ABSTRACT
OBJECTIVE: To explore the regularity of serological conversion of blood group in BM empty phase of ABO-incompatible allogeneic stem cell transplantation so as to provide the basis for selecting the blood components in blood transfusion. METHODS: Before hematpoietic stem cell transplantation (HSCT), the ABO and RhD blood groups of recipients and donors were identified by salt medium tube method and microcolumn gel method; after transplantation the changes of antigen intensity and antibody titer of ABO blood group in patients were periodically detected. RESULTS: After blood group shift of 33 patients received ABO-incompatible allo-HSCT, the consistent rate of positive and regative types in major ABO incompatible group was 100%; the consistent rate of positive and negative types in minor ABO-incompatible group was 33%, no-consistent rate was 66.7%; the consistent rate of positive and negative types in bidirextional ABO incompatible group was 20%, the no-consistent rate was 80%. CONCLUSION: After ABO-incompatible allo-HSCT, blood group antgen of patients shifts to the blood group of donors, there is a significant difference in the serological indicators between the minor and bidireetional ABO-incompatible patients and normal people.
Subject(s)
ABO Blood-Group System , Blood Group Incompatibility , Hematopoietic Stem Cell Transplantation , Blood Transfusion , Humans , Tissue Donors , Transplantation, HomologousABSTRACT
Platelets play crucial roles in hemostasis, thrombosis, wound healing, inflammation, angiogenesis, and tumor metastases. Because they are anucleated blood cells, platelets lack nuclear DNA, but they do contain mitochondrial DNA, which plays a key role in regulating apoptosis. Recent evidence has suggested that miRNAs are also involved in regulating gene expression and apoptosis in platelets. Our previous study showed that the expression of miR-326 increased visibly when apheresis platelets were stored in vitro. The antiapoptotic Bcl-2 family regulator Bcl-xL has been identified as a putative target of miR-326. In the present study, dual reporter luciferase assays were used to characterize the function of miR-326 in the regulation of the apoptosis of platelet cells. These assays demonstrated that miR-326 bound to the 3'-translated region of Bcl-xL. To directly assess the functional effects of miR-326 expression, levels of Bcl-xL and the apoptotic status of stored apheresis platelets were measured after transfection of miR-326 mimic or inhibitor. Results indicated that miR-326 inhibited Bcl-xL expression and induced apoptosis in stored platelets. Additionally, miR-326 inhibited Bcl-2 protein expression and enhanced Bak expression, possibly through an indirect mechanism, though there was no effect on the expression of Bax. The effect of miR-326 appeared to be limited to apoptosis, with no significant effect on platelet activation. These results provide new insight into the molecular mechanisms affecting differential platelet gene regulation, which may increase understanding of the role of platelet apoptosis in multiple diseases.
