoxia - genetics</topic><topic>Hypoxia • Original Article</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Monocytes - metabolism</topic><topic>Neurology</topic><topic>Otorhinolaryngology</topic><topic>Pediatrics</topic><topic>Pneumology/Respiratory System</topic><topic>Polysomnography</topic><topic>Reference Values</topic><topic>Risk Factors</topic><topic>RNA, Messenger - genetics</topic><topic>Sleep apnea</topic><topic>Sleep Apnea, Obstructive - diagnosis</topic><topic>Sleep Apnea, Obstructive - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chuang, Li-Pang</creatorcontrib><creatorcontrib>Chen, Ning-Hung</creatorcontrib><creatorcontrib>Lin, Yuling</creatorcontrib><creatorcontrib>Ko, Wen-Shan</creatorcontrib><creatorcontrib>Pang, Jong-Hwei S.</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 Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Social Science Database (Alumni Edition)</collection><collection>ProQuest Pharma 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>Social Science Premium Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Social Science 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 One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Sleep & breathing</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chuang, Li-Pang</au><au>Chen, Ning-Hung</au><au>Lin, Yuling</au><au>Ko, Wen-Shan</au><au>Pang, Jong-Hwei S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased MCP-1 gene expression in monocytes of severe OSA patients and under intermittent hypoxia</atitle><jtitle>Sleep & breathing</jtitle><stitle>Sleep Breath</stitle><addtitle>Sleep Breath</addtitle><date>2016-03-01</date><risdate>2016</risdate><volume>20</volume><issue>1</issue><spage>425</spage><epage>433</epage><pages>425-433</pages><issn>1520-9512</issn><eissn>1522-1709</eissn><abstract>Purpose
Obstructive sleep apnea (OSA) is known to be a risk factor of coronary artery disease. Monocyte chemoattractant protein-1 (MCP-1), as a critical factor for monocyte infiltration, is known to play a role in the development of atherosclerosis. This study aimed to investigate the effect of intermittent hypoxia, the hallmark of OSA, on the MCP-1 expression of monocytes.
Methods
Peripheral blood was sampled from 61 adults enrolled for suspected OSA. RNA was prepared from the isolated monocytes for the analysis of MCP-1. The effect of in vitro intermittent hypoxia on the regulation and function of MCP-1 was investigated on THP-1 monocytic cells and human monocytes. The mRNA and secreted protein levels were investigated by RT/real-time PCR and enzyme-linked immunosorbent assay, respectively.
Results
Monocytic MCP-1 gene expression was found to be increased significantly in severe OSA patients. In vitro intermittent hypoxia was demonstrated to increase the mRNA and protein expression levels of MCP-1 dose- and time-dependently in THP-1 monocytic cells. The MCP-1 mRNA expression in monocytes isolated from OSA patient was induced to a much higher level compared to that from normal control. Pre-treatment with inhibitor for p42/44 MAPK or p38 MAPK suppressed the activation of MCP-1 expression by intermittent hypoxia.
Conclusions
This is the first study to demonstrate the increase of MCP-1 gene expression in monocytes of severe OSA patients. In addition, monocytic MCP-1 gene expression can be induced under intermittent hypoxia.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26354107</pmid><doi>10.1007/s11325-015-1252-5</doi><tpages>9</tpages></addata></record> |
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| subjects | Adult Atherosclerosis - diagnosis Atherosclerosis - genetics Chemokine CCL2 - genetics Dentistry Female Gene expression Gene Expression - genetics Humans Hypoxia Hypoxia - diagnosis Hypoxia - genetics Hypoxia • Original Article Internal Medicine Male Medicine Medicine & Public Health Middle Aged Monocytes - metabolism Neurology Otorhinolaryngology Pediatrics Pneumology/Respiratory System Polysomnography Reference Values Risk Factors RNA, Messenger - genetics Sleep apnea Sleep Apnea, Obstructive - diagnosis Sleep Apnea, Obstructive - genetics |
| title | Increased MCP-1 gene expression in monocytes of severe OSA patients and under intermittent hypoxia |
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