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Rescue of early-stage myelodysplastic syndrome-deriving erythroid precursors by the ectopic expression of a dominant-negative form of FADD
Myelodysplastic syndromes (MDSs) are characterized by peripheral blood cytopenia including anemia. We have investigated the implication of the extrinsic pathway of apoptosis in MDS-ineffective erythropoiesis by in vitro expansion of erythroid precursors from early stage (low and intermediate-1 Inter...
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| Published in: | Blood 2005-05, Vol.105 (10), p.4035-4042 |
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| creator | Claessens, Yann-Erick Park, Sophie Dubart-Kupperschmitt, Anne Mariot, Virginie Garrido, Carmen Chrétien, Stany Dreyfus, François Lacombe, Catherine Mayeux, Patrick Fontenay, Michaëla |
| description | Myelodysplastic syndromes (MDSs) are characterized by peripheral blood cytopenia including anemia. We have investigated the implication of the extrinsic pathway of apoptosis in MDS-ineffective erythropoiesis by in vitro expansion of erythroid precursors from early stage (low and intermediate-1 International Prognosis Scoring System [IPSS]) MDS, advanced stage (intermediate-2 IPSS) MDS, and control bone marrow samples. We have previously shown that Fas and its ligand were overexpressed in early stage MDS erythroid cells. Here, we show that caspase-8 activity is significantly increased, whereas the expression of death receptors other than Fas, including the type 1 receptor for tumor necrosis factor α (TNF-α) and the receptors for the TNF-related apoptosis-inducing ligand (TRAIL), DR4 and DR5, was normal. We also observed that the adapter Fas-associated death domain (FADD) was overexpressed in early stage MDS erythroid cells. Transduction of early stage MDS-derived CD34+ progenitors with a FADD-encoding construct increased apoptosis of erythroid cells and dramatically reduced erythroid burst-forming unit (BFU-E) growth. Transduction of a dominant-negative (dn) mutant of FADD inhibited caspase-8 activity and cell death and rescued BFU-E growth without abrogating erythroid differentiation. These results extend the observation that Fas-dependent activation of caspase-8 accounts for apoptosis of early stage MDS erythroid cells and demonstrate for the first time that FADD is a valuable target to correct ineffective erythropoiesis in these syndromes. |
| doi_str_mv | 10.1182/blood-2004-08-3166 |
| format | article |
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We have investigated the implication of the extrinsic pathway of apoptosis in MDS-ineffective erythropoiesis by in vitro expansion of erythroid precursors from early stage (low and intermediate-1 International Prognosis Scoring System [IPSS]) MDS, advanced stage (intermediate-2 IPSS) MDS, and control bone marrow samples. We have previously shown that Fas and its ligand were overexpressed in early stage MDS erythroid cells. Here, we show that caspase-8 activity is significantly increased, whereas the expression of death receptors other than Fas, including the type 1 receptor for tumor necrosis factor α (TNF-α) and the receptors for the TNF-related apoptosis-inducing ligand (TRAIL), DR4 and DR5, was normal. We also observed that the adapter Fas-associated death domain (FADD) was overexpressed in early stage MDS erythroid cells. Transduction of early stage MDS-derived CD34+ progenitors with a FADD-encoding construct increased apoptosis of erythroid cells and dramatically reduced erythroid burst-forming unit (BFU-E) growth. Transduction of a dominant-negative (dn) mutant of FADD inhibited caspase-8 activity and cell death and rescued BFU-E growth without abrogating erythroid differentiation. These results extend the observation that Fas-dependent activation of caspase-8 accounts for apoptosis of early stage MDS erythroid cells and demonstrate for the first time that FADD is a valuable target to correct ineffective erythropoiesis in these syndromes.</description><identifier>ISSN: 0006-4971</identifier><identifier>EISSN: 1528-0020</identifier><identifier>DOI: 10.1182/blood-2004-08-3166</identifier><identifier>PMID: 15677568</identifier><language>eng</language><publisher>Washington, DC: Elsevier Inc</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; Adult ; Aged ; Aged, 80 and over ; Apoptosis ; Apoptosis Regulatory Proteins ; Biological and medical sciences ; Caspase 8 ; Caspases - metabolism ; Cell Differentiation ; Cells, Cultured ; Erythroid Cells - metabolism ; Erythroid Cells - pathology ; Fas-Associated Death Domain Protein ; Female ; Gene Expression Regulation, Neoplastic ; Genes, Dominant - genetics ; Hematologic and hematopoietic diseases ; Humans ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Male ; Medical sciences ; Membrane Glycoproteins - metabolism ; Middle Aged ; Myelodysplastic Syndromes - genetics ; Myelodysplastic Syndromes - metabolism ; Myelodysplastic Syndromes - pathology ; Myelodysplastic Syndromes - therapy ; Neoplasm Staging ; Stem Cells - cytology ; Stem Cells - metabolism ; TNF-Related Apoptosis-Inducing Ligand ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Blood, 2005-05, Vol.105 (10), p.4035-4042</ispartof><rights>2005 American Society of Hematology</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-1250da06666ee35d301f8a3c21a2f8513f7366745af2aafa3a0f8eb6c6fdfc8a3</citedby><cites>FETCH-LOGICAL-c494t-1250da06666ee35d301f8a3c21a2f8513f7366745af2aafa3a0f8eb6c6fdfc8a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0006497120454953$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>315,786,790,3568,27957,27958,45815</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16847277$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15677568$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Claessens, Yann-Erick</creatorcontrib><creatorcontrib>Park, Sophie</creatorcontrib><creatorcontrib>Dubart-Kupperschmitt, Anne</creatorcontrib><creatorcontrib>Mariot, Virginie</creatorcontrib><creatorcontrib>Garrido, Carmen</creatorcontrib><creatorcontrib>Chrétien, Stany</creatorcontrib><creatorcontrib>Dreyfus, François</creatorcontrib><creatorcontrib>Lacombe, Catherine</creatorcontrib><creatorcontrib>Mayeux, Patrick</creatorcontrib><creatorcontrib>Fontenay, Michaëla</creatorcontrib><title>Rescue of early-stage myelodysplastic syndrome-deriving erythroid precursors by the ectopic expression of a dominant-negative form of FADD</title><title>Blood</title><addtitle>Blood</addtitle><description>Myelodysplastic syndromes (MDSs) are characterized by peripheral blood cytopenia including anemia. We have investigated the implication of the extrinsic pathway of apoptosis in MDS-ineffective erythropoiesis by in vitro expansion of erythroid precursors from early stage (low and intermediate-1 International Prognosis Scoring System [IPSS]) MDS, advanced stage (intermediate-2 IPSS) MDS, and control bone marrow samples. We have previously shown that Fas and its ligand were overexpressed in early stage MDS erythroid cells. Here, we show that caspase-8 activity is significantly increased, whereas the expression of death receptors other than Fas, including the type 1 receptor for tumor necrosis factor α (TNF-α) and the receptors for the TNF-related apoptosis-inducing ligand (TRAIL), DR4 and DR5, was normal. We also observed that the adapter Fas-associated death domain (FADD) was overexpressed in early stage MDS erythroid cells. Transduction of early stage MDS-derived CD34+ progenitors with a FADD-encoding construct increased apoptosis of erythroid cells and dramatically reduced erythroid burst-forming unit (BFU-E) growth. Transduction of a dominant-negative (dn) mutant of FADD inhibited caspase-8 activity and cell death and rescued BFU-E growth without abrogating erythroid differentiation. These results extend the observation that Fas-dependent activation of caspase-8 accounts for apoptosis of early stage MDS erythroid cells and demonstrate for the first time that FADD is a valuable target to correct ineffective erythropoiesis in these syndromes.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins</subject><subject>Biological and medical sciences</subject><subject>Caspase 8</subject><subject>Caspases - metabolism</subject><subject>Cell Differentiation</subject><subject>Cells, Cultured</subject><subject>Erythroid Cells - metabolism</subject><subject>Erythroid Cells - pathology</subject><subject>Fas-Associated Death Domain Protein</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Dominant - genetics</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Humans</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>Middle Aged</subject><subject>Myelodysplastic Syndromes - genetics</subject><subject>Myelodysplastic Syndromes - metabolism</subject><subject>Myelodysplastic Syndromes - pathology</subject><subject>Myelodysplastic Syndromes - therapy</subject><subject>Neoplasm Staging</subject><subject>Stem Cells - cytology</subject><subject>Stem Cells - metabolism</subject><subject>TNF-Related Apoptosis-Inducing Ligand</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0006-4971</issn><issn>1528-0020</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNp9kU-LFDEQxYMo7rj6BTxILnqL5k93uge8LLuuCguC6DlkkspspLszptLD9lfwU5t2BvZmXepQv_co3iPkteDvhejlh92QkmeS84bxnimh9ROyEa3sGeeSPyUbzrlmzbYTF-QF4i_ORaNk-5xciFZ3Xav7DfnzHdDNQFOgYPOwMCx2D3RcYEh-wcNgsURHcZl8TiMwDzke47SnkJdyn1P09JDBzRlTRrpbaLkHCq6kQ1XBQ70hxjSt_pb6NMbJToVNsLclHoGGlMf1dnt1c_OSPAt2QHh13pfk5-2nH9df2N23z1-vr-6Ya7ZNYUK23Fuu6wCo1isuQm-Vk8LK0LdChU5p3TWtDdLaYJXloYeddjr44Cp5Sd6dfA85_Z4BixkjOhgGO0Ga0dRotrxRqoLyBLqcEDMEc8hxtHkxgpu1AfOvAbM2YHhv1gaq6M3Zfd6N4B8l58gr8PYMWHR2CNlOLuIjp_umk11XuY8nDmoWxwjZoIswOfCxBl6MT_F_f_wF8Panrw</recordid><startdate>20050515</startdate><enddate>20050515</enddate><creator>Claessens, Yann-Erick</creator><creator>Park, Sophie</creator><creator>Dubart-Kupperschmitt, Anne</creator><creator>Mariot, Virginie</creator><creator>Garrido, Carmen</creator><creator>Chrétien, Stany</creator><creator>Dreyfus, François</creator><creator>Lacombe, Catherine</creator><creator>Mayeux, Patrick</creator><creator>Fontenay, Michaëla</creator><general>Elsevier Inc</general><general>The Americain Society of Hematology</general><scope>6I.</scope><scope>AAFTH</scope><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>7X8</scope></search><sort><creationdate>20050515</creationdate><title>Rescue of early-stage myelodysplastic syndrome-deriving erythroid precursors by the ectopic expression of a dominant-negative form of FADD</title><author>Claessens, Yann-Erick ; Park, Sophie ; Dubart-Kupperschmitt, Anne ; Mariot, Virginie ; Garrido, Carmen ; Chrétien, Stany ; Dreyfus, François ; Lacombe, Catherine ; Mayeux, Patrick ; Fontenay, Michaëla</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-1250da06666ee35d301f8a3c21a2f8513f7366745af2aafa3a0f8eb6c6fdfc8a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins</topic><topic>Biological and medical sciences</topic><topic>Caspase 8</topic><topic>Caspases - metabolism</topic><topic>Cell Differentiation</topic><topic>Cells, Cultured</topic><topic>Erythroid Cells - metabolism</topic><topic>Erythroid Cells - pathology</topic><topic>Fas-Associated Death Domain Protein</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Dominant - genetics</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Humans</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>Middle Aged</topic><topic>Myelodysplastic Syndromes - genetics</topic><topic>Myelodysplastic Syndromes - metabolism</topic><topic>Myelodysplastic Syndromes - pathology</topic><topic>Myelodysplastic Syndromes - therapy</topic><topic>Neoplasm Staging</topic><topic>Stem Cells - cytology</topic><topic>Stem Cells - metabolism</topic><topic>TNF-Related Apoptosis-Inducing Ligand</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Claessens, Yann-Erick</creatorcontrib><creatorcontrib>Park, Sophie</creatorcontrib><creatorcontrib>Dubart-Kupperschmitt, Anne</creatorcontrib><creatorcontrib>Mariot, Virginie</creatorcontrib><creatorcontrib>Garrido, Carmen</creatorcontrib><creatorcontrib>Chrétien, Stany</creatorcontrib><creatorcontrib>Dreyfus, François</creatorcontrib><creatorcontrib>Lacombe, Catherine</creatorcontrib><creatorcontrib>Mayeux, Patrick</creatorcontrib><creatorcontrib>Fontenay, Michaëla</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>MEDLINE - Academic</collection><jtitle>Blood</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Claessens, Yann-Erick</au><au>Park, Sophie</au><au>Dubart-Kupperschmitt, Anne</au><au>Mariot, Virginie</au><au>Garrido, Carmen</au><au>Chrétien, Stany</au><au>Dreyfus, François</au><au>Lacombe, Catherine</au><au>Mayeux, Patrick</au><au>Fontenay, Michaëla</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rescue of early-stage myelodysplastic syndrome-deriving erythroid precursors by the ectopic expression of a dominant-negative form of FADD</atitle><jtitle>Blood</jtitle><addtitle>Blood</addtitle><date>2005-05-15</date><risdate>2005</risdate><volume>105</volume><issue>10</issue><spage>4035</spage><epage>4042</epage><pages>4035-4042</pages><issn>0006-4971</issn><eissn>1528-0020</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Myelodysplastic syndromes (MDSs) are characterized by peripheral blood cytopenia including anemia. We have investigated the implication of the extrinsic pathway of apoptosis in MDS-ineffective erythropoiesis by in vitro expansion of erythroid precursors from early stage (low and intermediate-1 International Prognosis Scoring System [IPSS]) MDS, advanced stage (intermediate-2 IPSS) MDS, and control bone marrow samples. We have previously shown that Fas and its ligand were overexpressed in early stage MDS erythroid cells. Here, we show that caspase-8 activity is significantly increased, whereas the expression of death receptors other than Fas, including the type 1 receptor for tumor necrosis factor α (TNF-α) and the receptors for the TNF-related apoptosis-inducing ligand (TRAIL), DR4 and DR5, was normal. We also observed that the adapter Fas-associated death domain (FADD) was overexpressed in early stage MDS erythroid cells. Transduction of early stage MDS-derived CD34+ progenitors with a FADD-encoding construct increased apoptosis of erythroid cells and dramatically reduced erythroid burst-forming unit (BFU-E) growth. Transduction of a dominant-negative (dn) mutant of FADD inhibited caspase-8 activity and cell death and rescued BFU-E growth without abrogating erythroid differentiation. These results extend the observation that Fas-dependent activation of caspase-8 accounts for apoptosis of early stage MDS erythroid cells and demonstrate for the first time that FADD is a valuable target to correct ineffective erythropoiesis in these syndromes.</abstract><cop>Washington, DC</cop><pub>Elsevier Inc</pub><pmid>15677568</pmid><doi>10.1182/blood-2004-08-3166</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Adult Aged Aged, 80 and over Apoptosis Apoptosis Regulatory Proteins Biological and medical sciences Caspase 8 Caspases - metabolism Cell Differentiation Cells, Cultured Erythroid Cells - metabolism Erythroid Cells - pathology Fas-Associated Death Domain Protein Female Gene Expression Regulation, Neoplastic Genes, Dominant - genetics Hematologic and hematopoietic diseases Humans Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Medical sciences Membrane Glycoproteins - metabolism Middle Aged Myelodysplastic Syndromes - genetics Myelodysplastic Syndromes - metabolism Myelodysplastic Syndromes - pathology Myelodysplastic Syndromes - therapy Neoplasm Staging Stem Cells - cytology Stem Cells - metabolism TNF-Related Apoptosis-Inducing Ligand Tumor Necrosis Factor-alpha - metabolism |
| title | Rescue of early-stage myelodysplastic syndrome-deriving erythroid precursors by the ectopic expression of a dominant-negative form of FADD |
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