Hengxing Meng

Government of the People's Republic of China, Peping, Beijing, China

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Publications (7)24.75 Total impact

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    ABSTRACT: Secondary monoclonal gammopathy of undetermined significance (MGUS) is a special phenomenon during the treatment of multiple myeloma (MM). The incidence, biological characteristics and prognostic value of secondary MGUS in patients with MM remain undefined. We proceed with a retrospective systematic review of serum immunofixation electrophoresis (IFE) studies performed in 438 cases of patients with plasma cell dyscrasias, including 409 cases of newly diagnosed MM and 29 cases of primary plasma cell leukemia (pPCL). Secondary MGUS was more common in patients with myeloma who had undergone SCT than in those who had not (17 [29.8%] out of 57 versus 5 [1.4%] out of 352, P < 0.001). The clinical parameters and cytogenetic characteristics in patients with or without secondary MGUS were comparable. The overall CR rates in patients with or without secondary MGUS were 81.8% and 21.8% respectively (p<0.01). For the cohort as a whole, secondary MGUS was associated with significantly prolonged progression free survival (median: 52.0 months vs. 22.5 months, p =0.002) and overall survival (median: not reached vs. 35.0 months, p<0.001).The presence of secondary MGUS retained independent prognostic value with a moderate impact on OS (HR 0.128 [95% CI 0.018-0.922], p=0.041) in the multivariate Cox regression model. However, when analysis was restricted to patients undergoing stem cell transplantation, no statistical difference in PFS and OS was found. In conclusion, we observe that secondary MGUS was frequently observed in MM patients after transplantation and conferred a survival prolongation. The favorable survival in patients with secondary MGUS may be explained by beneficial effect from myeloablative therapy.
    Biology of blood and marrow transplantation: journal of the American Society for Blood and Marrow Transplantation 11/2013; DOI:10.1016/j.bbmt.2013.11.022 · 3.35 Impact Factor
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    ABSTRACT: The majority of hematopoietic stem/progenitor cells (HSPCs) reside in bone marrow (BM) surrounded by a specialized environment, which governs HSPC function. Here we investigated the potential role of bone remodeling cells (osteoblasts and osteoclasts) in homeostasis and stress-induced HSPC mobilization. Peripheral blood (PB) and BM in steady/mobilized state were collected from healthy donors undergoing allogeneic transplantation and from mice treated with granulocyte colony stimulating factor (G-CSF), parathyroid hormone (PTH), or receptor activator of nuclear factor kappa-B ligand (RANKL). The number and the functional markers of osteoblasts and osteoclasts were checked by a series of experiments. Our data showed that the number of CD45(-) Ter119(-) osteopontin (OPN)(+) osteoblasts was significantly reduced from 4085 ± 135 cells/femur on day 0 to 1032 ± 55 cells/femur on day 5 in mice (P = 0.02) and from 21.38 ± 0.66 on day 0 to 14.78 ± 0.65 on day 5 in healthy donors (P < 0.01). Decrease of osteoblast number leads to reduced level of HSPC mobilization regulators stromal cell-derived factor-1 (SDF-1), stem cell factor (SCF) and OPN. The osteoclast number at bone surface (OC.N/B.s) was significantly increased from 1.53 ± 0.12 on day 0 to 4.42 ± 0.46 on day 5 (P < 0.01) in G-CSF-treated mice and from 0.88 ± 0.20 on day 0 to 3.24 ± 0.31 on day 5 (P < 0.01) in human. Serum TRACP-5b level showed a biphasic trend during G-CSF treatment. The ratio of osteoblasts number per bone surface (OB.N/B.s) to OC.N/B.s was changed after adding PTH plus RANKL during G-CSF treatment. In conclusion, short term G-CSF treatment leads to reduction of osteoblasts and stimulation of osteoclasts, and interrupting bone remodeling balance may contribute to HSPC mobilization. J. Cell. Physiol. © 2012 Wiley Periodicals, Inc.
    Journal of Cellular Physiology 05/2013; 228(5). DOI:10.1002/jcp.24246 · 3.87 Impact Factor
  • Heart (British Cardiac Society) 10/2011; 97(Suppl 3):A10-A10. DOI:10.1136/heartjnl-2011-300867.29 · 6.02 Impact Factor
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    ABSTRACT: Despite unsurpassed anti-tumor activity of bortezomib for multiple myeloma (MM), drug resistance has emerged as a challenge, especially when MM cells adhere to the stroma. This study aimed to determine whether bone marrow stromal cells (BMSCs) have a role in the development of chemoresistance in MM. Our data demonstrate that the secretion of interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), and cell-to-cell contact with microenvironment-derived stromal cells from patients with multiple myeloma (MM-BMSCs) significantly decreased the sensitivity of myeloma cells to bortezomib treatment. Mechanistically, we found that microRNA (miRNA)- 15a expression was up-regulated in U266 and NCI-H929 cells treated by bortezomib, which was inhibited by MM-BMSCs. miRNA-15a transfected myeloma cells were arrested in G1/S checkpoint and secreted less VEGF compared to control transfected cells, although no significant difference was found in VEGF mRNA levels. In conclusion, our data suggest that via suppressing miRNA-15a expression, BMSCs provide survival support and protect myeloma cells from bortezomib induced apoptosis.
    Leukemia & lymphoma 05/2011; 52(9):1787-94. DOI:10.3109/10428194.2011.576791 · 2.61 Impact Factor
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    ABSTRACT: There are two types of endothelial progenitor cell (EPC) in circulation, early EPC and outgrowth endothelial cell (OEC). Diabetes impairs the function of EPC, but it is not clear whether transplantation of OECs can rescue ischemic myocardium in diabetes. In this study, we compared the function of diabetic and healthy OECs in vitro. Then we administered diabetic and healthy OECs intramyocardially and compared their contribution to vasculogenesis in diabetic rabbits. Outgrowth endothelial cells from diabetic and healthy rabbits were isolated and subjected to in vitro proliferation, tube-forming, angiogenic cytokine assays. Exogenous diabetic and healthy OECs were analyzed for therapeutic efficacy in an acute ischemia model of diabetic rabbits. LV function was assessed using echocardiography. The capillary density and fibrosis area were evaluated. MRNA expression of VEGF and bFGF was analyzed using relative realtime quantitive PCR. Proliferation, tube-forming, secretion of VEGF and bFGF of diabetic OECs were significantly reduced compared with healthy OECs. In diabetic rabbits, healthy OECs transplantation could increase capillary density and improve cardiac function, decrease fibrosis area compared with diabetic OEC and the control group. Real time PCR indicated that mRNA expression of VEGF and bFGF were augmented more in the healthy OEC group than those in the control and diabetic OEC groups. These findings suggest that diabetes impairs the function of OECs. Transplantation of healthy OECs may rescue the ischemic myocardium by neovasculogenesis and paracrine effect in diabetic rabbits. However, autologous transplantation of diabetic OEC could not enhance cardiac function.
    Scandinavian journal of clinical and laboratory investigation 05/2010; 70(5):313-21. DOI:10.3109/00365511003774593 · 2.01 Impact Factor
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    ABSTRACT: Stem cells transplantation holds great promise for the treatment of ischemic diseases through functional revascularization. Umbilical cord-derived mesenchymal stem cells (UC-MSCs) are also an ideal candidate for cell-based bioengineering. Herein, we report on the development of a simple and effective protocol to isolate UC-MSCs, and confirm their endothelial potential both in vitro and in vivo. UC-MSCs were isolated by a novel explantation technique and induced to differentiate into endothelial-like cells. Then UC-MSCs were transplanted into ischemic mouse model and cultured on 3D gel/MMT-CS composite scaffolds. Morphological and proliferation assessments show that sufficient UC-MSCs can be generated during a relatively short culture period with explantation technique. Increased expression of endothelial-specific markers (KDR and vWF), and functional markers (ac-LDL uptake and UEA-1 binding), indicate that functional endothelial progenitor cells are induced after 9 days of in vitro culture. In an ischemic hindlimb mouse model, the ratio of ischemic/nonischemic limb perfusion 4 weeks after MSCs transplantation reached 0.84 +/- 0.09. The capillary density of this group was 2.57-fold greater than that of sham-injected mice (P < 0.05). Immunofluorescence and immunohistological analyses indicate that MSCs may act to salvage the ischemic tissue by incorporating into the local vasculature. In vitro, UC-MSCs were observed to incorporate into 3D gel/MMT-CS composite scaffolds, to secrete extracellular matrix, to remain viable, and to retain their proliferation capacity. In conclusion, UC-MSCs isolated by novel yet simple explantation technique are well suited for application in the development of novel stem cell-based revascularization therapies.
    Stem cells and development 02/2010; 19(10):1511-22. DOI:10.1089/scd.2009.0321 · 4.20 Impact Factor
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    ABSTRACT: Dendritic-like leukemia cells (DLLC) originating from leukemic cells could potentially induce a T cell-mediated anti-leukemia immune response. It has been demonstrated that B7-H1, a newly identified homologue of CD80/CD86, is abundant in human carcinomas and dendritic cells (DC), can exert co-stimulatory and immune regulatory functions. We demonstrated that B7-H1 was significantly expressed on AML cells and was strongly enhanced after differentiation to DLLC. Blockade of B7-H1 expressed on DLLC results in increased T cell proliferation and Th1 cytokine production, and decreased Th2 cytokine production. Importantly, autologous CTLs induced by DLLC treated with B7-H1 mAb showed significantly increased specific cytotoxcity against AML blasts. We further demonstrated that a significant decrease in IL-12 production, increase in IL-10 production by DLLC, and an increased CD4(+)CD25(+)Foxp3(+) T regulatory population lead to the defective T cell immune response that is induced by B7-H1 up-regulation on DLLC. Our data suggest that up-regulated B7-H1 on DLLC acts as a strong inhibitor of anti-leukemia T cell response, and that blockade of B7-H1 can improve DLLC-mediated anti-leukemia immunity.
    Leukemia research 03/2009; 33(7):948-57. DOI:10.1016/j.leukres.2009.01.007 · 2.69 Impact Factor