Sulphydryl modifications alter scramblase activity in murine sickle cell disease
Summary Increased oxidant stress has been suggested to play a role in the process of phosphatidylserine (PS) externalisation in the red blood cells of sickle cell patients. Inhibition of the ATP‐driven translocation from outer to inner monolayer (flippase) by sulphydryl modification has been establi...
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| Veröffentlicht in: | British journal of haematology 2006-05, Vol.133 (4), p.427-432 |
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| container_title | British journal of haematology |
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| creator | Jong, Kitty Kuypers, Frans A. |
| description | Summary
Increased oxidant stress has been suggested to play a role in the process of phosphatidylserine (PS) externalisation in the red blood cells of sickle cell patients. Inhibition of the ATP‐driven translocation from outer to inner monolayer (flippase) by sulphydryl modification has been established. The present study showed that phospholipid scrambling was also sensitive to protein sulphydryl modification. Treatment with N‐ethylmaleimide lead to enhanced PS exposure and a lower Ca++ requirement for scrambling. In contrast, pyridyldithioethylamine treatment inhibited PS exposure. Red blood cells from a murine model for sickle cell disease exhibited a reduced response to both reagents, suggestive of previous sulphydryl modifications to the protein(s) involved in phospholipid scrambling. We conclude that sulphydryl modifications to both scramblase and flippase underlie the enhanced formation of PS‐exposing cells in sickle cell disease. |
| doi_str_mv | 10.1111/j.1365-2141.2006.06045.x |
| format | Article |
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Increased oxidant stress has been suggested to play a role in the process of phosphatidylserine (PS) externalisation in the red blood cells of sickle cell patients. Inhibition of the ATP‐driven translocation from outer to inner monolayer (flippase) by sulphydryl modification has been established. The present study showed that phospholipid scrambling was also sensitive to protein sulphydryl modification. Treatment with N‐ethylmaleimide lead to enhanced PS exposure and a lower Ca++ requirement for scrambling. In contrast, pyridyldithioethylamine treatment inhibited PS exposure. Red blood cells from a murine model for sickle cell disease exhibited a reduced response to both reagents, suggestive of previous sulphydryl modifications to the protein(s) involved in phospholipid scrambling. We conclude that sulphydryl modifications to both scramblase and flippase underlie the enhanced formation of PS‐exposing cells in sickle cell disease.</description><identifier>ISSN: 0007-1048</identifier><identifier>EISSN: 1365-2141</identifier><identifier>DOI: 10.1111/j.1365-2141.2006.06045.x</identifier><identifier>PMID: 16643451</identifier><identifier>CODEN: BJHEAL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Anemia, Sickle Cell - blood ; Anemias. Hemoglobinopathies ; Animals ; Biological and medical sciences ; Calcium - pharmacology ; Diseases of red blood cells ; Dose-Response Relationship, Drug ; Erythrocyte Membrane - metabolism ; Erythrocytes - drug effects ; Hematologic and hematopoietic diseases ; Hematology ; Humans ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Oxidative Stress ; Phosphatidylserines - blood ; Phospholipid Transfer Proteins - antagonists & inhibitors ; Phospholipid Transfer Proteins - blood ; Phospholipid Transfer Proteins - physiology ; phospholipids ; red cell membrane ; sickle cell anaemia ; Sickle cell anemia ; Sulfhydryl Compounds - blood ; transgenic mice model</subject><ispartof>British journal of haematology, 2006-05, Vol.133 (4), p.427-432</ispartof><rights>2006 INIST-CNRS</rights><rights>Copyright Blackwell Publishing May 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4245-e8ec62d261d5279efd5d7fbbac3c707a0dfe3441646b23c17c9497e5b2778b393</citedby><cites>FETCH-LOGICAL-c4245-e8ec62d261d5279efd5d7fbbac3c707a0dfe3441646b23c17c9497e5b2778b393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1365-2141.2006.06045.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2141.2006.06045.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17701561$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16643451$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jong, Kitty</creatorcontrib><creatorcontrib>Kuypers, Frans A.</creatorcontrib><title>Sulphydryl modifications alter scramblase activity in murine sickle cell disease</title><title>British journal of haematology</title><addtitle>Br J Haematol</addtitle><description>Summary
Increased oxidant stress has been suggested to play a role in the process of phosphatidylserine (PS) externalisation in the red blood cells of sickle cell patients. Inhibition of the ATP‐driven translocation from outer to inner monolayer (flippase) by sulphydryl modification has been established. The present study showed that phospholipid scrambling was also sensitive to protein sulphydryl modification. Treatment with N‐ethylmaleimide lead to enhanced PS exposure and a lower Ca++ requirement for scrambling. In contrast, pyridyldithioethylamine treatment inhibited PS exposure. Red blood cells from a murine model for sickle cell disease exhibited a reduced response to both reagents, suggestive of previous sulphydryl modifications to the protein(s) involved in phospholipid scrambling. We conclude that sulphydryl modifications to both scramblase and flippase underlie the enhanced formation of PS‐exposing cells in sickle cell disease.</description><subject>Anemia, Sickle Cell - blood</subject><subject>Anemias. Hemoglobinopathies</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium - pharmacology</subject><subject>Diseases of red blood cells</subject><subject>Dose-Response Relationship, Drug</subject><subject>Erythrocyte Membrane - metabolism</subject><subject>Erythrocytes - drug effects</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematology</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Oxidative Stress</subject><subject>Phosphatidylserines - blood</subject><subject>Phospholipid Transfer Proteins - antagonists & inhibitors</subject><subject>Phospholipid Transfer Proteins - blood</subject><subject>Phospholipid Transfer Proteins - physiology</subject><subject>phospholipids</subject><subject>red cell membrane</subject><subject>sickle cell anaemia</subject><subject>Sickle cell anemia</subject><subject>Sulfhydryl Compounds - blood</subject><subject>transgenic mice model</subject><issn>0007-1048</issn><issn>1365-2141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkF2L1TAQhoMo7tnVvyBB0LvWTPPVXnjhLq6rLCio1yFNpphj2h6TVrf_3tZzcMEr52YG5pnh5SGEAithrVf7EriSRQUCyooxVTLFhCzvHpDd38VDsmOM6QKYqM_Iec57xoAzCY_JGSgluJCwI58-z_HwbfFpibQffeiCs1MYh0xtnDDR7JLt22gzUuum8DNMCw0D7ecUBqQ5uO8RqcMYqQ8ZV-wJedTZmPHpqV-Qr9dvv1zdFLcf372_enNbOFEJWWCNTlW-UuBlpRvsvPS6a1vruNNMW-Y75EKAEqqtuAPtGtFolG2ldd3yhl-Ql8e_hzT-mDFPpg95C2IHHOdslG6Aa16v4PN_wP04p2HNZqCpFdRc6xWqj5BLY84JO3NIobdpMcDMptzszWbWbGbNptz8UW7u1tNnp_9z26O_Pzw5XoEXJ8BmZ2OX7OBCvue0ZiDVxr0-cr9CxOW_A5jLDzfbxH8D2P-cOg</recordid><startdate>200605</startdate><enddate>200605</enddate><creator>Jong, Kitty</creator><creator>Kuypers, Frans A.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>200605</creationdate><title>Sulphydryl modifications alter scramblase activity in murine sickle cell disease</title><author>Jong, Kitty ; Kuypers, Frans A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4245-e8ec62d261d5279efd5d7fbbac3c707a0dfe3441646b23c17c9497e5b2778b393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Anemia, Sickle Cell - blood</topic><topic>Anemias. Hemoglobinopathies</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Calcium - pharmacology</topic><topic>Diseases of red blood cells</topic><topic>Dose-Response Relationship, Drug</topic><topic>Erythrocyte Membrane - metabolism</topic><topic>Erythrocytes - drug effects</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematology</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Oxidative Stress</topic><topic>Phosphatidylserines - blood</topic><topic>Phospholipid Transfer Proteins - antagonists & inhibitors</topic><topic>Phospholipid Transfer Proteins - blood</topic><topic>Phospholipid Transfer Proteins - physiology</topic><topic>phospholipids</topic><topic>red cell membrane</topic><topic>sickle cell anaemia</topic><topic>Sickle cell anemia</topic><topic>Sulfhydryl Compounds - blood</topic><topic>transgenic mice model</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jong, Kitty</creatorcontrib><creatorcontrib>Kuypers, Frans A.</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of haematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jong, Kitty</au><au>Kuypers, Frans A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sulphydryl modifications alter scramblase activity in murine sickle cell disease</atitle><jtitle>British journal of haematology</jtitle><addtitle>Br J Haematol</addtitle><date>2006-05</date><risdate>2006</risdate><volume>133</volume><issue>4</issue><spage>427</spage><epage>432</epage><pages>427-432</pages><issn>0007-1048</issn><eissn>1365-2141</eissn><coden>BJHEAL</coden><abstract>Summary
Increased oxidant stress has been suggested to play a role in the process of phosphatidylserine (PS) externalisation in the red blood cells of sickle cell patients. Inhibition of the ATP‐driven translocation from outer to inner monolayer (flippase) by sulphydryl modification has been established. The present study showed that phospholipid scrambling was also sensitive to protein sulphydryl modification. Treatment with N‐ethylmaleimide lead to enhanced PS exposure and a lower Ca++ requirement for scrambling. In contrast, pyridyldithioethylamine treatment inhibited PS exposure. Red blood cells from a murine model for sickle cell disease exhibited a reduced response to both reagents, suggestive of previous sulphydryl modifications to the protein(s) involved in phospholipid scrambling. We conclude that sulphydryl modifications to both scramblase and flippase underlie the enhanced formation of PS‐exposing cells in sickle cell disease.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16643451</pmid><doi>10.1111/j.1365-2141.2006.06045.x</doi><tpages>6</tpages></addata></record> |
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| subjects | Anemia, Sickle Cell - blood Anemias. Hemoglobinopathies Animals Biological and medical sciences Calcium - pharmacology Diseases of red blood cells Dose-Response Relationship, Drug Erythrocyte Membrane - metabolism Erythrocytes - drug effects Hematologic and hematopoietic diseases Hematology Humans Medical sciences Mice Mice, Inbred C57BL Mice, Transgenic Oxidative Stress Phosphatidylserines - blood Phospholipid Transfer Proteins - antagonists & inhibitors Phospholipid Transfer Proteins - blood Phospholipid Transfer Proteins - physiology phospholipids red cell membrane sickle cell anaemia Sickle cell anemia Sulfhydryl Compounds - blood transgenic mice model |
| title | Sulphydryl modifications alter scramblase activity in murine sickle cell disease |
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