HIV1 protease inhibitors selectively induce inflammatory chemokine expression in primary human osteoblasts
HIV-infected patients are at increased risk of decreased bone mineral density. Several studies have implicated antiretroviral therapy as a contributor to the decreased bone mineral density seen in treated HIV-1 patients. Whilst the exact molecular mechanisms underlying decreased bone density remain...
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| Veröffentlicht in: | Antiviral research 2007-04, Vol.74 (1), p.72-76 |
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| creator | Malizia, Andrea P. Vioreanu, Mihai H. Doran, Peter P. Powderly, William G. |
| description | HIV-infected patients are at increased risk of decreased bone mineral density. Several studies have implicated antiretroviral therapy as a contributor to the decreased bone mineral density seen in treated HIV-1 patients. Whilst the exact molecular mechanisms underlying decreased bone density remain to be elucidated, inflammation has been postulated to be an important pathogenomic mechanism. In this study, we have explored primary human osteoblast gene expression in response to protease inhibitors (PIs), by oligonucleotide microarray analysis. A list of dysregulated genes, correlated with the inflammatory response, increased significantly after NFV and RTV exposure. Analysis of gene and protein expression determined a selectively increase of the pro-inflammatory cytokines monocyte chemoattractant protein (MCP)-1 and interleukin-8 (IL-8) following exposure to a pharmacological concentration of NFV and RTV. These data suggested that generation of local inflammatory cascades may contribute to the development of decreased bone mineral density in highly active antiretroviral therapy (HAART)-treated HIV patients. |
| doi_str_mv | 10.1016/j.antiviral.2006.12.003 |
| format | Article |
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Several studies have implicated antiretroviral therapy as a contributor to the decreased bone mineral density seen in treated HIV-1 patients. Whilst the exact molecular mechanisms underlying decreased bone density remain to be elucidated, inflammation has been postulated to be an important pathogenomic mechanism. In this study, we have explored primary human osteoblast gene expression in response to protease inhibitors (PIs), by oligonucleotide microarray analysis. A list of dysregulated genes, correlated with the inflammatory response, increased significantly after NFV and RTV exposure. Analysis of gene and protein expression determined a selectively increase of the pro-inflammatory cytokines monocyte chemoattractant protein (MCP)-1 and interleukin-8 (IL-8) following exposure to a pharmacological concentration of NFV and RTV. 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Antiparasitic agents ; Antiviral agents ; Biological and medical sciences ; Cells, Cultured ; Chemokine CCL2 - genetics ; Chemokine CCL2 - metabolism ; Chemokines - genetics ; Chemokines - metabolism ; Gene Expression Profiling ; Gene Expression Regulation - drug effects ; HAART ; HIV Protease Inhibitors - pharmacology ; Human immunodeficiency virus 1 ; Humans ; IL-8 ; Inflammation ; Interleukin-8 - genetics ; Interleukin-8 - metabolism ; MCP-1 ; Medical sciences ; Nelfinavir ; Nelfinavir - pharmacology ; Oligonucleotide Array Sequence Analysis ; Osteoblasts ; Osteoblasts - drug effects ; Osteoblasts - metabolism ; Pharmacology. 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Several studies have implicated antiretroviral therapy as a contributor to the decreased bone mineral density seen in treated HIV-1 patients. Whilst the exact molecular mechanisms underlying decreased bone density remain to be elucidated, inflammation has been postulated to be an important pathogenomic mechanism. In this study, we have explored primary human osteoblast gene expression in response to protease inhibitors (PIs), by oligonucleotide microarray analysis. A list of dysregulated genes, correlated with the inflammatory response, increased significantly after NFV and RTV exposure. Analysis of gene and protein expression determined a selectively increase of the pro-inflammatory cytokines monocyte chemoattractant protein (MCP)-1 and interleukin-8 (IL-8) following exposure to a pharmacological concentration of NFV and RTV. These data suggested that generation of local inflammatory cascades may contribute to the development of decreased bone mineral density in highly active antiretroviral therapy (HAART)-treated HIV patients.</description><subject>Antibiotics. Antiinfectious agents. Antiparasitic agents</subject><subject>Antiviral agents</subject><subject>Biological and medical sciences</subject><subject>Cells, Cultured</subject><subject>Chemokine CCL2 - genetics</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Chemokines - genetics</subject><subject>Chemokines - metabolism</subject><subject>Gene Expression Profiling</subject><subject>Gene Expression Regulation - drug effects</subject><subject>HAART</subject><subject>HIV Protease Inhibitors - pharmacology</subject><subject>Human immunodeficiency virus 1</subject><subject>Humans</subject><subject>IL-8</subject><subject>Inflammation</subject><subject>Interleukin-8 - genetics</subject><subject>Interleukin-8 - metabolism</subject><subject>MCP-1</subject><subject>Medical sciences</subject><subject>Nelfinavir</subject><subject>Nelfinavir - pharmacology</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Osteoblasts</subject><subject>Osteoblasts - drug effects</subject><subject>Osteoblasts - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Ritonavir</subject><subject>Ritonavir - pharmacology</subject><issn>0166-3542</issn><issn>1872-9096</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u1DAUhS0EotOBV4BsYJdgO8lNvKwqoJUqdQNsLce-0Xhw4uKbVPTt8WgiuuzKks937t9h7KPgleACvhwrMy_-0ScTKsk5VEJWnNev2E70nSwVV_Ca7TIJZd028oJdEh15BjvVv2UXopMNb4Dv2PHm9pcoHlJc0BAWfj74wS8xUUEY0OYeGJ7yt1vtSR2DmSaT9afCHnCKv_2MBf59SEjk45yJXMtPJuuHdTJzEWnBOARDC71jb0YTCN9v7579_Pb1x_VNeXf__fb66q60Tc2XUoKDTvROKBCGN26Ug-2FBGW6cWhBjqbmFmswwjSgXDsq1bW1BeQDV66Bes8-n-vmrf6sSIuePFkMwcwYV9Idl03f9vWLYJ4AoM1n3bPuDNoUiRKOeltSC65Peeij_p-HPuWhhdTZmJ0fthbrMKF79m0BZODTBhiyJozJzNbTM9eDFMDbzF2dOcyXe_SYNFmPs0XnU45Ju-hfHOYfuESvXA</recordid><startdate>20070401</startdate><enddate>20070401</enddate><creator>Malizia, Andrea P.</creator><creator>Vioreanu, Mihai H.</creator><creator>Doran, Peter P.</creator><creator>Powderly, William G.</creator><general>Elsevier B.V</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>7QP</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20070401</creationdate><title>HIV1 protease inhibitors selectively induce inflammatory chemokine expression in primary human osteoblasts</title><author>Malizia, Andrea P. ; Vioreanu, Mihai H. ; Doran, Peter P. ; Powderly, William G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c430t-26d6718d1961a04df2bc81269a7fb562fa30ce36a1a469d5f99753c6e0b09d463</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Antibiotics. Antiinfectious agents. Antiparasitic agents</topic><topic>Antiviral agents</topic><topic>Biological and medical sciences</topic><topic>Cells, Cultured</topic><topic>Chemokine CCL2 - genetics</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Chemokines - genetics</topic><topic>Chemokines - metabolism</topic><topic>Gene Expression Profiling</topic><topic>Gene Expression Regulation - drug effects</topic><topic>HAART</topic><topic>HIV Protease Inhibitors - pharmacology</topic><topic>Human immunodeficiency virus 1</topic><topic>Humans</topic><topic>IL-8</topic><topic>Inflammation</topic><topic>Interleukin-8 - genetics</topic><topic>Interleukin-8 - metabolism</topic><topic>MCP-1</topic><topic>Medical sciences</topic><topic>Nelfinavir</topic><topic>Nelfinavir - pharmacology</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Osteoblasts</topic><topic>Osteoblasts - drug effects</topic><topic>Osteoblasts - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Ritonavir</topic><topic>Ritonavir - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Malizia, Andrea P.</creatorcontrib><creatorcontrib>Vioreanu, Mihai H.</creatorcontrib><creatorcontrib>Doran, Peter P.</creatorcontrib><creatorcontrib>Powderly, William G.</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>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Antiviral research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Malizia, Andrea P.</au><au>Vioreanu, Mihai H.</au><au>Doran, Peter P.</au><au>Powderly, William G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HIV1 protease inhibitors selectively induce inflammatory chemokine expression in primary human osteoblasts</atitle><jtitle>Antiviral research</jtitle><addtitle>Antiviral Res</addtitle><date>2007-04-01</date><risdate>2007</risdate><volume>74</volume><issue>1</issue><spage>72</spage><epage>76</epage><pages>72-76</pages><issn>0166-3542</issn><eissn>1872-9096</eissn><coden>ARSRDR</coden><abstract>HIV-infected patients are at increased risk of decreased bone mineral density. Several studies have implicated antiretroviral therapy as a contributor to the decreased bone mineral density seen in treated HIV-1 patients. Whilst the exact molecular mechanisms underlying decreased bone density remain to be elucidated, inflammation has been postulated to be an important pathogenomic mechanism. In this study, we have explored primary human osteoblast gene expression in response to protease inhibitors (PIs), by oligonucleotide microarray analysis. A list of dysregulated genes, correlated with the inflammatory response, increased significantly after NFV and RTV exposure. Analysis of gene and protein expression determined a selectively increase of the pro-inflammatory cytokines monocyte chemoattractant protein (MCP)-1 and interleukin-8 (IL-8) following exposure to a pharmacological concentration of NFV and RTV. These data suggested that generation of local inflammatory cascades may contribute to the development of decreased bone mineral density in highly active antiretroviral therapy (HAART)-treated HIV patients.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>17240460</pmid><doi>10.1016/j.antiviral.2006.12.003</doi><tpages>5</tpages></addata></record> |
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| subjects | Antibiotics. Antiinfectious agents. Antiparasitic agents Antiviral agents Biological and medical sciences Cells, Cultured Chemokine CCL2 - genetics Chemokine CCL2 - metabolism Chemokines - genetics Chemokines - metabolism Gene Expression Profiling Gene Expression Regulation - drug effects HAART HIV Protease Inhibitors - pharmacology Human immunodeficiency virus 1 Humans IL-8 Inflammation Interleukin-8 - genetics Interleukin-8 - metabolism MCP-1 Medical sciences Nelfinavir Nelfinavir - pharmacology Oligonucleotide Array Sequence Analysis Osteoblasts Osteoblasts - drug effects Osteoblasts - metabolism Pharmacology. Drug treatments Ritonavir Ritonavir - pharmacology |
| title | HIV1 protease inhibitors selectively induce inflammatory chemokine expression in primary human osteoblasts |
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