Role of altered mitochondria functions in the pathogenesis of systemic lupus erythematosus
Mitochondria, main producers of reactive-oxygen species (ROS), were studied to examine their role in the pathogenesis of systemic lupus erythematosus (SLE). PBMCs and mitochondria were isolated from SLE patients and healthy volunteers for various parameters. Mitochondrial ROS, swelling, hyperpolariz...
Gespeichert in:
| Veröffentlicht in: | Lupus 2016-03, Vol.25 (3), p.272-281 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 281 |
|---|---|
| container_issue | 3 |
| container_start_page | 272 |
| container_title | Lupus |
| container_volume | 25 |
| creator | Leishangthem, B D Sharma, A Bhatnagar, A |
| description | Mitochondria, main producers of reactive-oxygen species (ROS), were studied to examine their role in the pathogenesis of systemic lupus erythematosus (SLE). PBMCs and mitochondria were isolated from SLE patients and healthy volunteers for various parameters. Mitochondrial ROS, swelling, hyperpolarization and levels of cytochrome c, caspase3 in the cells were assessed by flow cytometry. ROS was significantly increased in SLE patients (SLE vs controls: 1.83 ± 1.03 vs 1.10 ± 0.35; p |
| doi_str_mv | 10.1177/0961203315605370 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1773833648</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_0961203315605370</sage_id><sourcerecordid>1768167242</sourcerecordid><originalsourceid>FETCH-LOGICAL-c398t-fd529e5244d7f486961f5186bbec99b6fc3a9300c5ee250c0732359dc8b972bd3</originalsourceid><addsrcrecordid>eNqNkUtr3DAUhUVISCbT7rsqgmy6caKH9VqWkDaFQCAkm26MLF9nHGxrqisv5t9Hw6SlBApdCXS-c3SvDiGfOLvk3Jgr5jQXTEquNFPSsCOy4rUxVbkXx2S1l6u9fkbOEV8YY5I7fUrOhJZWCa5X5OdDHIHGnvoxQ4KOTkOOYRPnLg2e9ssc8hBnpMNM8wbo1udNfIYZcMC9C3eYYRoCHZftghTSrlCTzxEX_EBOej8ifHw71-Tp283j9W11d__9x_XXuypIZ3PVd0o4UKKuO9PXVpeZe8WtblsIzrW6D9I7yVhQAEKxwIwUUrku2NYZ0XZyTb4ccrcp_loAczMNGGAc_QxxwaZ8lLRS6tr-B6ot10bUoqAX79CXuKS5LNJwy4QSgjtZKHagQoqICfpmm4bJp13DWbOvqHlfUbF8fgte2gm6P4bfnRSgOgDon-GvV_8V-ApzyZf8</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1802522193</pqid></control><display><type>article</type><title>Role of altered mitochondria functions in the pathogenesis of systemic lupus erythematosus</title><source>SAGE Complete A-Z List</source><source>MEDLINE</source><creator>Leishangthem, B D ; Sharma, A ; Bhatnagar, A</creator><creatorcontrib>Leishangthem, B D ; Sharma, A ; Bhatnagar, A</creatorcontrib><description><![CDATA[Mitochondria, main producers of reactive-oxygen species (ROS), were studied to examine their role in the pathogenesis of systemic lupus erythematosus (SLE). PBMCs and mitochondria were isolated from SLE patients and healthy volunteers for various parameters. Mitochondrial ROS, swelling, hyperpolarization and levels of cytochrome c, caspase3 in the cells were assessed by flow cytometry. ROS was significantly increased in SLE patients (SLE vs controls: 1.83 ± 1.03 vs 1.10 ± 0.35; p < 0.0001). Depolarized state of mitochondria was greater in patients (SLE vs controls: 7.10 ± 5.50% vs 2.5 ± 1.8%; p < 0.05). Mitochondria swelling was found to be significantly altered in patients (SLE vs controls: 112.65 ± 36.56 vs 60.49 ± 20.69; p < 0.001). Expression of cytochrome c and caspase 3 (SLE vs controls: 1.37 ± 0.37% vs 1.01 ± 0.03%; 1.57 ± 0.46% vs 1.06 ± 0.07%; p < 0.05) respectively was found to be significantly increased in SLE. Further, the enzymatic activity of mitochondrial complex was assessed in isolated mitochondria. A significant decrease in activity of Complex I (SLE vs controls: 11.79 ± 3.18 vs 15.10 ± 6.38 nmol NADH oxidized/min/mg protein, p < 0.05); Complex IV (SLE vs control: 9.41 ± 5.16 vs 13.56 ± 5.92 nmol cytochrome c oxidized/min/mg protein, p < 0.05) and Complex V (SLE vs controls: 4.85 ± 1.39 vs 6.17 ± 2.02 nmol ATP hydrolyzed/min/mg protein, p < 0.05) was found in SLE patients in comparison to healthy controls. However, Complex II did not show significant variation in either group (SLE vs controls: 42.2 ± 28.6 vs 61.71 ± 42.3 nmol succinate oxidized/min/mg protein; ns). The decrease in enzyme activities of mitochondrial Complexes I, IV and V on one hand and ROS, hyperpolarization and apoptosis on the other points toward a possible role of mitochondria in the pathogenesis of lupus.]]></description><identifier>ISSN: 0961-2033</identifier><identifier>EISSN: 1477-0962</identifier><identifier>DOI: 10.1177/0961203315605370</identifier><identifier>PMID: 26385216</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adult ; Apoptosis ; Case-Control Studies ; Caspase 3 - analysis ; Cytochromes c - analysis ; Electron Transport Chain Complex Proteins - analysis ; Female ; Humans ; Leukocytes, Mononuclear - enzymology ; Leukocytes, Mononuclear - pathology ; Lupus Erythematosus, Systemic - diagnosis ; Lupus Erythematosus, Systemic - enzymology ; Lupus Erythematosus, Systemic - pathology ; Membrane Potential, Mitochondrial ; Mitochondria - enzymology ; Mitochondria - pathology ; Mitochondrial Diseases - diagnosis ; Mitochondrial Diseases - enzymology ; Mitochondrial Diseases - pathology ; Mitochondrial Swelling ; Reactive Oxygen Species - analysis</subject><ispartof>Lupus, 2016-03, Vol.25 (3), p.272-281</ispartof><rights>The Author(s) 2015</rights><rights>The Author(s) 2015.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c398t-fd529e5244d7f486961f5186bbec99b6fc3a9300c5ee250c0732359dc8b972bd3</citedby><cites>FETCH-LOGICAL-c398t-fd529e5244d7f486961f5186bbec99b6fc3a9300c5ee250c0732359dc8b972bd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0961203315605370$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0961203315605370$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,776,780,21798,27901,27902,43597,43598</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26385216$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Leishangthem, B D</creatorcontrib><creatorcontrib>Sharma, A</creatorcontrib><creatorcontrib>Bhatnagar, A</creatorcontrib><title>Role of altered mitochondria functions in the pathogenesis of systemic lupus erythematosus</title><title>Lupus</title><addtitle>Lupus</addtitle><description><![CDATA[Mitochondria, main producers of reactive-oxygen species (ROS), were studied to examine their role in the pathogenesis of systemic lupus erythematosus (SLE). PBMCs and mitochondria were isolated from SLE patients and healthy volunteers for various parameters. Mitochondrial ROS, swelling, hyperpolarization and levels of cytochrome c, caspase3 in the cells were assessed by flow cytometry. ROS was significantly increased in SLE patients (SLE vs controls: 1.83 ± 1.03 vs 1.10 ± 0.35; p < 0.0001). Depolarized state of mitochondria was greater in patients (SLE vs controls: 7.10 ± 5.50% vs 2.5 ± 1.8%; p < 0.05). Mitochondria swelling was found to be significantly altered in patients (SLE vs controls: 112.65 ± 36.56 vs 60.49 ± 20.69; p < 0.001). Expression of cytochrome c and caspase 3 (SLE vs controls: 1.37 ± 0.37% vs 1.01 ± 0.03%; 1.57 ± 0.46% vs 1.06 ± 0.07%; p < 0.05) respectively was found to be significantly increased in SLE. Further, the enzymatic activity of mitochondrial complex was assessed in isolated mitochondria. A significant decrease in activity of Complex I (SLE vs controls: 11.79 ± 3.18 vs 15.10 ± 6.38 nmol NADH oxidized/min/mg protein, p < 0.05); Complex IV (SLE vs control: 9.41 ± 5.16 vs 13.56 ± 5.92 nmol cytochrome c oxidized/min/mg protein, p < 0.05) and Complex V (SLE vs controls: 4.85 ± 1.39 vs 6.17 ± 2.02 nmol ATP hydrolyzed/min/mg protein, p < 0.05) was found in SLE patients in comparison to healthy controls. However, Complex II did not show significant variation in either group (SLE vs controls: 42.2 ± 28.6 vs 61.71 ± 42.3 nmol succinate oxidized/min/mg protein; ns). The decrease in enzyme activities of mitochondrial Complexes I, IV and V on one hand and ROS, hyperpolarization and apoptosis on the other points toward a possible role of mitochondria in the pathogenesis of lupus.]]></description><subject>Adult</subject><subject>Apoptosis</subject><subject>Case-Control Studies</subject><subject>Caspase 3 - analysis</subject><subject>Cytochromes c - analysis</subject><subject>Electron Transport Chain Complex Proteins - analysis</subject><subject>Female</subject><subject>Humans</subject><subject>Leukocytes, Mononuclear - enzymology</subject><subject>Leukocytes, Mononuclear - pathology</subject><subject>Lupus Erythematosus, Systemic - diagnosis</subject><subject>Lupus Erythematosus, Systemic - enzymology</subject><subject>Lupus Erythematosus, Systemic - pathology</subject><subject>Membrane Potential, Mitochondrial</subject><subject>Mitochondria - enzymology</subject><subject>Mitochondria - pathology</subject><subject>Mitochondrial Diseases - diagnosis</subject><subject>Mitochondrial Diseases - enzymology</subject><subject>Mitochondrial Diseases - pathology</subject><subject>Mitochondrial Swelling</subject><subject>Reactive Oxygen Species - analysis</subject><issn>0961-2033</issn><issn>1477-0962</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUtr3DAUhUVISCbT7rsqgmy6caKH9VqWkDaFQCAkm26MLF9nHGxrqisv5t9Hw6SlBApdCXS-c3SvDiGfOLvk3Jgr5jQXTEquNFPSsCOy4rUxVbkXx2S1l6u9fkbOEV8YY5I7fUrOhJZWCa5X5OdDHIHGnvoxQ4KOTkOOYRPnLg2e9ssc8hBnpMNM8wbo1udNfIYZcMC9C3eYYRoCHZftghTSrlCTzxEX_EBOej8ifHw71-Tp283j9W11d__9x_XXuypIZ3PVd0o4UKKuO9PXVpeZe8WtblsIzrW6D9I7yVhQAEKxwIwUUrku2NYZ0XZyTb4ccrcp_loAczMNGGAc_QxxwaZ8lLRS6tr-B6ot10bUoqAX79CXuKS5LNJwy4QSgjtZKHagQoqICfpmm4bJp13DWbOvqHlfUbF8fgte2gm6P4bfnRSgOgDon-GvV_8V-ApzyZf8</recordid><startdate>201603</startdate><enddate>201603</enddate><creator>Leishangthem, B D</creator><creator>Sharma, A</creator><creator>Bhatnagar, A</creator><general>SAGE Publications</general><general>Sage Publications Ltd</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>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201603</creationdate><title>Role of altered mitochondria functions in the pathogenesis of systemic lupus erythematosus</title><author>Leishangthem, B D ; Sharma, A ; Bhatnagar, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-fd529e5244d7f486961f5186bbec99b6fc3a9300c5ee250c0732359dc8b972bd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adult</topic><topic>Apoptosis</topic><topic>Case-Control Studies</topic><topic>Caspase 3 - analysis</topic><topic>Cytochromes c - analysis</topic><topic>Electron Transport Chain Complex Proteins - analysis</topic><topic>Female</topic><topic>Humans</topic><topic>Leukocytes, Mononuclear - enzymology</topic><topic>Leukocytes, Mononuclear - pathology</topic><topic>Lupus Erythematosus, Systemic - diagnosis</topic><topic>Lupus Erythematosus, Systemic - enzymology</topic><topic>Lupus Erythematosus, Systemic - pathology</topic><topic>Membrane Potential, Mitochondrial</topic><topic>Mitochondria - enzymology</topic><topic>Mitochondria - pathology</topic><topic>Mitochondrial Diseases - diagnosis</topic><topic>Mitochondrial Diseases - enzymology</topic><topic>Mitochondrial Diseases - pathology</topic><topic>Mitochondrial Swelling</topic><topic>Reactive Oxygen Species - analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Leishangthem, B D</creatorcontrib><creatorcontrib>Sharma, A</creatorcontrib><creatorcontrib>Bhatnagar, A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Lupus</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Leishangthem, B D</au><au>Sharma, A</au><au>Bhatnagar, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of altered mitochondria functions in the pathogenesis of systemic lupus erythematosus</atitle><jtitle>Lupus</jtitle><addtitle>Lupus</addtitle><date>2016-03</date><risdate>2016</risdate><volume>25</volume><issue>3</issue><spage>272</spage><epage>281</epage><pages>272-281</pages><issn>0961-2033</issn><eissn>1477-0962</eissn><abstract><![CDATA[Mitochondria, main producers of reactive-oxygen species (ROS), were studied to examine their role in the pathogenesis of systemic lupus erythematosus (SLE). PBMCs and mitochondria were isolated from SLE patients and healthy volunteers for various parameters. Mitochondrial ROS, swelling, hyperpolarization and levels of cytochrome c, caspase3 in the cells were assessed by flow cytometry. ROS was significantly increased in SLE patients (SLE vs controls: 1.83 ± 1.03 vs 1.10 ± 0.35; p < 0.0001). Depolarized state of mitochondria was greater in patients (SLE vs controls: 7.10 ± 5.50% vs 2.5 ± 1.8%; p < 0.05). Mitochondria swelling was found to be significantly altered in patients (SLE vs controls: 112.65 ± 36.56 vs 60.49 ± 20.69; p < 0.001). Expression of cytochrome c and caspase 3 (SLE vs controls: 1.37 ± 0.37% vs 1.01 ± 0.03%; 1.57 ± 0.46% vs 1.06 ± 0.07%; p < 0.05) respectively was found to be significantly increased in SLE. Further, the enzymatic activity of mitochondrial complex was assessed in isolated mitochondria. A significant decrease in activity of Complex I (SLE vs controls: 11.79 ± 3.18 vs 15.10 ± 6.38 nmol NADH oxidized/min/mg protein, p < 0.05); Complex IV (SLE vs control: 9.41 ± 5.16 vs 13.56 ± 5.92 nmol cytochrome c oxidized/min/mg protein, p < 0.05) and Complex V (SLE vs controls: 4.85 ± 1.39 vs 6.17 ± 2.02 nmol ATP hydrolyzed/min/mg protein, p < 0.05) was found in SLE patients in comparison to healthy controls. However, Complex II did not show significant variation in either group (SLE vs controls: 42.2 ± 28.6 vs 61.71 ± 42.3 nmol succinate oxidized/min/mg protein; ns). The decrease in enzyme activities of mitochondrial Complexes I, IV and V on one hand and ROS, hyperpolarization and apoptosis on the other points toward a possible role of mitochondria in the pathogenesis of lupus.]]></abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>26385216</pmid><doi>10.1177/0961203315605370</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0961-2033 |
| ispartof | Lupus, 2016-03, Vol.25 (3), p.272-281 |
| issn | 0961-2033 1477-0962 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1773833648 |
| source | SAGE Complete A-Z List; MEDLINE |
| subjects | Adult Apoptosis Case-Control Studies Caspase 3 - analysis Cytochromes c - analysis Electron Transport Chain Complex Proteins - analysis Female Humans Leukocytes, Mononuclear - enzymology Leukocytes, Mononuclear - pathology Lupus Erythematosus, Systemic - diagnosis Lupus Erythematosus, Systemic - enzymology Lupus Erythematosus, Systemic - pathology Membrane Potential, Mitochondrial Mitochondria - enzymology Mitochondria - pathology Mitochondrial Diseases - diagnosis Mitochondrial Diseases - enzymology Mitochondrial Diseases - pathology Mitochondrial Swelling Reactive Oxygen Species - analysis |
| title | Role of altered mitochondria functions in the pathogenesis of systemic lupus erythematosus |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-30T02%3A30%3A05IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Role%20of%20altered%20mitochondria%20functions%20in%20the%20pathogenesis%20of%20systemic%20lupus%20erythematosus&rft.jtitle=Lupus&rft.au=Leishangthem,%20B%20D&rft.date=2016-03&rft.volume=25&rft.issue=3&rft.spage=272&rft.epage=281&rft.pages=272-281&rft.issn=0961-2033&rft.eissn=1477-0962&rft_id=info:doi/10.1177/0961203315605370&rft_dat=%3Cproquest_cross%3E1768167242%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1802522193&rft_id=info:pmid/26385216&rft_sage_id=10.1177_0961203315605370&rfr_iscdi=true |