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  • 2005-2009  (79)
  • Medicine  (79)
  • 11
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    Online Resource
    Platelet-Derived Microparticels Stimulate Proliferation of Colony-Forming Unit Granulocyte-Macrophage of Umbilical Cord Blood Hematopoietic Stem Cells.
    American Society of Hematology ; 2005
    In:  Blood Vol. 106, No. 11 ( 2005-11-16), p. 4191-4191
    Details
    In: Blood, American Society of Hematology, Vol. 106, No. 11 ( 2005-11-16), p. 4191-4191
    Abstract: Umbilical Cord blood has become an important source of hematopoietic stem-progenitor cells for transplantation, however hematopoietic recovery after transplantation with umbilical cord blood is slower than with bone marrow or mobilized peripheral blood. Adhesion molecules on hematopoietic cells are involved in hematopoietic cells’ homing, which is considered the most important step of hematological recovery. Some articles indicated that expressions of adhesion molecules on CD34+ cells could predict the time to hematopoietic recovery after transplantation with bone marrow and peripheral blood of many adhesion molecules (such as CD62, CXCR4) are significantly lower on umbilical cord blood than on bone marrow. It is a possible reason for the difficulty in hematopoietic recovery after umbilical cord blood transplant. Platelet -derived microparticles (PMPs) are submicroscopic ( & lt;1 μm) membrane vesicles released from platelet if they are stimulated with agonists such as thrombin, collagen, or calcium ionophore A23187 or if exposed to high-stress shear forces. PMPs express several platelet-endothelium attachment receptors on their surface, for example, glycoprotein IIb/IIIa (CD41), Ib and IaIIa, and P-selectin (CD62P) and several other platelet relevant receptors such as CXCR4 and PAR-1. Some articles indicate that PMPs can affect the function of hematopoietic stem cells by increasing the adhesion of hematopoietic cells to fibrinogen, which suggests that PMP-transferred CD41 antigen plays an important role in this process. PMPs can also increase the survival of human hematopoietic cells including human CD34+ clonogenic progenitors. In our research, we observe the function of PMP to affect the cloning efficiency of colony-forming unit granulocyte-macrophage (CFU-GM). We adopt different concentrations of Thrombin (2U/ml, 1.5U/ml, 1.0U/ml and 0.5U/ml) to activate the platelet and acquire PMPs. Then PMPs were evaluated by using flow cytometry. Based on the result that stimulation of platelets by Thrombin (1U/ml) can acquire the best efficiency of PMPs, we used this concentration in all subsequent experiments. Umbilical cord mononuclear cells (MNCs) were obtained from healthy donors and isolate the MNCs by Ficoll-Hypaque density gradient centrifugation. Briefly, MNCs incubated with or without PMPs cultured in 2.7% methylcellulose. CFU-GM growth was stimulated with 30% umbilical cord serum, rhIL-3 and rh GM-CSF. Cultures were incubated at 37°C in a fully humidified atmosphere supplemented with 5% CO2. Colonies were counted under an inverted microscope after 7 or 10 days. The research was divided into four groups: 1. control group; 2. PMPs(10μg/ml); 3. PMPs(50μg/ml); 4. PMPs(100μg/ml). The colony formation was enhanced with PMPs and is dependently stimulated with PMPs. The number of colonies in the group of PMPs(100μg/ml) is more than that of other groups. The number of colonies in control group, PMPs(10μg/ml), PMPs(50μg/ml) and PMPs(100μg/ml) are 57.4±3.2, 65.6±5.6, 77.1±1.7 and 87.8±5.0 per 1×105 respectively. These increases in different groups were statistically significant when compared with control group(p & lt;0.05). To sum up, PMPs can affect the cloning efficiency of CFU-GM of umbilical cord hematopoietic stem cells and the efficiencies are depended on the concentration of PMPs.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V106.11.4191.4191
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2005
    detail.hit.zdb_id: 1468538-3
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  • 12
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    Variation of p21, P-Gp Expression in K562/A02 Cell Line with Tetrandrine
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5066-5066
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5066-5066
    Abstract: Object: To study the variation of p21, P-gp expression in reversion of multidrug resistance of K562/A02 leukemic line with different concentration of tetrandrine(TET), to provide new theoretic evidence for the clinical application of TET. Methods: The IC50 (the concentration causing 50% inhibition of cell growth) of DNR was analyzed by MTT method; The Expressions of p21 were assayed by westernblot; The Expressions of P-gp were assayed by FCM; The expressions of mdr1 were assayed by RT-PCR; The variation of p21 was accentuation with the accrescence concentration of TET(P & lt;0.05). Results: The variation of p21 protein in K562/A02 cells was accentuation with the accrescence concentration of TET(p & lt;0.05), Mdr1 mRNA was lowly displayed in K562 cells and highly displayed in K562/A02 cells(p & lt;0.01), the variation of mdr1 was attenuation with the accrescence concentration of TET(p & lt;0.05); P-gp was lowly displayed in K562 cells and highly displayed in K562/A02 cells(p & lt;0.01), the variation of P-gp was attenuation with the accrescence concentration of TET(p & lt;0.05). Conclusion: TET may reverse multidrug resistance of K562/A02 cells by the regulation of p21,P-gp and mdr1.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5066.5066
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 13
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    Research of Apoptosis Induction by the Application of Magnetic Nanoparticle of Fe3O4 Loaded with Daunorubicin and 5-Bromotetrandrine in K562/A02 Leukemic Cells
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5060-5060
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5060-5060
    Abstract: Objective: To observe the apoptosis of K562/A02 cells induced by application of Fe3O4-Magnetic Nanoparticle (Fe3O4-MNPs) loaded with Daunorubicin(DNR) and 5-Bromotetrandrine (BrTet) and to explore its possible molecular mechanism. Methods: We detected the apoptosis of K562/A02 cells after treatment with Fe3O4-MNPs and BrTet with DNR alone or their combination by flow cytometry(FCM),Wright staining and DNA ladder. The expression of Bax and Bcl-2 protein was measured by Western blot. Results: The result showed apoptotic characteristics after treated with this composite for 48 hours. Flow cytometry assay showed the percentage of apoptotic cells which were treated with Fe3O4-MNPs and BrTet with DNR alone or their combination for 48 hours increased from (7.9%±0.35)% to (15.5%±0.87)%, (19.7%±1.04)% and(40.8%±1.74)%, (P & lt;0.05. After treated with this composite, the typical apoptotic morphological features appeared: condensation of cells and nuclear, disintegration of nuclear chromatin, and apoptotic body could be observed under microscope; DNA agarose gel electrophoresis showed ladder bands; the expression level of Bax protein increased (P & lt; 0.01) and Bcl-2 protein decreased markedly (P & lt; 0.01). Conclusion: Our results suggest that Fe3O4-MNPs or BrTet with DNR induces apoptosis in K562/ADM cells, and when used together,they have distinct synergism. The up-regulation of Bax protein and the down-regulation of Bcl-2 protein may play important roles.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5060.5060
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
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  • 14
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    Daunorubicin Loaded Magnetic Nanoparticles of Fe3O4 Greatly Enhance the Responses to Chemotherapy and Induce Apoptosis of Multidrug-Resistant K562 Cells in a Human-Nude Mice Xenograft Leukemia Model
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5038-5038
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5038-5038
    Abstract: Object: To the effect of Fe3O4-magnetic nanoparticle loaded with DNR on multidrugresistant K562 cells in vivo. Methods: K562-n and its MDR counterpart K562-n/VCR cell were inoculated subcutaneously into both sides of the back of nude mice (5×106 cells/each) to establish a human leukemia xenograft model. The mice were randomly divided into group A receiving normal saline every other day for 20days, group B receiving DNR every other day for 20days, group C receiving Fe3O4-magnetic nanoparticle every other day for 20days, group D receiving Fe3O4-magnetic nanoparticle loaded with DNR every other day for 20days, and group E receiving Fe3O4-magnetic nanoparticle containing DNR every other day for 20days with a magnetic field built on the surface of the tumor tissue. The tumor volume was measured on the day 1, 5, 9, 13, 17 and 21d after the first treatment. Tumor tissues were isolated for examination of the expression of mdr-1, bcl-2, bax and caspase-3 by reverse transcription polymerase chain reaction and Western blotting. Results: For K562-n/VCR tumor, the tumor volume was markedly lower in groups D and E than in groups A, B and C (group D or E vs group A, B or C, P & lt; 0.05). The transcription of mdr-1 and Bcl-2 gene was significantly lower in groups D and E than in groups A, B and C (group D or E vs group A, B or C, P & lt; 0.05). So did the protein expression of Bcl-2. However, there were no differences among these groups about the protein expression of P-gp. The protein and mRNA expressions of Bax and Caspase-3 in groups D and E were increased significantly compared with groups A, B and C (group D or E vs group A, B or C, P & lt; 0.05). The tumor volume of K562-n was markedly lower in groups C, D and E than in groups A and B (group C, D or E vs group A or B, P & lt; 0.05). Conclusion: In conclusion, DNR loaded Fe3O4-magnetic nanoparticles can suppress the growth and induce apoptosis further on the MDR K562-n/VCR tumor in vivo compared to DNR alone but not on the K562-n tumor. The external magnetic field failed to improve the antitumor effect.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5038.5038
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
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  • 15
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    Comparison of the Effects on Reversal of Multi-Drug Resistance of 5-Bromotetrandrine and Tetrandrine in K562/A02 Cell Line in Vivo and in Vitro
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5059-5059
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5059-5059
    Abstract: Objective This study was to compare the reversal effect of 5-bromotetrandrine (BrTet) with Tetrandrine (Tet) when combined with ADM on multidrug resistance cell line K562/A02 and to investigate the reversal mechanism of this new derivative. Methods The protein levels of P-glycoprotein (P-gp) were detected by fluorospectrophotometry and Western blot. The mRNA levels of P-gp were determined by RT-PCR. The in vivo effect of Tet was investigated using nude mice grafted with sensitive human leukemia cell line K562 and MDR cell line K562/A02. Results Flow cytometry assay showed that 1.0 μMol/L BrTet significantly increased the apoptosis percentage. BrTet also enhanced the intracellular accumulation of ADM in K562/A02 cells and its potency was greater than that of Tet at the same concentrations. BrTet inhibited the overexpression of P-gp and down regulated MDR1 mRNA expression in K562/A02 cells in a dose-dependent manner. In nude mice bearing K562 xenografts on the left flank and K562/A02 xenografts on the right flank, i.p. injection of 10 mg/kg BrTet significantly enhanced the antitumor activity of ADM against K562/A02 xenografts with inhibitory rates of 26.1%, while ADM alone inhibited the growth of KBv200 xenografts by only 5.8%. Conclusion BrTet showed significant MDR reversal activity in vitro and in vivo. Its activity may be related to the inhibition of P-gp overexpression and the increase in intracellular accumulation of anticancer drugs, which lead to more K562/A02 cells apoptosis.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5059.5059
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
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  • 16
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    Effect of Cyclosporine A and Estrogen-Receptor Inhibitor on the Reversion of Multidrug Resistance of K562/A02 Line.
    American Society of Hematology ; 2006
    In:  Blood Vol. 108, No. 11 ( 2006-11-16), p. 4358-4358
    Details
    In: Blood, American Society of Hematology, Vol. 108, No. 11 ( 2006-11-16), p. 4358-4358
    Abstract: Objective: This paper was to study the reverse effect of cyclosporine A and the estrogen-receptor inhibitor, raloxifene, on multidrug resistance cell line K562/A02 and to investigate the reversal mechanism of this combination, and to provide theoretic evidence for the clinical application of them as resistance modifying agents. Method: The IC50 (the concentration causing 50% inhibition of cell growth) of DNR were assayed by MTT method; mdr-1 mRNA was assayed by semi-quantitative reverse transcriptase polymerase chain reaction (RT-PCR).; intracellular DNR concentrations and the apoptosis and p-glycoprotein (p-gp) expression in K562 and K562/A02 were detected by fluorometry . Results: The IC50 of DNR for K562/A02 and K562 cells were 23.51mg/L and 0.29mg/L respectively. Pretreating K562/A02 cells with CsA(1mg/L) or raloxifene(2.5mg/L) for 48 hours partially restored the sensitivity of K562/A02 cells to DNR (IC50 were5.98mg/L and 8.15mg/L respectively) ,but had no effect on K562 cells;IC50 of combined cyclosporine A and raloxifene was 3.68mg/L The intracellular DNR concentrations( [DNR]i) in K562 cells were higher than that in K562/A02 cells,[DNR] i in K562/A02 cells was 12% of K562. Pretreating K562/A02 cells with cyclosporine A and raloxifene alone or combination for 48 hours induced the enhancement of [DNR]i in K562/A02 cells([DNR] i:CsA alone 33% of K562; raloxifene alone 12.78%of K562;CsA+raloxifene 45.29% of K562 Cyclosporine A and raloxifene alone or combination could decrease the expression of P-gp in K562/A02,the effect for 48 hours as follows: control(K562) 3.58,control(K562/A02) 104.96; CsA alone 78.29; raloxifene alone 85.02;CsA+raloxifene 59.89 K562/A02 showed apoptotic characteristics after treated with cyclosporine A for 48 hours and no apoptotic characteristics after treated with raloxifene for 48 hours Cyclosporine A and raloxifene alone could down regulate the expression of mdr-1 gene mRNA in K562/A02, cyclosporine A and raloxifene combination could markedly down regulate the expression of mdr-1 gene mRNA in K562/A02, the effect for 48 hours as follows(mdr1/β-action):control 1.313;CsA alone 1.232;raloxifene alone 1.052;CsA+raloxifene 0.449. Data was analyzed by SPSS 11.0 software and expressed as mean ± SD. Conclusions: Activation of P-gp may be involved in the mechanism of MDR of K562/A02 cell line; Multidrug resistance (MDR) can be partially reversed by CsA or raloxifene, of which the combination shows a great synergistic reversal effect.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V108.11.4358.4358
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2006
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  • 17
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    Mechanism Research of Reversal of Multidrug Resistance by the Application of 5-Bromotetrandrine and Magnetic Nanoparticle of Fe3O4 Combined with Daunorubicin in a Human-Nude Mice Xenograft Model
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5058-5058
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5058-5058
    Abstract: Objective: To establish the xenograft leukemia model with stable multiple drug resistance in nude mice; to investigate the reversal effect of 5-Bromotetrandrine and Magnetic nanoparticle of Fe3O4 combined with DNR in vivo and to search for the possible reversal mechanisms. Methods: K562 and K562/A02 cells were respectively inoculated subcutaneously into back of athymic nude mice (1×107 cells/each) to establish the xenograft models. The tumor formation was evaluated by animal ultrasonic inspection. Tumors-bearing nude mice were assigned randomly to five groups which were treated with NS (A group); DNR 1mg/kg (B group); nanoparticle of Fe3O4 combined with DNR 0.63mg/kg(C group): 5-BrTet 2.5mg/kg combined with DNR(D group); 5-Bromotetrandrine 2.5mg/kg and Magnetic nanoparticle of Fe3O4 combined with DNR 0.63mg/kg(E group) respectively. The incidence of tumor formation, growth characteristics, weight and volume of tumor were observed. The histopathologic examination of tumors and organs were detected. For resistant tumors, the protein levels of P-glycoprotein (P-gp) were detected by Western blot. Results: The tumor incidence was 100% in the nude mice inoculated with either K562 or K562/A02 cells. In 6 to 9 days,the tumors reached a volume of more than 1 00 mm3. In vivo, MTT assay showed K562/A02 tumor maintained the drug resistance. For K562 cells xenograft tumors, there were no apparent differences in tumor suppression effect between the B AC AD AE group. For K562/A02 cells xenograft tumors, 5-BrTet and Magnetic nanoparticle of Fe3O4 combined with DNR significantly suppressed growth of tumor: the inhibition rate was 62.76% while DNR alone be used, the inhibition rate was 3.68%. Pathologic examination of resistant tumors showed the tumors necrosis obviously in E group. Application of 5-BrTet and Magnetic nanoparticle of Fe3O4 inhibited the overexpression of P-gp. Conclusion: The xenograft leukemia nude mice model was maintain the multiple drug resistance. 5-Bromotetrandrine and Magnetic nanoparticle of Fe3O4 combined with DNR had a significant tumor-suppressing effect on MDR leukemia cells xenograft model.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5058.5058
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
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  • 18
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    Reversal of P-Glycoprotein-Dependent Resistance to Adriamycin by 5-bromotetrandrine in K562/A02 Cell Line.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 4175-4175
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 4175-4175
    Abstract: Objective: The present study aimed to evaluate the MDR reversal activity of bromotetrandrine (BrTet), a bromized derivative of tetrandrine (Tet), in vitro. Methods: Drug sensitivity was determined using the MTT assay. Adriamycin (ADM) accumulation, the protein levels of P-glycoprotein (P-gp) and the apoptotic changes were analyzed by fluorospectrophotometry, respectively. The mRNA levels of P-gp was determined by RT-PCR. Results: BrTet at 0.25, 0.5 and reversed ADM resistance in MDR K562/A02 cells dose-dependently and its potency was greater than that of Tet at the same concentrations. The IC50 of ADM for K562 and K562/A02 cells were 55.122 mg/l and 1.1373 mg/l, respectively. Treating K562/A02 cells with BrTet(1uM)and TTD(1uM)both for 48 hours partially restored the sensitivity of K562/A02 cells to ADM (IC50 were 4.7729 mg/l and 13.584 mg/l respectively) but had not effect on K562 cells. The fold reversal (FR) were 11.55 and 4.06 respectively. K562/A02 cells showed apoptotic characteristics after treated with Brtet and Tet both for 48 hours compared with control group(apoptosis rate was 61.1%, 11.1% and 9.9%,respectively); Fluorospectrophotometric assay showed that BrTet significantly increased the intracellular accumulation of ADM in K562/A02 cells in a dose-dependent manner. The fluorescence intensity of intracellelar ADM in K562/A02 cells treated with ADM(1mg/L)was 33% of that in K562 cells. BrTet and Tet elevated the intracellular ADM concentration in K562/A02 cells up to 52% and 69%,respectively. BrTet also inhibited the overexpression of P-gp in K562/A02 cells. The fluorescence intensity of P-gp in K562 and K562/A02 cells was 0.5 and 97.97.The P-gp expression was down after treated with BrTet and TTD (65.05 and 54.86). The mdr1 mRNA was also down regulated. Conclusions: BrTet showed significant MDR reversal activity in vitro. Its activity may be related to the inhibition of P-gp overexpression and the increase in intracellular accumulation of anticancer drugs. BrTet may be a promising MDR modulator for eventual assessment in the clinic.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.4175.4175
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
    detail.hit.zdb_id: 1468538-3
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  • 19
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    The Effect of Phenylhexyl Isothiocyanate on Drug Resistance of K562/A02 Cell Line
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 5061-5061
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 5061-5061
    Abstract: Objective: To investigate the effect of 6-phenylhexyl isothiocyanate (PHI) on drug resistance and sensitivity on K562/A02 cell line to ADM and elucidate the probable mechanisms. Methods: We measured growth inhibition of ADM on K562/A02 cell line by MTT assay. Apoptosis rate of K562/A02 cell line, the change of intracellular ADM and MRP1 protein level were detected by Flow Cytometry. Intracellular deoxidized GSH by spectrometric enzyme assay and MRP1 mRNA by RT-PCR semiquantitative assay were observed anteroposterior using PHI. Results: PHI can enhance the sensitivity of K562/A02 cell line to ADM, survival rate of K562/A02 cell line decreased with the increasing concentration of PHI and ADM. Apoptosis rate increased with treating by combination of two above drugs, and multiple of drug resistance had statistical significance (P & lt;0.05) when the concentration of PHI was more than 20μmol/l. Intracellular GSH of K562/A02 cell line reduced 5% when 1μg/ml ADM was single used, and when more than 10μmol/l PHI was used it increased slightly at first then decreased. When more than 20μmol/l PHI and 1μg/ml ADM were used combination, intracellular GSH of K562/A02 cell line decreased progressively with increasing the concentration of PHI. Protein and gene level of MRP1 have no statistical significance (P & gt;0.05) no matter after or before PHI was used on different concentration. Conlusion: The depletion effect of PHI on the intracellular GSH can not only partly enhance the reverse effect of ADM, but also enhance the sensitivity of K562/A02 cell line to ADM. Such depletion may diminish side effect and treatment dosage of ADM. It provides a new view to the therapy of leukaemia.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.5061.5061
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
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  • 20
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    Platelet-Derived Microparticles Induce Angiogenesis In Vitro and In Vivo.
    American Society of Hematology ; 2007
    In:  Blood Vol. 110, No. 11 ( 2007-11-16), p. 3901-3901
    Details
    In: Blood, American Society of Hematology, Vol. 110, No. 11 ( 2007-11-16), p. 3901-3901
    Abstract: Objective: An attempt was made to investigate the effect of platelet-derived microparticles (PMPs) on the angiogenesis. Methods: Thrombin was adopted to activate the platelets to release PMPs. Flow cytometry(FCM)was adopted to evaluate the efficiencies of different concentrations of thrombin to produce PMPs and BCA was adopted to evaluate the content of PMPs. By the carrier of human umbilical vein cell line ECV-304 cultivated in vitro, investigate the effect of PMPs on the proliferation and apoptosis of human umbilical vein endothelial cells using MTT and FCM. PMPs were put into CAM and observe the effects of PMPs on angiogenesis in Chick embryo chorioallantoic membrane (CAM). Results: The efficiencies of PMPs activated by 1.0U/ml thrombin were 50.1%; PMPs induced proliferation of human umbilical vein cell line ECV-304 in a dose dependent manner. At the concentration of 40ug/ml PMPs, the proliferation rate of human umbilical vein cell line ECV-304 was as 1.8±0.3 times as control and there was no difference with the group of vascular endothelial growth factor (VEGF),which the proliferation rate was 1.9±0.5 times vs. control, p & gt; 0.05;PMPs inhibited human umbilical vein cell line ECV-304 apoptosis. Compared with control group (apoptosis rate 9.4%±0.5%), apoptosis rate of PMPs (40μg/ml) is 3.9%±0.4%, which was significantly reduced, p & lt;0.05. The addition of VEGF (10μl/ml) did not successfully prevented apoptosis of human umbilical vein cell line ECV-304 (apoptosis rate 8.0%±0.8%);After 72 h of incubation, showing an implant of PMPs by allantoic vessels developing radially towards it (implant) in a ’spoked-wheel’ pattern, at the concentration of 80μg/ml PMPs, number of vessel ramification is 112.5±11.31 and vessel area/CAM area is (6.19±1.29)%, compared with the VEGF(p & gt;0.05). But there are not localized allantoic vessels developing in the NS control group(P & lt;0.05). Conclusion: 1.0U/ml thrombin activated platelet could get the best efficiency of PMPs, which could stimulate proliferation of human umbilical vein cell line ECV-304 and inhibit its apoptosis and PMPs have certain promotive effect on the formation of capillary in chick chorioallantoic membranes.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V110.11.3901.3901
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2007
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