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Zhao B.,Second Hospital | Wang Q.,Second Hospital | Tao T.,Second Hospital | Lin Q.,Harbin Medical University | Lin Q.,Immunity and Infection Key Laboratory of Heilongjiang Province
International Journal of Molecular Medicine | Year: 2013

This study aimed to compare the treatment effects of lentiviral vector-mediated hBMP2 which was overexpressed in the femoral bone marrow stromal cells of osteoporotic rats through genetic infection in vitro and in vivo. Comparison of the two transgenic effects may be crucial to determining the lentivirus infection method to be used. Following a comparison of the rat bone marrow stromal cells (rBMSCs) in osteoporotic (MSCs OVX) and normal (MSCs CON) groups, the lentiviral vector-mediated human bone morphogenetic protein 2 (hBMP2), which overexpressed the BMSCs of osteoporotic rats in vitro (rBMSCs in OE group), was constructed. The osteogenic ability in the overexpressed (OE) group was then compared to that of the MSCs CON. The rBMSCs in the OE group (transplants of genetic infection in vitro) and the lentivirus-containing solution (injected material of genetic infection in vivo) were injected into the femurs. The treatment effect of each group was compared via bone mineral density (BMD) and bone histomorphometry. The hBMP2-modified osteoporosis rBMSCs formed by genetic infection in vitro (n=7) had an ameliorated treatment effect on the femur as compared to that of the in vivo (n=7) (BMD: 0.315 vs. 0.19 g/cm2, P<0.01; bone histomorphometry: For bone trabeculars (Tb.Ar/T.Ar): 0.301 vs. 0.114, P<0.01; for trabecular thickness (Tb.Th): 43.54 vs. 21.39 μm, P<0.01; for trabecular separation (Tb.Sp): 115.7 vs. 304.87 μm, P<0.01). The results showed that the treatment effects of osteoporotic rBMSCs on local osteoporosis performed by genetic infection were improved in vitro as compared to those in vivo. Source

Dong Y.,Harbin Medical University | Dong Y.,Immunity and Infection Key Laboratory of Heilongjiang Province | Han Q.,Harbin Medical University | Han Q.,Immunity and Infection Key Laboratory of Heilongjiang Province | And 14 more authors.
Molecular and Cellular Biochemistry | Year: 2012

Glioblastoma multiforme (GBM) was shown to harbor therapy-resistant cancer stem cells that were major causes of recurrence. PDGFR (platelet-derived growth factor receptor) and c-Kit (stem cell factor receptor) signaling play important roles in initiation and maintenance of malignant glioma. This study demonstrated that long-term culture with imatinib mesylate, the tyrosine kinase inhibitor against PDGFR and c-Kit resulted in reduced cancer stem cell ability in glioblastoma cells through cell differentiation. Derived from RG glioblastoma cells co-cultured with imatinib for 3 months, RG-IM cells showed distinct properties of cell cycle distribution and morphology in addition to significantly decreased ability to form aggregates and colonies in vitro and tumorigenicity in vivo. Increased expression of GFAP (astrocyte marker) and class III β-tubulin isotype (Tuj1, neuron marker) were detected with morphology like neurons or astrocytes in RG-IM cells. Furthermore, decreased expression of stem cell markers, i.e., CD133, Oct-3/4, nestin, and Bmi1, and increased terminal neural cell markers, GFAP, Tuj1, etc., were identified in RG-IM at the mRNA level. All these markers were changed in RG cells when PDGFRB and c-Kit expression were double knocked down by siRNA. Cell differentiation agent, all-trans retinoic acid (ATRA) caused similar effect as that with imatinib in RG cells, while adding PDGF-B and SCF in RG-IM resulted in cell dedifferentiation to some extent. Moreover, differentiation in RG cells treated by imatinib or ATRA was mainly driven by MAPK signaling pathways. In summary, continuous inhibition on PDGFR and c-Kit signaling disturbed glioma stem cells biology in subsets of GBM cells and may have potentials in clinical applications. © 2012 Springer Science+Business Media, LLC. Source

Sui M.,Harbin Medical University | Lin Q.,Harbin Medical University | Lin Q.,Immunity and Infection Key Laboratory of Heilongjiang Province | Xu Z.,Harbin Medical University | And 9 more authors.
Journal of Clinical Immunology | Year: 2013

Objective: The purpose of this study is to examine autoantibody profile of systemic lupus erythematosus (SLE) patients with lupus nephritis (LN) and to establish the correlation between the antibody reactivity and disease activity of LN. Methods: Autoantibodies and serological parameters were measured and analyzed in 589 SLE patients. The associations of the co-positivity of anti-dsDNA, -nucleosome and - histone antibodies (3-pos) with clinical, serological and outcome parameters were analyzed. Results: At the study entry, the prevalence for anti-dsDNA (61.52 % vs. 34.11 %, P<0.0001), anti-nucleosome (56.09 % vs. 37.21 %, P=0.0002) and anti-histone (49.35 % vs. 33.33 %, P=0.0013) antibodies in patients with LN were significantly higher than that in patients without LN. Patients with 3-pos had a higher proportion of proliferative renal lesions (class III+IV). The incidence of a poor renal outcome (7.14 % vs. 2.52 %, P=0.0174) in LN patients with 3-pos was significantly higher than those without 3-pos. Moreover, the rate of remission (73.63 % vs. 82.37 %, P=0.0245) was significantly reduced and recurrence increased (58.90 % vs. 23.44 %, P<0.0001) in 3-pos patients as compared to that in non 3-pos within the LN group. Conclusion Our data indicate a strong association between the 3-pos and renal disease activities, especially proliferative glomerulonephritis. The ability of 3-pos to predict renal flares may lead to major additional benefits in the followup of these patients. Source

Yang J.,Harbin Medical University | Yang J.,Immunity and Infection Key Laboratory of Heilongjiang Province | Xu Z.,Harbin Medical University | Sui M.,Harbin Medical University | And 16 more authors.
PLoS ONE | Year: 2015

Objective To characterize the significance of correlated autoantibodies in systemic lupus erythematosus (SLE) and its complication lupus nephritis (LN) in a large cohort of patients. Methods Clinical data were statistically analyzed in 1699 SLE patients with or without nephritis who were diagnosed and treated during 2002-2013 in the northeast region of China. Reactivity to a list of 16 autoantibodies was detected by the serum test Euroline ANA profile (IgG). Serum titers of the anti-nucleosome autoantibodies were measured by ELISA assays. Kidney biopsies were examined by pathologists. Immune complex deposition was identified by immunohistochemistry stain. Results Simultaneous positivity of anti-dsDNA,-nucleosome and-histone antibodies (3-pos) was prevalent in SLE patients with LN compared to Non-renal SLE patients (41% vs 11%, p< 0.001). Significant correlations were found between any two of the above three anti-nucleosome antibodies in LN patients. In comparison to non-3-pos cohorts, 3-pos patients with LN had significantly higher serum levels of the three antibodies and more active disease; was associated with type IV disease; suffered from more severe renal damages; received more intensive treatment and had worse disease outcome. The serum levels of these three autoantibodies in 3-pos LN patients were significantly decreased when they underwent clinical recovery. Conclusions Simultaneous reactivity to anti-dsDNA,-nucleosome and-histone antibodies by Euroline ANA profile (IgG) may indicate severe nephropathy in patients with SLE. Copyright: © 2015 Yang et al.This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Source

Shi M.,Harbin Medical University | Shi M.,Immunity and Infection Key Laboratory of Heilongjiang Province | Huang R.,Harbin Medical University | Pei C.,Harbin Medical University | And 6 more authors.
Oncology Letters | Year: 2012

TP53 codon 72 polymorphism has been reported to affect regulatory networks central to glioma development. Although a number of published studies noted the association between TP53 codon 72 polymorphism and glioma risk, their conclusions were inconsistent. A meta-analysis was used to assess the possible association between TP53 codon 72 polymorphism and glioma risk. The PubMed databases were searched, relevant articles were identified and data were retrieved based on the inclusion criteria. The odds ratio (OR) and 95% confidence interval (95% CI) were determined on the pooled dataset. We retrieved eight different studies including 2,260 glioma cases and 3,506 controls. However, no association was found between the TP53 codon 72 polymorphism and glioma risk regarding the comparison between glioma cases and the controls. By further stratification based on criteria such as tumor grade, and the geographical location of the patients and the relevant controls, we found a significant association in the subgroup of patients with high-grade glioma in Europeans compared to controls in two models of TP53 codon 72 polymorphism, which include the dominant model [C/C + G/C vs. G/G: OR=1.35, 95% CI (1.14, 1.59), P=0.0005, P h=0.13] and the additive model [C allele vs. G allele: OR=1.16, 95% CI (1.02, 1.33), P=0.03, P h=0.37]. Our analysis suggests that TP53 codon 72 polymorphism is associated with an increased risk of high-grade glioma development in Europeans. Source

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