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PubMed2003

[Role of platelet membrane glycoprotein II b/III a receptor activation in no-reflow after myocardial reperfusion].

OBJECTIVE: To observe the changes in the activity of platelet glycoprotein (GP) IIb/IIIa receptor following the occurrence of no-reflow after myocardial reperfusion, to explore the measures for clinical management of this condition. METHODS: Nine canine models of no-reflow following myocardial ischemia verified by reperfusion myocardial contrast echocardiography were used in this investigation. The peripheral venous blood (PVB) and sinus venous blood (SVB) were sampled before myocardial reperfusion (after a 3-hour myocardial ischemia) and after a 3-hour reperfusion for determinating GP IIb/IIIa receptor activities by means of enzyme-linked immunosorbent assay (ELISA). RESULTS: The activity of platelet GP IIb/IIIa of PVB, either in 3-hour ischemic group or in 3-hour reperfusion group, was elevated significantly (P < 0.001), suggesting platelet activation. Elevated platelet GP IIb/IIIa receptor activity in SVB occurred only in 3-hour ischemic group, and the 3-hour reperfusion group (P < 0.001) and the no-reflow group had significantly decreased activities, which was more obvious in the latter group (P < 0.01). The findings signified the consumption of the platelet GP IIb/IIIa receptors in the myocardial microcirculation and the presence of platelet aggregation. CONCLUSIONS: Myocardial ischemia may activate the platelets to express GP IIb/IIIa receptors through stress response mechanism and damage the endothelia of the microvasculature to incur adhesion and aggregation of the platelets within the microcirculation, which may be one of the pathogeneses for myocardial no-reflow phenomenon.

Animals↗
PubMed2003

[Effect of insulin on the expression of platelet membrane glycoprotein II b/III a and its mechanisms].

OBJECTIVE: To investigate the effects of insulin on the expression of platelet membrane glycoprotein (GP) IIb/III a and its mechanism in normal subjects. METHODS: Flow cytometry was used to detect the expression of the whole-blood platelet membrane GP b/ a. The respective effects of insulin, L-nitro-arginine methyl ester (L-NAME) and methylene blue (MB) and their combination on the expression of GP b/ a were also studied. RESULTS: Insulin had no effect on the expression of GP II b/III a in healthy subjects, but significantly inhibited the up-regulated expression of GP II b/III a induced respectively by thrombin and collagen. The inhibitory effects of insulin on thrombin- or collagen-induced expression of platelet membrane GP II b/III a were dose- and time-dependent, and could be completely blocked by L-NAME or methylene blue. CONCLUSION: Insulin may inhibit the over-expression of platelet membrane GP IIb/III a by NOS-->NO-->GC-->GMP pathway.

Adolescent↗
PubMed1992

[Frequency of platelet specific alloantigens HPA-1a (P1A1) and HPA-4a (Pen(a)) expression in Chilean population].

The phenotype frequency of platelet-specific alloantigens has been reported to vary with the ethnic composition of the population under study and the only two HPA-4a negative individuals found in the United States were of Hispanic origin; therefore, the aim of this work was to define the frequency of expression of these systems in the Chilean population. Using an ELISA with captured antigen by monoclonal antibodies, 604 blood donors were typed for the platelet-specific antigen systems HPA-1 and HPA-4. Eight samples typed negative for HPA-1a (1.32%) and 596 typed positive (98.68%). The calculated gene frequencies were 0.88 for HPA-1a (gene frequency > 0.99). Since these antigens are involved in thrombocytopenic disorders such as neonatal alloimmune thrombocytopenia and post-transfusion purpura, their frequency in a population is of clinical relevance. The gene frequency found for HPA-1a is higher than in Europeans (0.85) and lower than in Mapuche Indians (0.99), which is to be expected from the ethnic origin of our population. The absence of HPA-4a negatives in this study does not support our original hypothesis of a higher polymorphism of this system among hispanics.

Antigens, Human Platelet↗
PubMed2003

Beta(3) integrin expression increases breast carcinoma cell responsiveness to the malignancy-enhancing effects of osteopontin.

Osteopontin (OPN) is a secreted phosphoprotein that has been associated with malignancy of breast and other cancers. OPN binds to several cell surface integrins including alpha(v)beta(3), alpha(v)beta(5), and alpha(v)beta(1). Although the relative contribution of these integrins to breast cancer cell malignancy is uncertain, correlative studies suggest that alpha(v)beta(3) may be particularly associated with increased tumor aggressiveness. Previously, we reported that tumorigenic, nonmetastatic 21NT mammary carcinoma cells respond to OPN through alpha(v)beta(5) and alpha(v)beta(1) but not alpha(v)beta(3). Here, we determined that 21NT cells lack beta(3) expression, and we asked whether expression of alpha(v)beta(3) could enhance the ability of breast cancer cells to respond to the malignancy-promoting effects of OPN both in vitro and in vivo. 21NT cells stably transfected with beta(3) showed significantly increased adhesion, migration, and invasion to OPN in vitro compared with vector control. To determine if beta(3) could also enhance the response of breast epithelial cells to OPN in vivo, cells stably transfected with both beta(3) and OPN (NT/Obeta(3)) were injected into the mammary fat pad of female nude mice and primary tumor growth was assessed relative to controls. Mice injected with NT/Obeta(3) cells demonstrated a significantly increased primary tumor take (75% of mice) compared with controls (0-12.5% of mice) as well as a decreased tumor doubling time and a decreased tumor latency period. These results suggest that increased expression of the alpha(v)beta(3) integrin during breast cancer progression can make tumor cells more responsive to malignancy-promoting ligands such as OPN and result in increased tumor cell aggressiveness.

Animals↗
PubMed1996

Acute megakaryoblastic leukaemia with mediastinal tumor.

Acute megakaryoblastic leukemia (AMKL) is a rare myeloproliferative syndrome with a fulminant clinical course characterized by progressive pancytopenia, pallor, weakness and severe hemorrhage. We present a 18-year old male with pancytopenia and massive hemorrhage, lymphadenopathy, organomegaly, and with unusual presentation of retrocardial mediastinal tumor on the right side. The diagnosis of AMKL was established by combining cytological and immunocytochemical analyses of peripheral blood cells (blasts were GPIIIa and GPIb positive); by immunohistochemical analysis of lymph node (dysplastic megakaryocytes were GPIIIa and F VIII positive); in vitro culture studies confirmed enormous growth of CFU-Mk with high proliferative capacity. In spite of therapy, the patient died 3 months after the first signs of the disease.

Adolescent↗
PubMedDate not supplied

Radiation induced-tubulogenesis in endothelial cells is antagonized by the antiangiogenic properties of green tea polyphenol (-) epigallocatechin-3-gallate.

Radiation therapy is a widely-used option for the treatment of a variety of solid tumors. Although effective, ionizing radiation (IR) may give rise to various side effects, including secondary tumors. In agreement with this, recent reports have demonstrated increased invasive potential in different tumor-derived cell lines following radiation treatment. Many of the molecular effects of IR specifically on the endothelial cells involved in tumor neo-vascularization remain unknown. In this study, we found that low sublethal single doses of IR applied to human umbilical vein endothelial cells stimulated cell migration and in vitro tubulogenesis. This correlated with an increase in membrane type-1 matrix metalloproteinase (MT1-MMP) protein expression, a crucial enzyme that promotes endothelial cell migration and tube formation, and of caveolin-1, a protein that regulates tube formation. Cell adhesion was also promoted by IR, reflected in increased gene expression levels of cell surface beta(3) integrin. Pretreatment of the cells with epigallocatechin-3-gallate (EGCg), a green tea catechin that possesses anti-angiogenic properties, prevented most of the IR-induced cellular and molecular events. These observations suggest that current protocols involving radiation therapy for the treatment of cancer can paradoxically promote angiogenesis, but can be improved by combination with anti-angiogenic molecules such as EGCg to target those tumor-derived endothelial cells that escaped IR-induced apoptosis.

Angiogenesis Inhibitors↗
PubMed2003

[The relationship between the peripheral blood of CD61, CD63, PAC-1 and the transplant kidney function].

OBJECTIVES: To explore the relationships between the peripheral blood levels of CD61, CD63, PAC-1 and the incidence of acute rejection and tubular necrosis after renal transplantation, and recovery of the graft function. METHODS: The peripheral blood levels of CD61, CD63, and PAC-1 of 86 patients with uremia in different stages before and after transplantations were analyzed by flow cytometry. The patients were divided into three groups: (1) twenty-nine patients with normal grafts function, (2) hirty with acute rejection and (3) twenty-seven with acute tubular necrosis. The patients with acute rejection were randomly divided into treatment group with anticoagulants and cntrol group. RESULTS: The peripheral blood levels of CD61, CD63 and PAC-1 significantly increased (P < 0.05) in the patients with acute rejection, in comparison with those with normal grafts function and those with acute tubular necrosis. The peripheral blood levels of CD61, CD63 and PAC-1 in patients with acute rejection in anticoagulants therapy was lower, recovery time of the grafts function was shorter, one-year survival rates of patients and grafts were higher, as compared with those of controls. CONCLUSIONS: The patients with acute rejection have significantly high peripheral blood levels of CD61, CD63 and PAC-1 before transplantation, however, these values in patients with acute tubular necrosis are not high, this suggesting that acute rejection might relate to platelet activation, while acute tubular necrosis might not relate to it. After anticoagulants therapy in patients with acute rejection, the grafts function might recover faster and their one-year survival rates and grafts might be higher in those with CD61, CD63 and PAC-1 decreasing remarkably.

Adult↗
PubMed2003

[Study of platelet membrane glycoprotein expression in mice with decompression sickness].

OBJECTIVE: To investigate the role of expression of platelet membrane glycoprotein CD31, CD61 and CD62p in the pathogenesis of decompression sickness. METHODS: Mice were randomly divided into decompression sickness group and normal control group. The animals in decompression sickness group were exposed to 600 kPa compressed air for 60 minute, then they were rapidly decompressed to normal pressure in one minute. At 60th minute after reducing to normal pressure, the expression of CD31, CD61 and CD62p on platelet membrane in mice was measured by flow cytometry. RESULTS: The mean fluorescence intensity of CD31, CD61 and positive percentage of CD62p on platelet membrane [(18.64 +/- 1.01), (271.06 +/- 24.25), (4.48% +/- 0.43%) respectively] in decompression sickness group were significantly increased compared with normal control group [(16.89 +/- 1.69), (234.09 +/- 15.96), (3.00% +/- 0.66%) respectively] (P < 0.05, P < 0.01). CONCLUSION: Inadequately rapid decompression may induce up regulation of platelet membrane glycoprotein CD31, CD61 and CD62p expression in mice, which may lead to thrombosis.

Animals↗
PubMed2004

Effects of chebulinic acid on differentiation of human leukemia K562 cells.

AIM: To study effects of chebulinic acid on erythroid and megakaryocytic differentiation in K562 cells. METHODS: The benzidine staining method was used to evaluate hemoglobin synthesis; the expression of erythroid specific glycophorin A (GPA) protein and megakaryocytic surface marker CD61 was determined by flow cytometry using fluorescence labeled antibodies; erythroid and megakaryocytic mRNA expression was analyzed by RT-PCR. RESULTS: During erythroid differentiation induced by butyric acid (BA) or hemin, chebulinic acid not only inhibited the hemoglobin synthesis of BA- and hemin-treated K562 cells in concentration-dependent manner with IC50 of 4 micromol/L and 40 micromol/L respectively, but also inhibited another erythroid differentiation marker acetylcholinesterase at the concentration of 50 micromol/L in the cells either treated or untreated with each erythroid differentiation inducers, whereas chebulinic acid 50 micromol/L did not change GPA protein expression in these cells significantly. When K562 cells were treated with TPA 50 microg/L for 72 h to induce megakaryocytic differentiation, the presence of chebulinic acid 50 micromol/L slightly provoked the decrease of GPA protein expression induced by TPA. Chebulinic acid did not change the TPA-induced CD61 expression at the same concentration. Chebulinic acid also reduced the mRNA levels of erythroid relative genes including gamma-globin, PBGD, NF-E2, and GATA-1 genes in K562 cells either treated or untreated with BA, whereas chebulinic acid upregulated the mRNA levels of GATA-2 transcription factor in these cells. CONCLUSION: Chebulinic acid had inhibitory effect on erythroid differentiation likely through changing transcriptional activation of differentiation relative genes, which suggests that chebulinic acid or other tannins might influence the efficiency of some anti-tumor drugs-induced differentiation or the hematopoiesis processes.

Acetylcholinesterase↗
PubMed1992

Antenatal treatment of fetal alloimmune thrombocytopenia.

OBJECTIVE: To review our experience with, and to evaluate the efficacy of, antenatal pharmacologic treatment of pregnancies complicated by alloimmune thrombocytopenia. METHODS: We reviewed the records of six pregnancies complicated by alloimmune thrombocytopenia recently cared for at the University of Iowa Fetal Diagnosis and Treatment Unit. All patients had a history consistent with alloimmune thrombocytopenia in a previous gestation. All fetuses had thrombocytopenia on funipuncture at 20-32 weeks' gestation, and all patients and fetuses demonstrated a platelet antigen incompatibility. Three women initially received weekly gamma globulin infusions, two received gamma globulin and dexamethasone, and one had no initial treatment but was given gamma globulin and dexamethasone at 32 weeks' gestation. Repeat funipuncture was performed at 3.5- to 7-week intervals, and therapeutic modifications were made as necessary. RESULTS: In five cases, the last funipuncture before delivery documented platelet counts adequate for vaginal delivery. One woman, who received gamma globulin alone with good initial response, was delivered by cesarean for a platelet count of 25,000/microL at 39 weeks. Following delivery, all infants were thoroughly evaluated, and none had evidence of intracranial hemorrhage or other alloimmune thrombocytopenia-associated morbidity. All had normal platelet counts at discharge from the hospital. CONCLUSIONS: Our experience confirms the efficacy of gamma globulin treatment, but indicates that not all fetuses will respond to it alone. Serial funipunctures are essential to evaluate patient response and allow appropriate therapeutic modifications. Randomized studies are needed to determine the optimal antenatal pharmacologic therapy for this disease.

Adult↗
PubMed2004

The activity of alpha1,6-fucosyltransferase during human megakaryocytic differentiation.

alpha1,6-Fucosyltransferase (6FucT, E.C. 2.4.1.68) is one of the enzymes involved in the synthesis of N-linked glycans of the GpIIb/IIIa complex (CD41a) which is present on megakaryocytes (MKs) and platelets. In this study, we examined 6FucT activity in ex vivo cultures of immunoselected cord blood CD34(+) cells grown in a medium promoting megakaryocytopoiesis. Our results show that the activity of 6FucT increased ahead of, and thereafter concomitantly with, cells expressing the CD41a antigen. When the CD41a(+) subpopulation of cells was immunoselected (using anti-CD61 i.e. anti-GpIIIa antibodies), its 6FucT activity increased proportionally to the yield of CD61(+)(+)(+) cells. Taking into account the heavy load of 6FucT in platelets and megakaryocytes, we regard this enzyme as a candidate for the earliest marker of MK-commitment in cultured hematopoietic stem cells. Such a marker should allow an earlier detection and earlier transplantation of patients' own, ex vivo expanded, Mk progenitors.

Antigens, CD34↗
PubMed2004

[Significance of detecting platelet associated antibody and platelet membrane glycoprotein for diagnosis of immune thrombocytopenia].

The aim of this study was to explore application value of detecting platelet associated antibody and platelet membrane glycoprotein in the diagnosis and prognosis for immune thrombocytopenia. The platelet associated immunoglobulin (PAIg) and platelet membrane glycoprotein (CD41, CD61, GPIIb/IIIa) in 76 cases of immune thrombocytopenia and 30 healthy subjects were determined by FCM. The results showed that PAIg level in ITP patients included PAIgG (31.25 +/- 18.06)%, PAIgM (32.41 +/- 15.51)%, PAIgA (23.39 +/- 16.67)% which were remarkedly higher than in health control (10.48 +/- 5.05)%, (9.40 +/- 4.42)% and (7.23 +/- 3.61)% (P < 0.001). In patients with secondary immune thrombocytopenia (chronic aplastic anemia, SLE, Evans syndrome, liver cirrhosis hypersplenism, etc), PAIg level was higher than that in control group, while the platelet membrane glycoprotein in the blood of these patients was lower than that in control group. The level of PAIg decreased (P < 0.05) after treatment, but platelet membrane glycoprotein increased (P < 0.01). The result suggested that measurements for platelet membrane glycoprotein and platelet associated antibody by FCM were practical with high sensitivity, rapidity and simplicity used as a routine method in diagnosis and evaluation of the therapeutic effects in immune thrombocytopenia patients.

Adolescent↗
PubMed1992

Further evidence that heparin-dependent thrombocytopenia may result from Fc receptor-mediated interactions.

Heparin-dependent thrombocytopenia (HDT) and associated thrombotic complications, are thought to be linked to the appearance of anti-platelet antibodies. Attempts were made to characterize the antibodies in the sera from 10 such patients. Western blotting against platelet antigens was inconclusive, often revealing multiple bands but with considerable variability from patient to patient. An often seen band of approximately 83 kDa was also given by some nonimmune sera and the antigen appeared to be predominantly intracellular in origin. Antibodies to major membrane glycoproteins were not readily apparent. This was confirmed by the MAIPA ("Monoclonal Antibody Immobilization of Platelet Antigens") test, performed to detect antibodies to GP Ib-IX and GP IIb-IIIa. Only one weak activity to GP Ib-IX and one weak activity to GP IIb-IIIa were detected. In contrast, an antibody to the PlA1 alloantigen was readily detected in the serum of an additional patient. The ability of HDT serum to induce the aggregation of control platelets was studied in detail. Aggregation was inhibited by EDU-3, a monoclonal antibody to GP IIb-IIIa complexes, and by the synthetic peptide RGDS, suggesting an involvement of the same pathway as used by physiologic agonists. However, in agreement with Chong et al (Thromb Res 55:291, 1989), we observed that aggregation was inhibited by rabbit IgG, suggesting that it was Fc-receptor mediated. Interestingly, 2E1, a monoclonal antibody to the Fc gamma RII receptor, induced platelet aggregation with a lag phase, a characteristic of HD antibodies. Nonetheless, for different donors, there was no correlation between the length of the lag phase induced by 2E1 and HD antibodies. Fc-receptor blockade should be considered as a means for diminishing the clinical complications of HDT.

Adult↗
PubMed2004

[Three special cases of pregnancy outcome to reflect about].

BACKGROUND: Neonatal alloimmune thrombocytopenia (NAITP) may be a serious condition with prenatal intracranial haemorrhages. Our three cases of serious NAITP raise the question of whether pregnant women should be screened for thrombocyte type and then for HPA-1a antibodies if they are HPA-1bb positive. CASE REPORTS: We present three cases of severe NAITP in which screening and follow up of HPA-1a antibodies prevented serious sequelae in two of the siblings. The first child was a stillbirth with congenital hydrocephalus caused by an intraventricular haemorrhage. In the second pregnancy, the mother was found to be platelet type HPA-1bb with platelet antibodies against HPA-1a. The antibody level was extremely high and an elective caesarean section was performed four weeks before term. The platelet count at birth was 3 and 5 x 10(9)/L and a transfusion of matched platelets was immediately performed followed by infusion of intravenous immunoglobulin. In the third pregnancy, an intracerebral haemorrhage was detected by ultrasound at 27 weeks of gestation. The mother was given steroids to induce foetal lung maturation followed by a caesarean section in week 28. The platelet count was 6 x 10(9)/L. The child was transfused with compatible platelets and given an infusion of intravenous immunoglobulin. OUTCOME: None of the two children have developed any psychomotor sequelae by the age of five and three years, respectively. The importance of screening for platelet type and anti-platelet antibodies and mode of delivery is discussed.

Adult↗
PubMedDate not supplied

beta(3)-Integrin cytoplasmic binding proteins.

Integrins are cell-surface adhesion receptors that play an important role in mediating numerous physiological processes,including inflammation, migration, adhesion, and proliferation. Integrin regulation by events within the cell has been termed "inside-out " signaling; this is a capacity that is unique to integrin receptors. As is typical of other cell-surface receptors, integrins can also transduce signals from outside the cell into the cytoplasm on binding extracellular ligands ("outside-in signaling "). Integrins are composed of an alpha and a beta subunit, which form a heterodimer. The beta(3)-integrin family consists of alpha(IIb)beta(3)-found on platelets and megakaryocytes, and the more widely distributed alpha(v)beta(3). beta Subunits consist of a large extracellular domain, a single transmembrane segment, and a relatively short cytoplasmic tail. The cytoplasmic domains do not contain intrinsic tyrosine kinase activity, and therefore signaling occurs primarily via recruitment of intracellular signaling molecules. Integrins form transmembrane connections, and the interactions between integrin cytoplasmic domains, intracellular factors (cytoplasmic proteins and intracellular signaling pathways), and membrane-anchored proteins play an important role in integrin-mediated events. There are at least 21 proteins that associate with integrin beta tails to regulate cell motility, proliferation, differentiation, and apoptosis. In this review, we will focus on 10 of these proteins and their function in integrin-mediated events.

Animals↗