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1.
Chinese Medical Journal ; (24): 839-843, 2009.
Article in English | WPRIM | ID: wpr-279824

ABSTRACT

<p><b>BACKGROUND</b>Bone morphogenetic protein (BMP) is a member of the superfamily of transforming growth factor-beta. Recent studies show that it is an indispensable factor in hematopoiesis. To better characterize the effect of recombinant human BMP (rhBMP)-2 in hematopoiesis, we set out to determine whether rhBMP-2 could promote the proliferation of mesenchymal stem cells (MSCs) and increase the levels of hematopoietic cytokines in MSCs.</p><p><b>METHODS</b>2, 3-bis (2-methoxy-4-nitro-5-sulfophenyl)-5-((phenylamino) carbonyl)-2H-tetrazolium hydroxide (XTT), real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) were used to detect the effects of rhBMP-2 on the proliferation and hematopoietic cytokine levels of MSCs. In addition, MSCs marked with Hoechst33342 were transplanted into BALB/c mice by the intravenous route or intra-bone marrow transplantation, and cluster numbers were counted.</p><p><b>RESULTS</b>The XTT test revealed that rhBMP-2 significantly induced proliferation of MSCs in doses ranging from 10 ng/ml to 0.1 mg/ml in a dose-dependent manner. The experiments in vivo showed that there were more clusters of donor cells in bone marrow, spleen, liver and lung of the BMP group than those in the control group after both intra-bone marrow transplantation (P < 0.001, P < 0.001, P < 0.001, and P = 0.001, respectively) and intravenous transplantation (P < 0.001, P < 0.001, and P < 0.001 respectively). The results of real-time PCR and ELISA revealed that rhBMP-2 significantly increased mRNA expressions and protein levels of IL-6, IL-7, IL-11, G-CSF, M-CSF and SCF.</p><p><b>CONCLUSIONS</b>The treatment with rhBMP-2 promotes the proliferation of MSCs in vivo and in vitro and increases the levels of hematopoietic cytokines in MSCs, which may contribute to the improvement of hematopoietic function.</p>


Subject(s)
Animals , Humans , Mice , Bone Morphogenetic Protein 2 , Bone Morphogenetic Proteins , Pharmacology , Cell Proliferation , Cells, Cultured , Dose-Response Relationship, Drug , Enzyme-Linked Immunosorbent Assay , Granulocyte Colony-Stimulating Factor , Genetics , Interleukin-11 , Genetics , Interleukin-6 , Genetics , Interleukin-7 , Genetics , Macrophage Colony-Stimulating Factor , Genetics , Mesenchymal Stem Cells , Cell Biology , Metabolism , Mice, Inbred BALB C , Polymerase Chain Reaction , Recombinant Proteins , Pharmacology , Stem Cell Factor , Genetics , Transforming Growth Factor beta , Pharmacology
2.
Chinese Journal of Surgery ; (12): 885-888, 2005.
Article in Chinese | WPRIM | ID: wpr-306190

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the expression level of inhibitor of apoptosis protein survivin gene in human brain glioma and its role in malignant proliferation and antiapoptosis of brain glioma.</p><p><b>METHODS</b>Eighty-three cases of brain glioma specimen was chosen, protein expression of survivin and proliferating cell nuclear antigen (PCNA) was investigated by immunohistochemistry streptavidin-biotin complex (SABC) method, the immunoreactivity score (IRS) of survivin and the proliferative index (PI) were counted. Apoptotic cells were screened by TdT-mediated dUTP-biotin nick-end labeling (TUNEL) method, and the apoptotic index (AI) of brain glioma was calculated.</p><p><b>RESULTS</b>The survivin IRS, PI and AI of brain glioma were 3.8 +/- 3.9, (28.4 +/- 19.5)% and (1.0 +/- 0.8)% respectively, and all of them were elevated with the increase of pathological grade of brain glioma (P < 0.01 for all). PI in survivin positive group was significantly higher than that in survivin negative group (P < 0.01), and PI was positively correlated with survivin IRS (r = 0.740, P < 0.01). There was no significant difference between AI in survivin positive group and that in survivin negative group (P > 0.05), however, AI was negatively correlated with survivin IRS (r = -0.307, P < 0.01).</p><p><b>CONCLUSIONS</b>Survivin is overexpressed in brain glioma, and which may play important roles in malignant proliferation and antiapoptosis of brain glioma.</p>


Subject(s)
Adolescent , Adult , Aged , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Apoptosis , Brain Neoplasms , Genetics , Metabolism , Pathology , Cell Proliferation , Glioma , Genetics , Metabolism , Pathology , Immunohistochemistry , In Situ Nick-End Labeling , Inhibitor of Apoptosis Proteins , Microtubule-Associated Proteins , Genetics , Neoplasm Proteins , Genetics , Proliferating Cell Nuclear Antigen
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