The Expressions of CD114, CD117 and STAT5 in CD34+CD59− and CD34+CD59+ Bone Marrow Cells of the Patients with Paroxysmal Nocturnal Hemoglobinuria

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4404-4404
Author(s):  
Rong Fu ◽  
Shaoxue Ding ◽  
Zonghong Shao ◽  
Lijuan Li ◽  
Hui Liu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Signaling Pathway ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Bone Marrow Cells ◽  
Conflicts Of Interest ◽  
Granulocyte Colony Stimulating Factor ◽  
Clone Cells ◽  
Stimulating Factor ◽  
Normal Controls ◽  
Marrow Cells

Abstract Abstract 4404 Objective: To measure the expressions of granulocyte colony-stimulating factor receptor (G-CSFR, CD114) and stem cell factor receptor (C-KIT, CD117) on the membrane of CD34+CD59− and CD34+CD59+ bone marrow cells of the patients with paroxysmal nocturnal hemoglobinuria(PNH), and the signaling pathway protein STAT5 within the cytoplasm of those cells. Methods: The expressions of CD114 and CD117 on the cell membrane and STAT5 protein within the cytoplasm of bone marrow CD34+CD59+ and CD34+CD59− cells from 26 PNH patients and 14 normal controls were examined by flow cytometry (FCM). Results: The percentage of CD114 positive cells in CD34+CD59− cells of PNH patients was (43.23±19.77)%,which was significantly lower than that in CD34+CD59+ cells of PNH patients (73.72±17.42) (P<0.01) or normal controls (65.91±13.70)% (P<0.01). There was no statistic difference between the two latter (P>0.05). The percentage of CD117 positive cells in CD34+CD59− cells of PNH patients was (49.20±26.80)%,which was significantly lower than that in CD34+CD59+ cells of PNH patients (67.62±17.41) (P<0.01) or normal controls (70.21±12.68)% (P<0.01). There was no statistic difference between the two latter (P>0.05). The STAT5 MFI in CD34+CD59− and CD34+CD59+ cells of PNH patients and CD34+CD59+ cells of normal controls was (270.01±181.26), (205.05±146.16), (227.39±156.65) respectively. There was no statistic difference among the three groups (P>0.05). Conclusions: In PNH, CD114 and CD117 expressed lower on bone marrow PNH clone cells than normal clone cells, but the expressions of signaling pathway protein STAT5 within the cytoplasm was normal. Disclosures: No relevant conflicts of interest to declare.

Expression of dlk1 in the Bone Marrow Cells of Patients with Myelodysplastic Syndrome and Its Clinical Significance

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 5042-5042
Author(s):  
Zonghong Shao ◽  
Lanzhu Yue ◽  
Rong Fu ◽  
Lijuan Li ◽  
Erbao Ruan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Early Diagnosis ◽  
Myelodysplastic Syndrome ◽  
Bone Marrow Cells ◽  
Conflicts Of Interest ◽  
Rt Pcr ◽  
Normal Controls ◽  
Lower Expression ◽  
Bone Marrow Blasts ◽  
Marrow Cells

Abstract Abstract 5042 Objective To investigate the expression of dlk1 gene (delta-like 1) in the bone marrow cells of patients with Myelodysplastic syndrome (MDS), and explore the molecular marker for early diagnosis of MDS. Methods The expression of dlk1 mRNA in the bone marrow cells of cases with MDS, AML and normal controls were measured by RT-PCR, aiming to search for the cytogenetic marker of MDS malignant clone. Results The expression of dlk1 mRNA in bone marrow cells of MDS patients (0.7342±0.3652) was significantly higher than that of normal controls (0.4801±0.1759) (P<0.05), and was significantly positively correlated with the proportion of bone marrow blasts(r=0.467,P<0.05). The expression of dlk1 mRNA significantly increased as the subtype of MDS advanced (P<0.05). Patients with abnormal karyotypes displayed significantly higher expression of dlk1 mRNA (0.9007±0.4334) than those with normal karyotypes (0.6411±0.2630) (P<0.05). Patients with higher expression of dlk1(≥0.8) presented significantly higher malignant clone burden (0.4134±0.3999) than those with lower expression (<0.8) of dlk1 (0.1517±0.3109) (P<0.05). Conclusion dlk1 gene was highly expressed in MDS patients, which increased as the subtype of MDS advanced. The expression of dlk1 mRNA was significantly positively correlated with the proportion of bone marrow blasts. High expression of dlk1 gene suggests high malignant clone burden of MDS. Disclosures: No relevant conflicts of interest to declare.

Tyrosine residues of the granulocyte colony-stimulating factor receptor transmit proliferation and differentiation signals in murine bone marrow cells

Blood ◽  
2002 ◽  
Vol 99 (3) ◽  
pp. 879-887 ◽  
Author(s):  
Shiva Akbarzadeh ◽  
Alister C. Ward ◽  
Dora O. M. McPhee ◽  
Warren S. Alexander ◽  
Graham J. Lieschke ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cell Proliferation ◽  
Bone Marrow Cells ◽  
Granulocyte Colony Stimulating Factor ◽  
Tyrosine Residues ◽  
Proliferation And Differentiation ◽  
Epidermal Growth ◽  
Mutant Receptors ◽  
Stimulating Factor ◽  
Marrow Cells

Abstract Granulocyte colony-stimulating factor (G-CSF) is the major regulator of granulopoiesis and acts through binding to its specific receptor (G-CSF-R) on neutrophilic granulocytes. Previous studies of signaling from the 4 G-CSF-R cytoplasmic tyrosine residues used model cell lines that may have idiosyncratic, nonphysiological responses. This study aimed to identify specific signals transmitted by the receptor tyrosine residues in primary myeloid cells. To bypass the presence of endogenous G-CSF-R, a chimeric receptor containing the extracellular domain of the epidermal growth factor receptor in place of the entire extracellular domain of the G-CSF-R was used. A series of chimeric receptors containing tyrosine mutations to phenylalanine, either individually or collectively, was constructed and expressed in primary bone marrow cells from G-CSF–deficient mice. Proliferation and differentiation responses of receptor-expressing bone marrow cells stimulated by epidermal growth factor were measured. An increased 50% effective concentration to stimulus of the receptor Ynullmutant indicated that specific signals from tyrosine residues were required for cell proliferation, particularly at low concentrations of stimulus. Impaired responses by mutant receptors implicated G-CSF-R Y764 in cell proliferation and Y729 in granulocyte differentiation signaling. In addition, different sensitivities to ligand stimulation between mutant receptors indicated that G-CSF-R Y744 and possibly Y729 have an inhibitory role in cell proliferation. STAT activation was not affected by tyrosine mutations, whereas ERK activation appeared to depend, at least in part, on Y764. These observations have suggested novel roles for the G-CSF-R tyrosine residues in primary cells that were not observed previously in studies in cell lines.

The Somatic Mutation of PIG-A Gene and the Expressions of EGR-1 and WT1 Genes in Bone Marrow Cells of the Patients with Paroxysmal Nocturnal Hemoglobinuria

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 4379-4379
Author(s):  
Rong Fu ◽  
Liyan Li ◽  
Zonghong Shao ◽  
Jun Wang ◽  
Lijuan Li ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Gene Mutation ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Bone Marrow Cells ◽  
Chinese Patients ◽  
Single Base Substitution ◽  
Base Substitution ◽  
Single Base ◽  
Normal Controls ◽  
Marrow Cells

Abstract Abstract 4379 Objective To investigate the somatic mutations of PIG-A gene and the expressions of EGR-1 and WT1 genes in the bone marrow cells of the patients with Paroxysmal nocturnal hemoglobinuria, then explore the characteristics of PIG-A gene mutation in Chinese patients with PNH and the possible mechanism of PNH clonal expansion related to EGR-1 and WT1 genes. Methods The quantities of CD55− cells and CD59− cells in both peripheral blood and bone marrow were examined with flow cytometric assay(FCM), and then sorting CD59− cells from bone marrow mononuclears (BMMNCs). The mutant segments of PIG-A gene were identified by DNA sequencing; The expressions of EGR-1 and WT1 mRNA in CD59− and CD59+ BMMNC were measured with semiquantitive RT-PCR. Results Nine in sixteen patients with PNH and one in four patients with AA-PNH were measured for their PIG-A gene mutation. Five single base substitution were found, including A→G, G→T, A→T, T→G and G→C, resulting in one consense and seven missense mutations. Each of 3 PNH patients had more than two point mutations of PIG-A gene. Insert or deletion mutation of PIG-A gene were not found. The relative mRNA expressions of EGR-1and WT1 genes in CD59− BMMNC, CD59+ BMMNC of PNH or AA-PNH patient and BMMNC of normal controls were (1.00±0.11), (0.86±0.14), (0.85±0.06) and (1.06±0.16), (0.90±0.14), (0.88±0.06), the expression in CD59− BMMNC was significantly higher than that in CD59+ BMMNC or normal controls (p<0.05). There was no significant difference between the expression in CD59+ BMMNC and normal controls(p>0.05). The relative mRNA expressions of EGR-1 and WT1 in BMMNC of PNH and AA-PNH cases were positively correlated with the proportion of CD59− cells(coefficient correlation was 0.509 and 0.481 respectively, p<0.05), but not related to the proportion of CD59+ cells. Conclusions The PIG-A gene mutation in some Chinese patients mainly manifested as single base substitution, occurred at random sites and without hot spot, the overexpression of EGR-1 and WT1 genes in PNH clone could promote the abnormal clone expansion. Disclosures: No relevant conflicts of interest to declare.

Granulocyte-colony stimulating factor enhanced the recruitment of bone marrow cells into the heart

2004 ◽  
Vol 52 (10) ◽  
pp. 451-455
Author(s):  
Yosuke Hisashi ◽  
Shinji Tomita ◽  
Takeshi Nakatani ◽  
Shinya Fukuhara ◽  
Chikao Yutani ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bone Marrow Cells ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor ◽  
Marrow Cells
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