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Chen J.-J.,PLA Fourth Military Medical University | Gao Y.,Shaanxi Province Peoples Hospital | Tian Q.,PLA Fourth Military Medical University | Liang Y.-M.,PLA Fourth Military Medical University | Yang L.,PLA Fourth Military Medical University
British Journal of Radiology | Year: 2014

Objective: The aimof this studywas to find a newradiation protector, platelet factor 4 (PF4) and to identify its effect on haemopoietic microenvironment in vitro and in vivo.Methods: Radiation damage on bone marrow mesenchymal stem cells ex and in vitro was set up as models. Growth curve analysis, clonogenic survival assay, FACSCalibur™ (BD Immunocytometry Systems, San Jose, CA), 5-ethynyl-2′-deoxyuridine immunofluorescence staining and quantitative reverse transcription-polymerase chain reaction were employed to assess the characterization of bone marrow mesenchymal stem cells (BMSCs), proliferation, apoptosis, cell cycle and gene expression.Results: A dose- and time-dependent enhancement of cell viability and survival was observed for PF4 treatment along with 500cGy γ-radiation in vitro. The same phenomena were noted in vivo, including enhancement of adherence and proliferation ability while inhibition of cell apoptosis, which were associated with a short-term decrease in the G0/G1 ratio owing to S phase arrest. These were accompanied with enhanced Bcl-2 expression and p53/p21 loss.Conclusion: These results uncover that PF4 might be a novel therapeutic approach, which could reduce DNA damage and increase survival of BMSCs, in part, by inhibiting p53/p21 axis and facilitating DNA damage repair. Advances in knowledge: This study explores the feasibility of a new radioprotector and hence may be clinically important. © 2014 The Authors. Source


Yang G.,Georgia Regents University | Yang G.,Xian Jiaotong University | Deng Y.-J.,CAS Beijing Institute of Genomics | Qin H.,Georgia Regents University | And 8 more authors.
International Journal of Immunogenetics | Year: 2010

To identify HLA-Bz.ast;15 subtypes distribution in Han population in Beijing, People's Republic of China, 826 unrelated healthy individuals were typed using the polymerase chain reaction-sequence-based typing method. Within the 246 HLA-Bz.ast;15 positive individuals, 29 HLA-Bz.ast;15 alleles were identified, the most predominant of which is Bz.ast;1501 (40.07%), followed by Bz.ast;1502 (12.87%), Bz.ast;1511 (12.87%), Bz.ast;1518 (9.19%) and Bz.ast;1532 (3.31%). The distribution of HLA-Bz.ast;15 subtype frequencies was compared between the Beijing Han, eight other Chinese ethnic minorities and six Chinese populations covering the mainland of China, Taiwan, Hong Kong and Singapore. A neighbor-joining phylogenetic tree was constructed and revealed that the Beijing Han population clustered into the northern populations group and had a closer relationship with northern Han and Hui than with southern Han or other ethnic minorities. These results thus provide useful information that can be used in anthropology, selection for bone marrow transplantation as well as in diseaseassociation study, such as in carbamazepine (CBZ)- induced Stevens-Johnson syndrome and toxic epidermal necrolysis. © 2010 Blackwell Publishing Ltd, International Journal of Immunogenetics. Source


Ma K.,Xian Jiaotong University | Wang C.,Xian Jiaotong University | Geng Q.,Xian Jiaotong University | Fan Y.,Xian Jiaotong University | And 8 more authors.
Oncology Reports | Year: 2016

Anginex is an artificial synthetic small molecule β-sheet-forming peptide shown to have anti- Angiogenesis and antitumor effects in various solid tumors. However,its molecular mechanism remains largely unclear and efficient delivery methods for anginex remains to be developed. We report on the development of recombinant adeno- Associated virus (rAAV2)-delivered anginex and the underlying mechanism of anti- Angiogenesis and antitumor effects of anginex. We have successfully developed the rAAV2 vector to efficiently express anginex (rAAV2- Anginex). Transduction of rAAV2- Anginex significantly induced apoptosis,and inhibited the proliferation,migration,invasion and tube formation of human umbilical vein endothelial cells in vitro. Western blot analysis revealed that rAAV2- Anginex inhibited the phosphorylation of Akt,while inducing the phosphorylation of JNK and activation of the NF-κB signaling pathway. In an in vivo CAM assay and xenograft model of SKOV3,rAAV2- Anginex significantly reduced microvessel density (MVD) and vascular endothelial growth factor 165 (VEGF165),as demonstrated by immunohistochemistry analysis. Importantly,rAAV2- Anginex inhibited tumor growth in an ovarian cancer SKOV3 cell nude mouse xenograft model. Our results suggest that rAAV2- Anginex may inhibit tumor angiogenesis and growth through regulating Akt,JNK and NF-κB signaling pathways. Source


Ma G.,Xian Jiaotong University | Pan Y.,Northwest Women and Childrens Hospital | Zhou C.,Xian Jiaotong University | Sun R.,Xian Jiaotong University | And 4 more authors.
Oncology Reports | Year: 2015

Tamoxifen resistance is a major clinical problem for ER-positive breast cancer, but the underlying mechanism is not completely elucidated. In the present study, we reported that mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1), a member of the family of MKPs, is involved in tamoxifen resistance. We found that MKP1 expression increased in tamoxifen resistant MCF7 cells. To explore the possible role of MKP1 in tamoxifen resistance, siRNA targeting MKP1 was transfected into tamoxifen resistant MCF7 cells. To our surprise, knockdown of MKP-1 promoted cell death induced by tamoxifen. On the other hand, the MKP1 overexpressed MCF7 cell clone was established and MKP1 overexpression effectively attenuated MCF7 cell death induced by tamoxifen. In addition, we revealed that MKP1 inhibited tamoxifen-mediated JNK activation in tamoxifen resistant MCF7 and MCF7 cells, and by this mechanism MKP1 was able to inhibit tamoxifen-induced cell death. We also showed that combined appliaction of MKP1 inhibitor triptolide and tamoxifen can effectively increase tamoxifen sensitivity in tamoxifen resistant MCF7 cells. Collectively, our results indicated that MKP-1 can attenuate tamoxifen-induced cell death through inhibiting the JNK signal pathway, which represents a novel mechanism of tamoxifen resistance in MCF7 cells. Source


Zhao N.,Shaanxi Province Peoples Hospital | Mi L.,Peking University | Liu X.,Shaanxi Province Peoples Hospital | Liu X.,Xian Jiaotong University | And 9 more authors.
PLoS ONE | Year: 2015

Global Registry of Acute Coronary Events (GRACE) risk score and red blood cell distribution width (RDW) content can both independently predictmajor adverse cardiac events (MACEs) in patients with acute coronary syndrome (ACS). We investigated the combined predictive value of RDW and GRACE risk score for cardiovascular events in patients with ACS undergoing percutaneous coronary intervention (PCI) for the first time. We enrolled 480 ACS patients. During a median follow-up time of 37.2 months, 70 (14.58%) patients experienced MACEs. Patients were divided into tertiles according to the baseline RDW content (11.30-12.90, 13.00-13.50, 13.60-16.40). GRACE score was positively correlated with RDW content. Multivariate Cox analysis showed that both GRACE score and RDW content were independent predictors of MACEs (hazard ratio 1.039; 95% confidence interval [CI] 1.024-1.055; p < 0.001; 1.699; 1.294-2.232; p < 0.001; respectively). Furthermore, Kaplan-Meier analysis demonstrated that the risk of MACEs increased with increasing RDW content (p < 0.001). For GRACE score alone, the area under the receiver operating characteristic (ROC) curve for MACEs was 0.749 (95% CI: 0.707-0.787). The area under the ROC curve for MACEs increased to 0.805 (0.766-0.839, p = 0.034) after adding RDW content. The incremental predictive value of combining RDW content and GRACE risk score was significantly improved, also shown by the net reclassification improvement (NRI = 0.352, p < 0.001) and integrated discrimination improvement (IDI = 0.023, p = 0.002). Combining the predictive value of RDW and GRACE risk score yielded a more accurate predictive value for long-term cardiovascular events in ACS patients who underwent PCI as compared to each measure alone. Copyright: © 2015 Zhao et al. Source

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