Haemolytic anaemia and alterations in hepatic iron metabolism in aged mice lacking Cu,Zn-superoxide dismutase
The continuous recycling of haem iron following phagocytosis and catabolism of senescent and damaged red blood cells by macrophages is a crucial process in the maintenance of systemic iron homoeostasis. However, little is known about macrophage iron handling in haemolytic states resulting from a def...
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| Veröffentlicht in: | Biochemical journal 2009-06, Vol.420 (3), p.383-390 |
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| creator | Starzyński, Rafał R Canonne-Hergaux, François Willemetz, Alexandra Gralak, Mikołaj A Woliński, Jarosław Styś, Agnieszka Olszak, Jarosław Lipiński, Paweł |
| description | The continuous recycling of haem iron following phagocytosis and catabolism of senescent and damaged red blood cells by macrophages is a crucial process in the maintenance of systemic iron homoeostasis. However, little is known about macrophage iron handling in haemolytic states resulting from a deficiency in antioxidant defences. Our observations indicate that the recently described chronic, but moderate regenerative, haemolytic anaemia of aged SOD1 (superoxide dismutase 1)-knockout mice is associated with red blood cell modifications and sensitivity to both intra- and extra-vascular haemolysis. In the present study, we have characterized the molecular pathways of iron turnover in the liver of Sod1-deficient mice. Despite iron accumulation in liver macrophages, namely Kupffer cells, we did not measure any significant change in non-haem liver iron. Interestingly, in Kupffer cells, expression of the rate-limiting enzyme in haem degradation, haem oxygenase-1, and expression of the iron exporter ferroportin were both up-regulated, whereas the hepcidin mRNA level in the liver was decreased in Sod1-/- mice. These results suggest that concerted changes in the hepatic expression of iron- and haem-related genes in response to haemolytic anaemia in Sod1-/- mice act to reduce toxic iron accumulation in the liver and respond to the needs of erythropoiesis. |
| doi_str_mv | 10.1042/BJ20082137 |
| format | Article |
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However, little is known about macrophage iron handling in haemolytic states resulting from a deficiency in antioxidant defences. Our observations indicate that the recently described chronic, but moderate regenerative, haemolytic anaemia of aged SOD1 (superoxide dismutase 1)-knockout mice is associated with red blood cell modifications and sensitivity to both intra- and extra-vascular haemolysis. In the present study, we have characterized the molecular pathways of iron turnover in the liver of Sod1-deficient mice. Despite iron accumulation in liver macrophages, namely Kupffer cells, we did not measure any significant change in non-haem liver iron. Interestingly, in Kupffer cells, expression of the rate-limiting enzyme in haem degradation, haem oxygenase-1, and expression of the iron exporter ferroportin were both up-regulated, whereas the hepcidin mRNA level in the liver was decreased in Sod1-/- mice. These results suggest that concerted changes in the hepatic expression of iron- and haem-related genes in response to haemolytic anaemia in Sod1-/- mice act to reduce toxic iron accumulation in the liver and respond to the needs of erythropoiesis.</description><identifier>ISSN: 0264-6021</identifier><identifier>EISSN: 1470-8728</identifier><identifier>DOI: 10.1042/BJ20082137</identifier><identifier>PMID: 19296829</identifier><language>eng</language><publisher>England: Portland Press</publisher><subject>Aging ; Anemia, Hemolytic ; Anemia, Hemolytic - blood ; Anemia, Hemolytic - metabolism ; Anemia, Hemolytic - pathology ; Animals ; Antimicrobial Cationic Peptides ; Antimicrobial Cationic Peptides - genetics ; Antimicrobial Cationic Peptides - metabolism ; Blotting, Western ; Cation Transport Proteins ; Cation Transport Proteins - genetics ; Cation Transport Proteins - metabolism ; Cellular Biology ; Erythrocytes ; Erythrocytes - metabolism ; Erythrocytes - pathology ; Female ; Flow Cytometry ; Fluorescent Antibody Technique ; Heme ; Heme - metabolism ; Heme Oxygenase-1 ; Heme Oxygenase-1 - genetics ; Heme Oxygenase-1 - metabolism ; Hemoglobins ; Hemoglobins - metabolism ; Hemolysis ; Hepcidins ; Iron ; Iron - blood ; Iron - metabolism ; Life Sciences ; Liver ; Liver - metabolism ; Liver - pathology ; Male ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Superoxide Dismutase ; Superoxide Dismutase - deficiency ; Superoxide Dismutase - genetics</subject><ispartof>Biochemical journal, 2009-06, Vol.420 (3), p.383-390</ispartof><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c355t-bf895dd39e1644b7af15b30a2c108af231c791ee404160d2e87517078195b29a3</citedby><cites>FETCH-LOGICAL-c355t-bf895dd39e1644b7af15b30a2c108af231c791ee404160d2e87517078195b29a3</cites><orcidid>0000-0002-0621-2157</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19296829$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00439841$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Starzyński, Rafał R</creatorcontrib><creatorcontrib>Canonne-Hergaux, François</creatorcontrib><creatorcontrib>Willemetz, Alexandra</creatorcontrib><creatorcontrib>Gralak, Mikołaj A</creatorcontrib><creatorcontrib>Woliński, Jarosław</creatorcontrib><creatorcontrib>Styś, Agnieszka</creatorcontrib><creatorcontrib>Olszak, Jarosław</creatorcontrib><creatorcontrib>Lipiński, Paweł</creatorcontrib><title>Haemolytic anaemia and alterations in hepatic iron metabolism in aged mice lacking Cu,Zn-superoxide dismutase</title><title>Biochemical journal</title><addtitle>Biochem J</addtitle><description>The continuous recycling of haem iron following phagocytosis and catabolism of senescent and damaged red blood cells by macrophages is a crucial process in the maintenance of systemic iron homoeostasis. However, little is known about macrophage iron handling in haemolytic states resulting from a deficiency in antioxidant defences. Our observations indicate that the recently described chronic, but moderate regenerative, haemolytic anaemia of aged SOD1 (superoxide dismutase 1)-knockout mice is associated with red blood cell modifications and sensitivity to both intra- and extra-vascular haemolysis. In the present study, we have characterized the molecular pathways of iron turnover in the liver of Sod1-deficient mice. Despite iron accumulation in liver macrophages, namely Kupffer cells, we did not measure any significant change in non-haem liver iron. Interestingly, in Kupffer cells, expression of the rate-limiting enzyme in haem degradation, haem oxygenase-1, and expression of the iron exporter ferroportin were both up-regulated, whereas the hepcidin mRNA level in the liver was decreased in Sod1-/- mice. These results suggest that concerted changes in the hepatic expression of iron- and haem-related genes in response to haemolytic anaemia in Sod1-/- mice act to reduce toxic iron accumulation in the liver and respond to the needs of erythropoiesis.</description><subject>Aging</subject><subject>Anemia, Hemolytic</subject><subject>Anemia, Hemolytic - blood</subject><subject>Anemia, Hemolytic - metabolism</subject><subject>Anemia, Hemolytic - pathology</subject><subject>Animals</subject><subject>Antimicrobial Cationic Peptides</subject><subject>Antimicrobial Cationic Peptides - genetics</subject><subject>Antimicrobial Cationic Peptides - metabolism</subject><subject>Blotting, Western</subject><subject>Cation Transport Proteins</subject><subject>Cation Transport Proteins - genetics</subject><subject>Cation Transport Proteins - metabolism</subject><subject>Cellular Biology</subject><subject>Erythrocytes</subject><subject>Erythrocytes - metabolism</subject><subject>Erythrocytes - pathology</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Fluorescent Antibody Technique</subject><subject>Heme</subject><subject>Heme - metabolism</subject><subject>Heme Oxygenase-1</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Hemoglobins</subject><subject>Hemoglobins - metabolism</subject><subject>Hemolysis</subject><subject>Hepcidins</subject><subject>Iron</subject><subject>Iron - blood</subject><subject>Iron - metabolism</subject><subject>Life Sciences</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mice, Knockout</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Superoxide Dismutase</subject><subject>Superoxide Dismutase - deficiency</subject><subject>Superoxide Dismutase - genetics</subject><issn>0264-6021</issn><issn>1470-8728</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkE1PwzAMhiMEYmNw4QegXEEU7DRtk-OYgIEmcYELl8pt0y3QLzUtYv-eVpvY6bXsx5b8MHaJcIcgxf3DqwBQAv3oiE1RRuCpSKhjNgURSi8EgRN25twXAEqQcMomqIUOldBTVi7JlHWx7WzKqRpqS0NmnIrOtNTZunLcVnxjGhoR29YVL01HSV1YV44jWpuMlzY1vKD021ZrvuhvPyvP9Y1p61-bGZ4NaN-RM-fsJKfCmYt9ztjH0-P7Yumt3p5fFvOVl_pB0HlJrnSQZb42GEqZRJRjkPhAIkVQlAsf00ijMcM3GEImjIoCjCBSqINEaPJn7Hp3d0NF3LS2pHYb12Tj5XwVjz0A6Wsl8QcH9mbHpm3tXGvy_wWEePQbH_wO8NUObvqkNNkB3Qv1_wDbaHSl</recordid><startdate>20090615</startdate><enddate>20090615</enddate><creator>Starzyński, Rafał R</creator><creator>Canonne-Hergaux, François</creator><creator>Willemetz, Alexandra</creator><creator>Gralak, Mikołaj A</creator><creator>Woliński, Jarosław</creator><creator>Styś, Agnieszka</creator><creator>Olszak, Jarosław</creator><creator>Lipiński, Paweł</creator><general>Portland Press</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>1XC</scope><orcidid>https://orcid.org/0000-0002-0621-2157</orcidid></search><sort><creationdate>20090615</creationdate><title>Haemolytic anaemia and alterations in hepatic iron metabolism in aged mice lacking Cu,Zn-superoxide dismutase</title><author>Starzyński, Rafał R ; Canonne-Hergaux, François ; Willemetz, Alexandra ; Gralak, Mikołaj A ; Woliński, Jarosław ; Styś, Agnieszka ; Olszak, Jarosław ; Lipiński, Paweł</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c355t-bf895dd39e1644b7af15b30a2c108af231c791ee404160d2e87517078195b29a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Aging</topic><topic>Anemia, Hemolytic</topic><topic>Anemia, Hemolytic - blood</topic><topic>Anemia, Hemolytic - metabolism</topic><topic>Anemia, Hemolytic - pathology</topic><topic>Animals</topic><topic>Antimicrobial Cationic Peptides</topic><topic>Antimicrobial Cationic Peptides - genetics</topic><topic>Antimicrobial Cationic Peptides - metabolism</topic><topic>Blotting, Western</topic><topic>Cation Transport Proteins</topic><topic>Cation Transport Proteins - genetics</topic><topic>Cation Transport Proteins - metabolism</topic><topic>Cellular Biology</topic><topic>Erythrocytes</topic><topic>Erythrocytes - metabolism</topic><topic>Erythrocytes - pathology</topic><topic>Female</topic><topic>Flow Cytometry</topic><topic>Fluorescent Antibody Technique</topic><topic>Heme</topic><topic>Heme - metabolism</topic><topic>Heme Oxygenase-1</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Hemoglobins</topic><topic>Hemoglobins - metabolism</topic><topic>Hemolysis</topic><topic>Hepcidins</topic><topic>Iron</topic><topic>Iron - blood</topic><topic>Iron - metabolism</topic><topic>Life Sciences</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mice, Knockout</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Superoxide Dismutase</topic><topic>Superoxide Dismutase - deficiency</topic><topic>Superoxide Dismutase - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Starzyński, Rafał R</creatorcontrib><creatorcontrib>Canonne-Hergaux, François</creatorcontrib><creatorcontrib>Willemetz, Alexandra</creatorcontrib><creatorcontrib>Gralak, Mikołaj A</creatorcontrib><creatorcontrib>Woliński, Jarosław</creatorcontrib><creatorcontrib>Styś, Agnieszka</creatorcontrib><creatorcontrib>Olszak, Jarosław</creatorcontrib><creatorcontrib>Lipiński, Paweł</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Biochemical journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Starzyński, Rafał R</au><au>Canonne-Hergaux, François</au><au>Willemetz, Alexandra</au><au>Gralak, Mikołaj A</au><au>Woliński, Jarosław</au><au>Styś, Agnieszka</au><au>Olszak, Jarosław</au><au>Lipiński, Paweł</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Haemolytic anaemia and alterations in hepatic iron metabolism in aged mice lacking Cu,Zn-superoxide dismutase</atitle><jtitle>Biochemical journal</jtitle><addtitle>Biochem J</addtitle><date>2009-06-15</date><risdate>2009</risdate><volume>420</volume><issue>3</issue><spage>383</spage><epage>390</epage><pages>383-390</pages><issn>0264-6021</issn><eissn>1470-8728</eissn><abstract>The continuous recycling of haem iron following phagocytosis and catabolism of senescent and damaged red blood cells by macrophages is a crucial process in the maintenance of systemic iron homoeostasis. However, little is known about macrophage iron handling in haemolytic states resulting from a deficiency in antioxidant defences. Our observations indicate that the recently described chronic, but moderate regenerative, haemolytic anaemia of aged SOD1 (superoxide dismutase 1)-knockout mice is associated with red blood cell modifications and sensitivity to both intra- and extra-vascular haemolysis. In the present study, we have characterized the molecular pathways of iron turnover in the liver of Sod1-deficient mice. Despite iron accumulation in liver macrophages, namely Kupffer cells, we did not measure any significant change in non-haem liver iron. Interestingly, in Kupffer cells, expression of the rate-limiting enzyme in haem degradation, haem oxygenase-1, and expression of the iron exporter ferroportin were both up-regulated, whereas the hepcidin mRNA level in the liver was decreased in Sod1-/- mice. These results suggest that concerted changes in the hepatic expression of iron- and haem-related genes in response to haemolytic anaemia in Sod1-/- mice act to reduce toxic iron accumulation in the liver and respond to the needs of erythropoiesis.</abstract><cop>England</cop><pub>Portland Press</pub><pmid>19296829</pmid><doi>10.1042/BJ20082137</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-0621-2157</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Biochemical journal, 2009-06, Vol.420 (3), p.383-390 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Aging Anemia, Hemolytic Anemia, Hemolytic - blood Anemia, Hemolytic - metabolism Anemia, Hemolytic - pathology Animals Antimicrobial Cationic Peptides Antimicrobial Cationic Peptides - genetics Antimicrobial Cationic Peptides - metabolism Blotting, Western Cation Transport Proteins Cation Transport Proteins - genetics Cation Transport Proteins - metabolism Cellular Biology Erythrocytes Erythrocytes - metabolism Erythrocytes - pathology Female Flow Cytometry Fluorescent Antibody Technique Heme Heme - metabolism Heme Oxygenase-1 Heme Oxygenase-1 - genetics Heme Oxygenase-1 - metabolism Hemoglobins Hemoglobins - metabolism Hemolysis Hepcidins Iron Iron - blood Iron - metabolism Life Sciences Liver Liver - metabolism Liver - pathology Male Mice Mice, Inbred Strains Mice, Knockout Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger RNA, Messenger - genetics RNA, Messenger - metabolism Superoxide Dismutase Superoxide Dismutase - deficiency Superoxide Dismutase - genetics |
| title | Haemolytic anaemia and alterations in hepatic iron metabolism in aged mice lacking Cu,Zn-superoxide dismutase |
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