Impairment of bone marrow endothelial progenitor cells in acute graft‐versus‐host disease patients after allotransplant

Summary Graft‐versus‐host disease (GVHD) is a major complication after allogeneic haematopoietic stem cell transplantation (allo‐HSCT) that is frequently associated with bone marrow (BM) suppression, and clinical management is challenging. BM endothelial progenitor cells (EPCs) play crucial roles in...

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Veröffentlicht in:British journal of haematology 2018-09, Vol.182 (6), p.870-886
Hauptverfasser: Cao, Xie‐Na, Kong, Yuan, Song, Yang, Shi, Min‐Min, Zhao, Hong‐Yan, Wen, Qi, Lyu, Zhong‐Shi, Duan, Cai‐Wen, Wang, Yu, Xu, Lan‐Ping, Zhang, Xiao‐Hui, Huang, Xiao‐Jun
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container_issue 6
container_start_page 870
container_title British journal of haematology
container_volume 182
creator Cao, Xie‐Na
Kong, Yuan
Song, Yang
Shi, Min‐Min
Zhao, Hong‐Yan
Wen, Qi
Lyu, Zhong‐Shi
Duan, Cai‐Wen
Wang, Yu
Xu, Lan‐Ping
Zhang, Xiao‐Hui
Huang, Xiao‐Jun
description Summary Graft‐versus‐host disease (GVHD) is a major complication after allogeneic haematopoietic stem cell transplantation (allo‐HSCT) that is frequently associated with bone marrow (BM) suppression, and clinical management is challenging. BM endothelial progenitor cells (EPCs) play crucial roles in the regulation of haematopoiesis and thrombopoiesis. However, little is known regarding the functional roles of BM EPCs in acute GVHD (aGVHD) patients. In the current prospective case‐control study, reduced and dysfunctional BM EPCs, characterized by decreased migration and angiogenesis capacities and increased levels of reactive oxygen species (ROS) and apoptosis, were found in aGVHD patients compared with those without aGVHD. Moreover, lower frequency and increased levels of ROS, apoptosis and DNA damage, but reduced colony‐forming unit‐plating efficiency were found in BM CD34+ cells of aGVHD patients compared with those without aGVHD. The severity of aGVHD and GVHD‐mediated cytopenia was associated with BM EPC impairment in aGVHD patients. In addition, the EPC impairment positively correlated with ROS level. Taken together, our results suggest that reduced and dysfunctional BM EPCs may be involved in the pathogenesis of aGVHD. Although these findings require validation, our data indicate that improvement of BM EPCs may represent a promising therapeutic approach for aGVHD patients.
doi_str_mv 10.1111/bjh.15456
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BM endothelial progenitor cells (EPCs) play crucial roles in the regulation of haematopoiesis and thrombopoiesis. However, little is known regarding the functional roles of BM EPCs in acute GVHD (aGVHD) patients. In the current prospective case‐control study, reduced and dysfunctional BM EPCs, characterized by decreased migration and angiogenesis capacities and increased levels of reactive oxygen species (ROS) and apoptosis, were found in aGVHD patients compared with those without aGVHD. Moreover, lower frequency and increased levels of ROS, apoptosis and DNA damage, but reduced colony‐forming unit‐plating efficiency were found in BM CD34+ cells of aGVHD patients compared with those without aGVHD. The severity of aGVHD and GVHD‐mediated cytopenia was associated with BM EPC impairment in aGVHD patients. In addition, the EPC impairment positively correlated with ROS level. Taken together, our results suggest that reduced and dysfunctional BM EPCs may be involved in the pathogenesis of aGVHD. 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BM endothelial progenitor cells (EPCs) play crucial roles in the regulation of haematopoiesis and thrombopoiesis. However, little is known regarding the functional roles of BM EPCs in acute GVHD (aGVHD) patients. In the current prospective case‐control study, reduced and dysfunctional BM EPCs, characterized by decreased migration and angiogenesis capacities and increased levels of reactive oxygen species (ROS) and apoptosis, were found in aGVHD patients compared with those without aGVHD. Moreover, lower frequency and increased levels of ROS, apoptosis and DNA damage, but reduced colony‐forming unit‐plating efficiency were found in BM CD34+ cells of aGVHD patients compared with those without aGVHD. The severity of aGVHD and GVHD‐mediated cytopenia was associated with BM EPC impairment in aGVHD patients. In addition, the EPC impairment positively correlated with ROS level. Taken together, our results suggest that reduced and dysfunctional BM EPCs may be involved in the pathogenesis of aGVHD. 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Kong, Yuan ; Song, Yang ; Shi, Min‐Min ; Zhao, Hong‐Yan ; Wen, Qi ; Lyu, Zhong‐Shi ; Duan, Cai‐Wen ; Wang, Yu ; Xu, Lan‐Ping ; Zhang, Xiao‐Hui ; Huang, Xiao‐Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3886-5b921da6f90b7ad283a1f22f7d6459b636dbc0ff6c7636b0a84a691a87fdad3d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>allotransplant</topic><topic>Angiogenesis</topic><topic>Apoptosis</topic><topic>Bone marrow</topic><topic>Bone marrow transplantation</topic><topic>CD34 antigen</topic><topic>DNA damage</topic><topic>endothelial progenitor cells</topic><topic>Graft-versus-host reaction</topic><topic>graft‐versus‐host disease</topic><topic>haematopoietic stem cells</topic><topic>Hematology</topic><topic>Hematopoietic stem cells</topic><topic>Impairment</topic><topic>Osteoprogenitor cells</topic><topic>Reactive oxygen species</topic><topic>Stem cell transplantation</topic><topic>Thrombopoiesis</topic><topic>Transplantation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cao, Xie‐Na</creatorcontrib><creatorcontrib>Kong, Yuan</creatorcontrib><creatorcontrib>Song, Yang</creatorcontrib><creatorcontrib>Shi, Min‐Min</creatorcontrib><creatorcontrib>Zhao, Hong‐Yan</creatorcontrib><creatorcontrib>Wen, Qi</creatorcontrib><creatorcontrib>Lyu, Zhong‐Shi</creatorcontrib><creatorcontrib>Duan, Cai‐Wen</creatorcontrib><creatorcontrib>Wang, Yu</creatorcontrib><creatorcontrib>Xu, Lan‐Ping</creatorcontrib><creatorcontrib>Zhang, Xiao‐Hui</creatorcontrib><creatorcontrib>Huang, Xiao‐Jun</creatorcontrib><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>Cao, Xie‐Na</au><au>Kong, Yuan</au><au>Song, Yang</au><au>Shi, Min‐Min</au><au>Zhao, Hong‐Yan</au><au>Wen, Qi</au><au>Lyu, Zhong‐Shi</au><au>Duan, Cai‐Wen</au><au>Wang, Yu</au><au>Xu, Lan‐Ping</au><au>Zhang, Xiao‐Hui</au><au>Huang, Xiao‐Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impairment of bone marrow endothelial progenitor cells in acute graft‐versus‐host disease patients after allotransplant</atitle><jtitle>British journal of haematology</jtitle><addtitle>Br J Haematol</addtitle><date>2018-09</date><risdate>2018</risdate><volume>182</volume><issue>6</issue><spage>870</spage><epage>886</epage><pages>870-886</pages><issn>0007-1048</issn><eissn>1365-2141</eissn><abstract>Summary Graft‐versus‐host disease (GVHD) is a major complication after allogeneic haematopoietic stem cell transplantation (allo‐HSCT) that is frequently associated with bone marrow (BM) suppression, and clinical management is challenging. 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subjects allotransplant
Angiogenesis
Apoptosis
Bone marrow
Bone marrow transplantation
CD34 antigen
DNA damage
endothelial progenitor cells
Graft-versus-host reaction
graft‐versus‐host disease
haematopoietic stem cells
Hematology
Hematopoietic stem cells
Impairment
Osteoprogenitor cells
Reactive oxygen species
Stem cell transplantation
Thrombopoiesis
Transplantation
title Impairment of bone marrow endothelial progenitor cells in acute graft‐versus‐host disease patients after allotransplant
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