细胞减少
医学
造血
骨髓
祖细胞
免疫学
川地34
血管生成
发病机制
移植物抗宿主病
干细胞
移植
癌症研究
内科学
生物
遗传学
作者
Xie-Na Cao,Yuan Kong,Yang Song,Min‐Min Shi,Hongyan Zhao,Qi Wen,Zhong‐Shi Lyu,Cai‐Wen Duan,Yu Wang,Lan‐Ping Xu,Xiaohui Zhang,Xiao‐Jun Huang
摘要
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 ( EPC s) play crucial roles in the regulation of haematopoiesis and thrombopoiesis. However, little is known regarding the functional roles of BM EPC s in acute GVHD ( aGVHD ) patients. In the current prospective case‐control study, reduced and dysfunctional BM EPC s, 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 CD 34 + 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 EPC s may be involved in the pathogenesis of aGVHD . Although these findings require validation, our data indicate that improvement of BM EPC s may represent a promising therapeutic approach for aGVHD patients.
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