Associations between acute GVHD-related biomarkers and endothelial cell activation after allogeneic hematopoietic stem cell transplantation
Hematopoietic stem cell transplantation (HSCT) can cause serious transplant-related complications such as graft-versus-host disease (GVHD). Acute GVHD (aGVHD) has been diagnosed by clinical manifestations, laboratory data and pathological effects until now, but recently the discovery of specific bio...
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| Veröffentlicht in: | Transplant immunology 2017-08, Vol.43-44, p.27-32 |
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| creator | Nomura, Shosaku Ishii, Kazuyoshi Fujita, Shinya Nakaya, Aya Satake, Atsushi Ito, Tomoki |
| description | Hematopoietic stem cell transplantation (HSCT) can cause serious transplant-related complications such as graft-versus-host disease (GVHD). Acute GVHD (aGVHD) has been diagnosed by clinical manifestations, laboratory data and pathological effects until now, but recently the discovery of specific biomarkers such as suppression of tumorigenicity 2 (ST2), elafin and regenerating islet-derived 3α (REG3α) is challenging this approach.
We investigated the expression of aGVHD-related markers (regulated on activation normal T-cell expressed and secretes: RANTES, elafin, REG3α and ST2) and endothelial cell activation markers (soluble vascular cell adhesion molecule: sVCAM-1 and plasminogen activator inhibitor: PAI-1) in patients undergoing allogeneic HSCT. Additionally, we studied the effects of recombinant soluble thrombomodulin (rTM) on the expression of these markers. Our study cohort included 225 patients who underwent allogeneic HSCT at several institutions in Japan.
RANTES, sVCAM-1, PAI-1, elafin, REG3α and ST2 exhibited significant increases in patients not receiving rTM after HSCT. When we examined patients with confirmed complications, the frequencies of aGVHD and VOD were significantly lower in the rTM-treated group. In addition, aGVHD-related biomarkers such as elafin, REG3α, and ST2 were elevated significantly in patients with aGVHD.
Our findings suggest that endothelial cell activation might be linked to aGVHD, and that rTM might act to prevent aGVHD, at least in part, through its effect on endothelial cells. |
| doi_str_mv | 10.1016/j.trim.2017.06.004 |
| format | Article |
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We investigated the expression of aGVHD-related markers (regulated on activation normal T-cell expressed and secretes: RANTES, elafin, REG3α and ST2) and endothelial cell activation markers (soluble vascular cell adhesion molecule: sVCAM-1 and plasminogen activator inhibitor: PAI-1) in patients undergoing allogeneic HSCT. Additionally, we studied the effects of recombinant soluble thrombomodulin (rTM) on the expression of these markers. Our study cohort included 225 patients who underwent allogeneic HSCT at several institutions in Japan.
RANTES, sVCAM-1, PAI-1, elafin, REG3α and ST2 exhibited significant increases in patients not receiving rTM after HSCT. When we examined patients with confirmed complications, the frequencies of aGVHD and VOD were significantly lower in the rTM-treated group. In addition, aGVHD-related biomarkers such as elafin, REG3α, and ST2 were elevated significantly in patients with aGVHD.
Our findings suggest that endothelial cell activation might be linked to aGVHD, and that rTM might act to prevent aGVHD, at least in part, through its effect on endothelial cells.</description><identifier>ISSN: 0966-3274</identifier><identifier>EISSN: 1878-5492</identifier><identifier>DOI: 10.1016/j.trim.2017.06.004</identifier><identifier>PMID: 28687251</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Acute Disease ; Adolescent ; Adult ; Aged ; aGVHD ; Allografts ; Biomarker ; Biomarkers - blood ; Chemokine CCL5 - blood ; Chemokine CCL5 - immunology ; Elafin - blood ; Elafin - immunology ; Endothelial Cells - immunology ; Endothelial Cells - metabolism ; Endothelial Cells - pathology ; Female ; Graft vs Host Disease - blood ; Graft vs Host Disease - immunology ; Graft vs Host Disease - pathology ; Hematologic Neoplasms - blood ; Hematologic Neoplasms - immunology ; Hematologic Neoplasms - therapy ; Hematopoietic Stem Cell Transplantation ; Humans ; Male ; Middle Aged ; Plasminogen Activator Inhibitor 1 - blood ; Plasminogen Activator Inhibitor 1 - immunology ; rTM ; Stem cell transplantation ; sVCAM-1 ; Vascular Cell Adhesion Molecule-1 - blood ; Vascular Cell Adhesion Molecule-1 - immunology</subject><ispartof>Transplant immunology, 2017-08, Vol.43-44, p.27-32</ispartof><rights>2017 The Authors</rights><rights>Copyright © 2017 The Authors. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c466t-46469822ba0719de5de2d8cda86fcc9874c6b00502650324e8cc752c05e699d83</citedby><cites>FETCH-LOGICAL-c466t-46469822ba0719de5de2d8cda86fcc9874c6b00502650324e8cc752c05e699d83</cites><orcidid>0000-0003-2152-9862</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.trim.2017.06.004$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28687251$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nomura, Shosaku</creatorcontrib><creatorcontrib>Ishii, Kazuyoshi</creatorcontrib><creatorcontrib>Fujita, Shinya</creatorcontrib><creatorcontrib>Nakaya, Aya</creatorcontrib><creatorcontrib>Satake, Atsushi</creatorcontrib><creatorcontrib>Ito, Tomoki</creatorcontrib><title>Associations between acute GVHD-related biomarkers and endothelial cell activation after allogeneic hematopoietic stem cell transplantation</title><title>Transplant immunology</title><addtitle>Transpl Immunol</addtitle><description>Hematopoietic stem cell transplantation (HSCT) can cause serious transplant-related complications such as graft-versus-host disease (GVHD). Acute GVHD (aGVHD) has been diagnosed by clinical manifestations, laboratory data and pathological effects until now, but recently the discovery of specific biomarkers such as suppression of tumorigenicity 2 (ST2), elafin and regenerating islet-derived 3α (REG3α) is challenging this approach.
We investigated the expression of aGVHD-related markers (regulated on activation normal T-cell expressed and secretes: RANTES, elafin, REG3α and ST2) and endothelial cell activation markers (soluble vascular cell adhesion molecule: sVCAM-1 and plasminogen activator inhibitor: PAI-1) in patients undergoing allogeneic HSCT. Additionally, we studied the effects of recombinant soluble thrombomodulin (rTM) on the expression of these markers. Our study cohort included 225 patients who underwent allogeneic HSCT at several institutions in Japan.
RANTES, sVCAM-1, PAI-1, elafin, REG3α and ST2 exhibited significant increases in patients not receiving rTM after HSCT. When we examined patients with confirmed complications, the frequencies of aGVHD and VOD were significantly lower in the rTM-treated group. In addition, aGVHD-related biomarkers such as elafin, REG3α, and ST2 were elevated significantly in patients with aGVHD.
Our findings suggest that endothelial cell activation might be linked to aGVHD, and that rTM might act to prevent aGVHD, at least in part, through its effect on endothelial cells.</description><subject>Acute Disease</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>aGVHD</subject><subject>Allografts</subject><subject>Biomarker</subject><subject>Biomarkers - blood</subject><subject>Chemokine CCL5 - blood</subject><subject>Chemokine CCL5 - immunology</subject><subject>Elafin - blood</subject><subject>Elafin - immunology</subject><subject>Endothelial Cells - immunology</subject><subject>Endothelial Cells - metabolism</subject><subject>Endothelial Cells - pathology</subject><subject>Female</subject><subject>Graft vs Host Disease - blood</subject><subject>Graft vs Host Disease - immunology</subject><subject>Graft vs Host Disease - pathology</subject><subject>Hematologic Neoplasms - blood</subject><subject>Hematologic Neoplasms - immunology</subject><subject>Hematologic Neoplasms - therapy</subject><subject>Hematopoietic Stem Cell Transplantation</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Plasminogen Activator Inhibitor 1 - blood</subject><subject>Plasminogen Activator Inhibitor 1 - immunology</subject><subject>rTM</subject><subject>Stem cell transplantation</subject><subject>sVCAM-1</subject><subject>Vascular Cell Adhesion Molecule-1 - blood</subject><subject>Vascular Cell Adhesion Molecule-1 - immunology</subject><issn>0966-3274</issn><issn>1878-5492</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1uFDEQhS0EIkPgAiyQl2y6Kbu7bbfEJgqQIEViA2wtt11DPLjtwfYEcQYujScTWLIqlfS-Vz-PkJcMegZMvNn1Nfu158BkD6IHGB-RDVNSddM488dkA7MQ3cDleEaelbIDAD7N8ik540ooySe2Ib8vSknWm-pTLHTB-hMxUmMPFenV1-t3XcZgKjq6-LSa_B1zoSY6itGleovBm0AthtCQ6u_ubajZVszUhJC-YURv6S2upqZ98lhbVyquJ6ZmE8s-mFjvwefkydaEgi8e6jn58uH958vr7ubT1cfLi5vOjkLUbhSjmBXniwHJZoeTQ-6UdUaJrbWzkqMVC8AEXEww8BGVtXLiFiYU8-zUcE5en3z3Of04YKl69eW4kImYDkWzmcmhDRlYk_KT1OZUSsat3reXm_xLM9DHEPROH0PQxxA0CN1CaNCrB__DsqL7h_z9ehO8PQmwXXnnMetiPUaLzme0Vbvk_-f_B1yTm7c</recordid><startdate>201708</startdate><enddate>201708</enddate><creator>Nomura, Shosaku</creator><creator>Ishii, Kazuyoshi</creator><creator>Fujita, Shinya</creator><creator>Nakaya, Aya</creator><creator>Satake, Atsushi</creator><creator>Ito, Tomoki</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</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><orcidid>https://orcid.org/0000-0003-2152-9862</orcidid></search><sort><creationdate>201708</creationdate><title>Associations between acute GVHD-related biomarkers and endothelial cell activation after allogeneic hematopoietic stem cell transplantation</title><author>Nomura, Shosaku ; Ishii, Kazuyoshi ; Fujita, Shinya ; Nakaya, Aya ; Satake, Atsushi ; Ito, Tomoki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-46469822ba0719de5de2d8cda86fcc9874c6b00502650324e8cc752c05e699d83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Acute Disease</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>aGVHD</topic><topic>Allografts</topic><topic>Biomarker</topic><topic>Biomarkers - blood</topic><topic>Chemokine CCL5 - blood</topic><topic>Chemokine CCL5 - immunology</topic><topic>Elafin - blood</topic><topic>Elafin - immunology</topic><topic>Endothelial Cells - immunology</topic><topic>Endothelial Cells - metabolism</topic><topic>Endothelial Cells - pathology</topic><topic>Female</topic><topic>Graft vs Host Disease - blood</topic><topic>Graft vs Host Disease - immunology</topic><topic>Graft vs Host Disease - pathology</topic><topic>Hematologic Neoplasms - blood</topic><topic>Hematologic Neoplasms - immunology</topic><topic>Hematologic Neoplasms - therapy</topic><topic>Hematopoietic Stem Cell Transplantation</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Plasminogen Activator Inhibitor 1 - blood</topic><topic>Plasminogen Activator Inhibitor 1 - immunology</topic><topic>rTM</topic><topic>Stem cell transplantation</topic><topic>sVCAM-1</topic><topic>Vascular Cell Adhesion Molecule-1 - blood</topic><topic>Vascular Cell Adhesion Molecule-1 - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nomura, Shosaku</creatorcontrib><creatorcontrib>Ishii, Kazuyoshi</creatorcontrib><creatorcontrib>Fujita, Shinya</creatorcontrib><creatorcontrib>Nakaya, Aya</creatorcontrib><creatorcontrib>Satake, Atsushi</creatorcontrib><creatorcontrib>Ito, Tomoki</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>Transplant immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nomura, Shosaku</au><au>Ishii, Kazuyoshi</au><au>Fujita, Shinya</au><au>Nakaya, Aya</au><au>Satake, Atsushi</au><au>Ito, Tomoki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Associations between acute GVHD-related biomarkers and endothelial cell activation after allogeneic hematopoietic stem cell transplantation</atitle><jtitle>Transplant immunology</jtitle><addtitle>Transpl Immunol</addtitle><date>2017-08</date><risdate>2017</risdate><volume>43-44</volume><spage>27</spage><epage>32</epage><pages>27-32</pages><issn>0966-3274</issn><eissn>1878-5492</eissn><abstract>Hematopoietic stem cell transplantation (HSCT) can cause serious transplant-related complications such as graft-versus-host disease (GVHD). Acute GVHD (aGVHD) has been diagnosed by clinical manifestations, laboratory data and pathological effects until now, but recently the discovery of specific biomarkers such as suppression of tumorigenicity 2 (ST2), elafin and regenerating islet-derived 3α (REG3α) is challenging this approach.
We investigated the expression of aGVHD-related markers (regulated on activation normal T-cell expressed and secretes: RANTES, elafin, REG3α and ST2) and endothelial cell activation markers (soluble vascular cell adhesion molecule: sVCAM-1 and plasminogen activator inhibitor: PAI-1) in patients undergoing allogeneic HSCT. Additionally, we studied the effects of recombinant soluble thrombomodulin (rTM) on the expression of these markers. Our study cohort included 225 patients who underwent allogeneic HSCT at several institutions in Japan.
RANTES, sVCAM-1, PAI-1, elafin, REG3α and ST2 exhibited significant increases in patients not receiving rTM after HSCT. When we examined patients with confirmed complications, the frequencies of aGVHD and VOD were significantly lower in the rTM-treated group. In addition, aGVHD-related biomarkers such as elafin, REG3α, and ST2 were elevated significantly in patients with aGVHD.
Our findings suggest that endothelial cell activation might be linked to aGVHD, and that rTM might act to prevent aGVHD, at least in part, through its effect on endothelial cells.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>28687251</pmid><doi>10.1016/j.trim.2017.06.004</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0003-2152-9862</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Disease Adolescent Adult Aged aGVHD Allografts Biomarker Biomarkers - blood Chemokine CCL5 - blood Chemokine CCL5 - immunology Elafin - blood Elafin - immunology Endothelial Cells - immunology Endothelial Cells - metabolism Endothelial Cells - pathology Female Graft vs Host Disease - blood Graft vs Host Disease - immunology Graft vs Host Disease - pathology Hematologic Neoplasms - blood Hematologic Neoplasms - immunology Hematologic Neoplasms - therapy Hematopoietic Stem Cell Transplantation Humans Male Middle Aged Plasminogen Activator Inhibitor 1 - blood Plasminogen Activator Inhibitor 1 - immunology rTM Stem cell transplantation sVCAM-1 Vascular Cell Adhesion Molecule-1 - blood Vascular Cell Adhesion Molecule-1 - immunology |
| title | Associations between acute GVHD-related biomarkers and endothelial cell activation after allogeneic hematopoietic stem cell transplantation |
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