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Alteration in endoglin-related angiogenesis in refractory cytopenia with multilineage dysplasia
The functional mechanisms involved in angiogenesis and the potential role of endoglin (ENG), recently described as a new marker for this process, have not been explored in Myelodysplastic Syndromes (MDS). In order to gain insight in MDS angiogenesis a combined analysis in bone marrow (BM) of gene ex...
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description | The functional mechanisms involved in angiogenesis and the potential role of endoglin (ENG), recently described as a new marker for this process, have not been explored in Myelodysplastic Syndromes (MDS). In order to gain insight in MDS angiogenesis a combined analysis in bone marrow (BM) of gene expression levels, angiogenesis-related soluble factors and functional angiogenesis-related studies was carried out. Ninety-seven MDS patients and forty-two normal BM samples were studied. The morphology of the capillary-like structures originated by two endothelial cells lines in the BM environment of patients with refractory cytopenia with multilineage dysplasia (RCMD) was different from those of the remaining MDS. In addition, the BM mononuclear cells from RCMD patients displayed over-expression of VEGF, HIF and FN1 while they showed reduced expression of ENG in contrast to the normal ENG expression of the remaining low-risk MDS and the high expression of ENG in high-risk MDS subtype. Moreover, higher soluble ENG and soluble FLT-1 levels in BM microenvironment were observed in RCMD cases, which distinguished them from other individuals. Therefore, the present study suggests that the patterns of angiogenesis are different between the MDS subtypes. The differences in angiogenesis observed in RCMD patients could be related to ENG abnormalities. |
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In order to gain insight in MDS angiogenesis a combined analysis in bone marrow (BM) of gene expression levels, angiogenesis-related soluble factors and functional angiogenesis-related studies was carried out. Ninety-seven MDS patients and forty-two normal BM samples were studied. The morphology of the capillary-like structures originated by two endothelial cells lines in the BM environment of patients with refractory cytopenia with multilineage dysplasia (RCMD) was different from those of the remaining MDS. In addition, the BM mononuclear cells from RCMD patients displayed over-expression of VEGF, HIF and FN1 while they showed reduced expression of ENG in contrast to the normal ENG expression of the remaining low-risk MDS and the high expression of ENG in high-risk MDS subtype. Moreover, higher soluble ENG and soluble FLT-1 levels in BM microenvironment were observed in RCMD cases, which distinguished them from other individuals. Therefore, the present study suggests that the patterns of angiogenesis are different between the MDS subtypes. The differences in angiogenesis observed in RCMD patients could be related to ENG abnormalities.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0053624</identifier><identifier>PMID: 23341958</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Abnormalities ; Analysis ; Anemia ; Anemia, Refractory - metabolism ; Anemia, Refractory - pathology ; Angiogenesis ; Angiogenesis Inducing Agents - metabolism ; Antigens, CD - genetics ; Antigens, CD - metabolism ; Biology ; Bone marrow ; Bone Marrow - metabolism ; Bone Marrow - pathology ; Cancer ; Cell Lineage ; Cell Proliferation ; Cellular Microenvironment ; Dysplasia ; Endoglin ; Endothelial cells ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Endothelium ; Fibronectins ; Gene expression ; Growth factors ; Humans ; Leukemia ; Leukocytes (mononuclear) ; Medical research ; Medicine ; Mitochondrial DNA ; Myelodysplastic syndrome ; Myelodysplastic syndromes ; Myelodysplastic Syndromes - metabolism ; Myelodysplastic Syndromes - pathology ; Neovascularization, Pathologic - metabolism ; Neovascularization, Pathologic - pathology ; Overexpression ; Patients ; Proteins ; Receptors, Cell Surface - genetics ; Receptors, Cell Surface - metabolism ; Signal transduction ; Solubility ; Studies ; Tumors ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - genetics ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>PloS one, 2013-01, Vol.8 (1), p.e53624-e53624</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 del Rey et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 del Rey et al 2013 del Rey et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-d918809c6712f2aaa731ba8f1cb9db100d13360175c91cd418a3ef0a514d67be3</citedby><cites>FETCH-LOGICAL-c692t-d918809c6712f2aaa731ba8f1cb9db100d13360175c91cd418a3ef0a514d67be3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1327274993/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1327274993?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,315,733,786,790,891,25783,27957,27958,37047,37048,44625,53827,53829,75483</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23341958$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gao, Jian-Xin</contributor><creatorcontrib>del Rey, Mónica</creatorcontrib><creatorcontrib>Pericacho, Miguel</creatorcontrib><creatorcontrib>Velasco, Soraya</creatorcontrib><creatorcontrib>Lumbreras, Eva</creatorcontrib><creatorcontrib>López-Novoa, José Miguel</creatorcontrib><creatorcontrib>Hernández-Rivas, Jesús María</creatorcontrib><creatorcontrib>Rodríguez-Barbero, Alicia</creatorcontrib><title>Alteration in endoglin-related angiogenesis in refractory cytopenia with multilineage dysplasia</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The functional mechanisms involved in angiogenesis and the potential role of endoglin (ENG), recently described as a new marker for this process, have not been explored in Myelodysplastic Syndromes (MDS). In order to gain insight in MDS angiogenesis a combined analysis in bone marrow (BM) of gene expression levels, angiogenesis-related soluble factors and functional angiogenesis-related studies was carried out. Ninety-seven MDS patients and forty-two normal BM samples were studied. The morphology of the capillary-like structures originated by two endothelial cells lines in the BM environment of patients with refractory cytopenia with multilineage dysplasia (RCMD) was different from those of the remaining MDS. In addition, the BM mononuclear cells from RCMD patients displayed over-expression of VEGF, HIF and FN1 while they showed reduced expression of ENG in contrast to the normal ENG expression of the remaining low-risk MDS and the high expression of ENG in high-risk MDS subtype. Moreover, higher soluble ENG and soluble FLT-1 levels in BM microenvironment were observed in RCMD cases, which distinguished them from other individuals. Therefore, the present study suggests that the patterns of angiogenesis are different between the MDS subtypes. The differences in angiogenesis observed in RCMD patients could be related to ENG abnormalities.</description><subject>Abnormalities</subject><subject>Analysis</subject><subject>Anemia</subject><subject>Anemia, Refractory - metabolism</subject><subject>Anemia, Refractory - pathology</subject><subject>Angiogenesis</subject><subject>Angiogenesis Inducing Agents - metabolism</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, CD - metabolism</subject><subject>Biology</subject><subject>Bone marrow</subject><subject>Bone Marrow - metabolism</subject><subject>Bone Marrow - pathology</subject><subject>Cancer</subject><subject>Cell Lineage</subject><subject>Cell Proliferation</subject><subject>Cellular Microenvironment</subject><subject>Dysplasia</subject><subject>Endoglin</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>Endothelium</subject><subject>Fibronectins</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Leukemia</subject><subject>Leukocytes (mononuclear)</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Mitochondrial DNA</subject><subject>Myelodysplastic syndrome</subject><subject>Myelodysplastic syndromes</subject><subject>Myelodysplastic Syndromes - 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metabolism</topic><topic>Anemia, Refractory - pathology</topic><topic>Angiogenesis</topic><topic>Angiogenesis Inducing Agents - metabolism</topic><topic>Antigens, CD - genetics</topic><topic>Antigens, CD - metabolism</topic><topic>Biology</topic><topic>Bone marrow</topic><topic>Bone Marrow - metabolism</topic><topic>Bone Marrow - pathology</topic><topic>Cancer</topic><topic>Cell Lineage</topic><topic>Cell Proliferation</topic><topic>Cellular Microenvironment</topic><topic>Dysplasia</topic><topic>Endoglin</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - pathology</topic><topic>Endothelium</topic><topic>Fibronectins</topic><topic>Gene expression</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Leukemia</topic><topic>Leukocytes (mononuclear)</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Mitochondrial DNA</topic><topic>Myelodysplastic syndrome</topic><topic>Myelodysplastic syndromes</topic><topic>Myelodysplastic Syndromes - metabolism</topic><topic>Myelodysplastic Syndromes - pathology</topic><topic>Neovascularization, Pathologic - metabolism</topic><topic>Neovascularization, Pathologic - pathology</topic><topic>Overexpression</topic><topic>Patients</topic><topic>Proteins</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Signal transduction</topic><topic>Solubility</topic><topic>Studies</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - genetics</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>del Rey, Mónica</creatorcontrib><creatorcontrib>Pericacho, Miguel</creatorcontrib><creatorcontrib>Velasco, Soraya</creatorcontrib><creatorcontrib>Lumbreras, Eva</creatorcontrib><creatorcontrib>López-Novoa, José Miguel</creatorcontrib><creatorcontrib>Hernández-Rivas, Jesús María</creatorcontrib><creatorcontrib>Rodríguez-Barbero, Alicia</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Opposing Viewpoints Resource Center</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>del Rey, Mónica</au><au>Pericacho, Miguel</au><au>Velasco, Soraya</au><au>Lumbreras, Eva</au><au>López-Novoa, José Miguel</au><au>Hernández-Rivas, Jesús María</au><au>Rodríguez-Barbero, Alicia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alteration in endoglin-related angiogenesis in refractory cytopenia with multilineage dysplasia</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-01-16</date><risdate>2013</risdate><volume>8</volume><issue>1</issue><spage>e53624</spage><epage>e53624</epage><pages>e53624-e53624</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><notes>Competing Interests: The authors have declared that no competing interests exist.</notes><notes>Collected the patients samples: EL. Conceived and designed the experiments: MDR MP JMLN JMHR ARB. Performed the experiments: MDR MP SV. Analyzed the data: MDR MP SV JMHR ARB. Wrote the paper: MDR ARB JMHR.</notes><abstract>The functional mechanisms involved in angiogenesis and the potential role of endoglin (ENG), recently described as a new marker for this process, have not been explored in Myelodysplastic Syndromes (MDS). In order to gain insight in MDS angiogenesis a combined analysis in bone marrow (BM) of gene expression levels, angiogenesis-related soluble factors and functional angiogenesis-related studies was carried out. Ninety-seven MDS patients and forty-two normal BM samples were studied. The morphology of the capillary-like structures originated by two endothelial cells lines in the BM environment of patients with refractory cytopenia with multilineage dysplasia (RCMD) was different from those of the remaining MDS. In addition, the BM mononuclear cells from RCMD patients displayed over-expression of VEGF, HIF and FN1 while they showed reduced expression of ENG in contrast to the normal ENG expression of the remaining low-risk MDS and the high expression of ENG in high-risk MDS subtype. Moreover, higher soluble ENG and soluble FLT-1 levels in BM microenvironment were observed in RCMD cases, which distinguished them from other individuals. Therefore, the present study suggests that the patterns of angiogenesis are different between the MDS subtypes. The differences in angiogenesis observed in RCMD patients could be related to ENG abnormalities.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23341958</pmid><doi>10.1371/journal.pone.0053624</doi><tpages>e53624</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Abnormalities Analysis Anemia Anemia, Refractory - metabolism Anemia, Refractory - pathology Angiogenesis Angiogenesis Inducing Agents - metabolism Antigens, CD - genetics Antigens, CD - metabolism Biology Bone marrow Bone Marrow - metabolism Bone Marrow - pathology Cancer Cell Lineage Cell Proliferation Cellular Microenvironment Dysplasia Endoglin Endothelial cells Endothelial Cells - metabolism Endothelial Cells - pathology Endothelium Fibronectins Gene expression Growth factors Humans Leukemia Leukocytes (mononuclear) Medical research Medicine Mitochondrial DNA Myelodysplastic syndrome Myelodysplastic syndromes Myelodysplastic Syndromes - metabolism Myelodysplastic Syndromes - pathology Neovascularization, Pathologic - metabolism Neovascularization, Pathologic - pathology Overexpression Patients Proteins Receptors, Cell Surface - genetics Receptors, Cell Surface - metabolism Signal transduction Solubility Studies Tumors Vascular endothelial growth factor Vascular Endothelial Growth Factor A - genetics Vascular Endothelial Growth Factor A - metabolism |
title | Alteration in endoglin-related angiogenesis in refractory cytopenia with multilineage dysplasia |
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