COX5B and COX2 gene expressions in Multiple Sclerosis
Multiple Sclerosis (MS) is an autoimmune inflammatory disease which affects the Central Nervous System (CNS) and leads to the destruction of myelin and atrophy of the axons. Genetic factors, in addition to environmental ones, seem to play a role in MS. Numerous studies have reported mitochondrial de...
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Veröffentlicht in: | Journal of cell and molecular biology 2012-12, Vol.10 (2), p.21-21 |
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description | Multiple Sclerosis (MS) is an autoimmune inflammatory disease which affects the Central Nervous System (CNS) and leads to the destruction of myelin and atrophy of the axons. Genetic factors, in addition to environmental ones, seem to play a role in MS. Numerous studies have reported mitochondrial defects including a reduction in COX complex function related to the decrease of mitochondrial gene expression in the cortex tissue of MS patients. This study aimed to assess COX5B and COX2 gene expression in MS patients and controls. By using Real-Time PCR method, expression levels of the COX5B and COX2 were determined, with reference to s-actin and GAPDH. The results showed that COX5B gene expression is significantly reduced in MS patients compared to control (P |
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Genetic factors, in addition to environmental ones, seem to play a role in MS. Numerous studies have reported mitochondrial defects including a reduction in COX complex function related to the decrease of mitochondrial gene expression in the cortex tissue of MS patients. This study aimed to assess COX5B and COX2 gene expression in MS patients and controls. By using Real-Time PCR method, expression levels of the COX5B and COX2 were determined, with reference to s-actin and GAPDH. The results showed that COX5B gene expression is significantly reduced in MS patients compared to control (P<0.05), whereas there was no significant difference in the COX2 gene expression. Thus, it can be claimed that down-regulation of mitochondrial electron transport chain genes supported the hypothesis that hypoxia-like tissue injury in MS may be due to mitochondrial gene expression impairments.</description><identifier>ISSN: 1303-3646</identifier><identifier>EISSN: 1306-0961</identifier><language>eng</language><subject>Atrophy</subject><ispartof>Journal of cell and molecular biology, 2012-12, Vol.10 (2), p.21-21</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids></links><search><creatorcontrib>Safavizadeh, Naeimeh</creatorcontrib><creatorcontrib>Rahmani, Seyed Ali</creatorcontrib><creatorcontrib>Zaefizadeh, Mohamad</creatorcontrib><title>COX5B and COX2 gene expressions in Multiple Sclerosis</title><title>Journal of cell and molecular biology</title><description>Multiple Sclerosis (MS) is an autoimmune inflammatory disease which affects the Central Nervous System (CNS) and leads to the destruction of myelin and atrophy of the axons. Genetic factors, in addition to environmental ones, seem to play a role in MS. Numerous studies have reported mitochondrial defects including a reduction in COX complex function related to the decrease of mitochondrial gene expression in the cortex tissue of MS patients. This study aimed to assess COX5B and COX2 gene expression in MS patients and controls. By using Real-Time PCR method, expression levels of the COX5B and COX2 were determined, with reference to s-actin and GAPDH. The results showed that COX5B gene expression is significantly reduced in MS patients compared to control (P<0.05), whereas there was no significant difference in the COX2 gene expression. Thus, it can be claimed that down-regulation of mitochondrial electron transport chain genes supported the hypothesis that hypoxia-like tissue injury in MS may be due to mitochondrial gene expression impairments.</description><subject>Atrophy</subject><issn>1303-3646</issn><issn>1306-0961</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><recordid>eNqNjMtqwzAQRUVpoSHNP2jZjWGkkcbysjV9QUIWzaK7IFvjIFBs14qhn1_T9gO6ugfu4VyJlUKgAipS1z-MBZKhW7HJOTYAzgIpcCth6_2HfZS-D3IhLU_cs-SvceJFHPosYy93c7rEMbF8bxNPQ475Ttx0PmXe_O1aHJ6fDvVrsd2_vNUP22IksoXxBsEAaG0BqUVDpWmoDNwBsUavKh-6xnXg2IXlQe8MhsroYJ0lRlyL-9_sOA2fM-fL8Rxzyyn5noc5HxUuRedA23-qxpaA30R7UEg</recordid><startdate>20121201</startdate><enddate>20121201</enddate><creator>Safavizadeh, Naeimeh</creator><creator>Rahmani, Seyed Ali</creator><creator>Zaefizadeh, Mohamad</creator><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7TK</scope></search><sort><creationdate>20121201</creationdate><title>COX5B and COX2 gene expressions in Multiple Sclerosis</title><author>Safavizadeh, Naeimeh ; Rahmani, Seyed Ali ; Zaefizadeh, Mohamad</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p665-4a430400225036c34674b67def06e23a19adfb8f08e8d4b63a843d942d5856e33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Atrophy</topic><toplevel>online_resources</toplevel><creatorcontrib>Safavizadeh, Naeimeh</creatorcontrib><creatorcontrib>Rahmani, Seyed Ali</creatorcontrib><creatorcontrib>Zaefizadeh, Mohamad</creatorcontrib><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Neurosciences Abstracts</collection><jtitle>Journal of cell and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Safavizadeh, Naeimeh</au><au>Rahmani, Seyed Ali</au><au>Zaefizadeh, Mohamad</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>COX5B and COX2 gene expressions in Multiple Sclerosis</atitle><jtitle>Journal of cell and molecular biology</jtitle><date>2012-12-01</date><risdate>2012</risdate><volume>10</volume><issue>2</issue><spage>21</spage><epage>21</epage><pages>21-21</pages><issn>1303-3646</issn><eissn>1306-0961</eissn><abstract>Multiple Sclerosis (MS) is an autoimmune inflammatory disease which affects the Central Nervous System (CNS) and leads to the destruction of myelin and atrophy of the axons. Genetic factors, in addition to environmental ones, seem to play a role in MS. Numerous studies have reported mitochondrial defects including a reduction in COX complex function related to the decrease of mitochondrial gene expression in the cortex tissue of MS patients. This study aimed to assess COX5B and COX2 gene expression in MS patients and controls. By using Real-Time PCR method, expression levels of the COX5B and COX2 were determined, with reference to s-actin and GAPDH. The results showed that COX5B gene expression is significantly reduced in MS patients compared to control (P<0.05), whereas there was no significant difference in the COX2 gene expression. Thus, it can be claimed that down-regulation of mitochondrial electron transport chain genes supported the hypothesis that hypoxia-like tissue injury in MS may be due to mitochondrial gene expression impairments.</abstract><tpages>1</tpages></addata></record> |
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subjects | Atrophy |
title | COX5B and COX2 gene expressions in Multiple Sclerosis |
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