Trimidox-Mediated Morphological Changes during Erythroid Differentiation Is Associated with the Stimulation of Hemoglobin and F-Cell Production in Human K562 Cells

1998 ◽  
Vol 247 (3) ◽  
pp. 759-764 ◽  
Author(s):  
Efe W. Iyamu ◽  
Samuel E. Adunyah ◽  
Howard L. Elford ◽  
Hugo Fasold ◽  
Ernest A. Turner
Keyword(s):  
Morphological Changes ◽  
K562 Cells ◽  
Erythroid Differentiation ◽  
Cell Production ◽  
Stimulation Of

scholarly journals Effects of innate immune receptor stimulation on extracellular α-synuclein uptake and degradation by brain resident cells

2021 ◽  
Author(s):  
Changyoun Kim ◽  
Somin Kwon ◽  
Michiyo Iba ◽  
Brian Spencer ◽  
Edward Rockenstein ◽  
...  
Keyword(s):  
Degradation Kinetics ◽  
Morphological Changes ◽  
Direct Interaction ◽  
Innate Immune ◽  
Pathological Feature ◽  
Tlr2 Expression ◽  
Immune Receptors ◽  
Age Related ◽  
Stimulation Of

AbstractSynucleinopathies are age-related neurological disorders characterized by the progressive deposition of α-synuclein (α-syn) aggregates and include Parkinson’s disease (PD) and dementia with Lewy bodies (DLB). Although cell-to-cell α-syn transmission is thought to play a key role in the spread of α-syn pathology, the detailed mechanism is still unknown. Neuroinflammation is another key pathological feature of synucleinopathies. Previous studies have identified several immune receptors that mediate neuroinflammation in synucleinopathies, such as Toll-like receptor 2 (TLR2). However, the species of α-syn aggregates varies from study to study, and how different α-syn aggregate species interact with innate immune receptors has yet to be addressed. Therefore, we investigated whether innate immune receptors can facilitate the uptake of different species of α-syn aggregates. Here, we examined whether stimulation of TLRs could modulate the cellular uptake and degradation of α-syn fibrils despite a lack of direct interaction. We observed that stimulation of TLR2 in vitro accelerated α-syn fibril uptake in neurons and glia while delaying the degradation of α-syn in neurons and astrocytes. Internalized α-syn was rapidly degraded in microglia regardless of whether TLR2 was stimulated. However, cellular α-syn uptake and degradation kinetics were not altered by TLR4 stimulation. In addition, upregulation of TLR2 expression in a synucleinopathy mouse model increased the density of Lewy-body-like inclusions and induced morphological changes in microglia. Together, these results suggest that cell type-specific modulation of TLR2 may be a multifaceted and promising therapeutic strategy for synucleinopathies; inhibition of neuronal and astroglial TLR2 decreases pathogenic α-syn transmission, but activation of microglial TLR2 enhances microglial extracellular α-syn clearance.

scholarly journals THE MORPHOLOGICAL CHANGES IN THE TISSUES OF THE RABBIT AS A RESULT OF REDUCED OXIDATION

1918 ◽  
Vol 27 (3) ◽  
pp. 399-412 ◽  
Author(s):  
H. G. Martin ◽  
A. S. Loevenhart ◽  
C. H. Bunting
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Content ◽  
Morphological Changes ◽  
Low Oxygen ◽  
High Carbon ◽  
Red Bone Marrow ◽  
Hydropic Degeneration ◽  
Thyroid Hyperplasia ◽  
High Carbon Dioxide ◽  
Stimulation Of

Exposure of rabbits to an atmosphere of low oxygen content results in a stimulation of the cardiorespiratory systems, in an extension (hyperplasia) of red bone marrow and probably of a thyroid hyperplasia, with the further production of hydropic and hyaline degeneration in the cells of the parenchymatous organs. An atmosphere of high carbon dioxide and normal oxygen content produces, however, a stimulation of the cardiorespiratory systems, but no marrow extension and, in the concentrations used, but slight hydropic degeneration in the parenchyma of the glandular organs.

scholarly journals Correction: Wogonin induces cell cycle arrest and erythroid differentiation in imatinib-resistant K562 cells and primary CML cells

Oncotarget ◽  
2020 ◽  
Vol 11 (3) ◽  
pp. 300-301
Author(s):  
Hao Yang ◽  
Hui Hui ◽  
Qian Wang ◽  
Hui Li ◽  
Kai Zhao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
K562 Cells ◽  
Erythroid Differentiation ◽  
Cycle Arrest ◽  
Imatinib Resistant

scholarly journals Expression and modulation of specific, high affinity binding sites for erythropoietin on the human erythroleukemic cell line K562

Blood ◽  
1988 ◽  
Vol 71 (1) ◽  
pp. 104-109 ◽  
Author(s):  
JK Fraser ◽  
FK Lin ◽  
MV Berridge
Keyword(s):  
Cell Line ◽  
K562 Cell ◽  
K562 Cells ◽  
Erythroid Differentiation ◽  
Receptor Expression ◽  
Target Cells ◽  
Epo Receptor ◽  
High Affinity ◽  
Erythroleukemic Cell ◽  
Erythroleukemic Cell Line

Erythroid differentiation is mediated by several interacting factors which include the glycoprotein hormone erythropoietin (Epo), interleukin-3 (IL-3) in the mouse, and erythroid-potentiating activity (EPA) in humans. Each of these factors binds to specific cell surface receptors on responsive target cells, but the way in which these factors interact to modulate erythropoiesis is unknown. In the present study, we used the human erythroleukemic cell line K562 to examine expression and regulation of the receptor for Epo using 125I-labeled, bioactive recombinant human Epo. K562 cells expressed low numbers of a single class of high-affinity Epo receptors corresponding to 4 to 6 receptors per K562 cell (KD = 270 to 290 pmol/L). Treatment of K562 cell cultures with medium conditioned by the EPA-secreting cell line U937 (U937CM) increased receptor expression 2.6 to 3.5-fold to 13 to 17 receptors/cell (KD = 260 to 300 pmol/L). That all of the Epo receptor- potentiating activity in U937CM was accounted for by EPA was shown by a similar increase in Epo receptor expression on K562 cells with recombinant EPA. The effect of U937CM on Epo receptors was reversed by culturing cells in inducer-free medium for 3 days. Medium conditioned by the 5637 cell line had no effect on Epo receptors on K562 cells. In methylcellulose culture, U937CM and Epo acted synergistically to increase erythroid differentiation of K562. Similarly, U937CM stimulated human cord blood CFU-E growth under conditions in which Epo was limiting or in excess. Increases in Epo receptor expression on K562 cells and on CFU-E in response to EPA may mediate the effects of Epo on these cells.

scholarly journals Monoclonal antibodies detecting antigenic determinants with restricted expression on erythroid cells: from the erythroid committed progenitor level to the mature erythroblast

Blood ◽  
1984 ◽  
Vol 63 (6) ◽  
pp. 1376-1384 ◽  
Author(s):  
T Yokochi ◽  
M Brice ◽  
PS Rabinovitch ◽  
T Papayannopoulou ◽  
G Stamatoyannopoulos
Keyword(s):  
Monoclonal Antibodies ◽  
K562 Cells ◽  
Erythroid Differentiation ◽  
Antigenic Determinants ◽  
Erythroid Progenitors ◽  
Cell Surface Antigens ◽  
Cytotoxicity Assays ◽  
Complement Dependent Cytotoxicity

Two new cell surface antigens specific for the erythroid lineage were defined with cytotoxic IgM monoclonal antibodies (McAb) (EP-1; EP-2) that were produced using BFU-E-derived colonies as immunogens. These two antigens are expressed on in vivo and in vitro derived adult and fetal erythroblasts, but not on erythrocytes. They are not detectable on resting lymphocytes, concanavalin-A (Con-A) activated lymphoblasts, granulocytes, and monocytes or granulocytic cells or macrophages present in peripheral blood or harvested from CFU-GM cultures. Cell line and tissue distributions distinguish McAb EP-1 and EP-2 from all previously described monoclonal antibodies. McAb EP-1 (for erythropoietic antigen-1) inhibits the formation of BFU-E and CFU-E, but not CFU-GM, colonies in complement-dependent cytotoxicity assays. By cell sorting analysis, about 90% of erythroid progenitors (CFU-E, BFU-E) were recovered in the antigen-positive fraction. Seven percent of the cells in this fraction were progenitors (versus 0.1% in the negative fraction). The expression of EP-1 antigen is greatly enhanced in K562 cells, using inducers of hemoglobin synthesis. McAb EP-2 fails to inhibit BFU-E and CFU-E colony formation in complement-dependent cytotoxicity assays. EP-2 antigen is predominantly expressed on in vitro derived immature erythroblasts, and it is weakly expressed on mature erythroblasts. The findings with McAb EP-1 provide evidence that erythroid progenitors (BFU-E and CFU-E) express determinants that fail to be expressed on other progenitor cells and hence appear to be unique to the erythroid lineage. McAb EP-1 and EP-2 are potentially useful for studies of erythroid differentiation and progenitor cell isolation.

scholarly journals Negative regulation of the human epsilon-globin gene by transcriptional interference: role of an Alu repetitive element.

1990 ◽  
Vol 10 (3) ◽  
pp. 1209-1216 ◽  
Author(s):  
J Wu ◽  
G J Grindlay ◽  
P Bushel ◽  
L Mendelsohn ◽  
M Allan
Keyword(s):  
Transcription Initiation ◽  
Repetitive Element ◽  
Globin Gene ◽  
K562 Cells ◽  
Erythroid Differentiation ◽  
Transcriptional Interference ◽  
Base Pairs ◽  
Transient Expression Assay ◽  
Down Regulation ◽  
Alternative Transcription

The human epsilon-globin gene has a number of alternative transcription initiation sites which correspond with regions of DNase I hypersensitivity upstream of the canonical cap site. Transcripts originating from the promoters located -4.3/-4.5 and -1.48 kilobase pairs (kbp) and -900 and -200 base pairs (bp) upstream of the major epsilon-globin cap site can, at certain stages of erythroid differentiation, extend through the gene and are polyadenylated. The 350-bp PolIII transcripts, originating within the Alu repetitive element -2.2 kbp upstream of the cap site, extend in the opposite direction from the gene, are nonpolyadenylated, nucleus confined, and are detectable only in mature K562 cells or mature embryonic red blood cells where the epsilon-globin major cap site is maximally transcribed. Fragments containing the promoters located between -4.5 and -4.3 kbp upstream of the gene down regulate transcription from the epsilon-globin gene 20- to 30-fold in a transient expression assay in which both erythroid and nonerythroid cell lines were used. This occurs only when the direction of transcription from the -4.3/-4.5-kbp promoters is towards the gene, and we hypothesize that down regulation is caused by transcriptional interference. Fragments containing the Alu repetitive element -2.2 kbp upstream of the gene can overcome down regulation of the epsilon-globin gene by the -4.5-kbp element when interposed in the direct orientation between this element and the epsilon-globin gene.

The effect of exogenous RNA extract on chick embryo fibroblasts in vitro

Development ◽  
1970 ◽  
Vol 23 (2) ◽  
pp. 509-517
Author(s):  
A. Sann ◽  
D. Sharp ◽  
J. McKenzie
Keyword(s):  
Cell Differentiation ◽  
Chick Embryo ◽  
Morphological Changes ◽  
Bacterial Cells ◽  
Baby Hamster Kidney ◽  
Exogenous Rna ◽  
Embryo Fibroblasts ◽  
Stimulation Of ◽  
Rna Extract

It is extremely difficult, if not impossible, to reconcile the conflicting claims of those who have treated different cells and tissues with exogenous RNA. Some authors (e.g. Niu, Cordova & Niu, 1961; Niu, Cordova & Radbill, 1962) maintain that RNA extracts alter the course of cell differentiation to conform in morphological terms to the source of the RNA; in the same vein, Amos, Askonas & Soeiro (1964) have shown that, under certain conditions, RNA from mouse and bacterial cells can stimulate chick embryo fibroblasts to synthesize protein related antigenically to the origin of the RNA. Shepley, Ambrose & Kirby (1965), however, obtained stimulation of growth with permanent morphological changes in baby hamster kidney fibroblasts by the addition of RNA from a variety of sources.

scholarly journals Anti-K562 cell monoclonal antibody RTF8X recognizes tumor-associated antigen of erythroid lineage

Blood ◽  
1988 ◽  
Vol 72 (5) ◽  
pp. 1487-1491 ◽  
Author(s):  
T Sakurai ◽  
H Hara ◽  
K Nagai
Keyword(s):  
Monoclonal Antibody ◽  
Cell Lines ◽  
Surface Antigen ◽  
K562 Cell ◽  
K562 Cells ◽  
Erythroid Differentiation ◽  
Enzyme Treatment ◽  
Normal Peripheral Blood ◽  
Marrow Cells

Abstract A new anti-K562 cell monoclonal antibody, RTF8X, a cytotoxic IgM, recognized a surface antigen on erythroblasts from patients with erythroleukemia and polycythemia vera. RTF8X, which is highly specific to K562 cells, did not react with the other 14 hematopoietic cell lines and the seven nonhematopoietic cell lines. RTF8X antigen was not detected in normal peripheral blood, but was found in less than 1% of normal marrow cells. RTF8X did not inhibit in vitro colony formation of CFU-E and BFU-E in a complement-dependent cytotoxicity assay. Cell- sorting analysis showed that, morphologically, the RTF8X-positive marrow cells from the patients and normal volunteers contained more than 60% erythroblasts and that CFU-E and BFU-E were not demonstrated in cells with RTF8X antigen. Enzyme treatment suggested that RTF8X antigen was a sialoglycolipid. These results indicate that RTF8X may recognize the surface antigen found increasingly in association with tumors of erythroid lineage. RTF8X should be useful for studies of erythroid differentiation and proliferation in patients.

scholarly journals Carbonic anhydrase I is an early specific marker of normal human erythroid differentiation

Blood ◽  
1985 ◽  
Vol 66 (5) ◽  
pp. 1162-1170 ◽  
Author(s):  
JL Villeval ◽  
U Testa ◽  
G Vinci ◽  
H Tonthat ◽  
A Bettaieb ◽  
...  
Keyword(s):  
Carbonic Anhydrase ◽  
K562 Cells ◽  
Erythroid Differentiation ◽  
Specific Marker ◽  
Glycophorin A ◽  
Erythroid Progenitors ◽  
Erythroid Progenitor ◽  
Hel Cells ◽  
I Cells ◽  
Marrow Cells

Abstract The expression of carbonic anhydrase (CA) as a marker of erythroid differentiation was investigated by immunologic and enzymatic procedures. A polyclonal anti-CA antibody was obtained by immunizing rabbits with purified CA I isozyme. This antibody is reactive with CA I but not with CA II. Within blood cells, CA I was only present in erythrocytes, whereas CA II was also detected in platelet lysates by enzymatic assay. Concerning marrow cells, identifiable erythroblasts and some blast cells expressed CA I. Most of the glycophorin A-positive marrow cells were clearly labeled by the anti-CA I antibody. However, rare CA I-positive cells were not reactive with anti-glycophorin A antibodies. We therefore investigated whether these cells were erythroid precursors or progenitors. In cell sorting experiments of marrow cells with the FA6 152 monoclonal antibody, which among hematopoietic progenitors is reactive only with CFU-E and a part of BFU- E, was performed, CA I+ cells were found mainly in the positive fraction. The percentage of CA I+ cells nonreactive with anti- glycophorin A antibodies contained in the two fractions was in the same range as the percentage of erythroid progenitors identified by their capacity to form colonies. In addition, the anti-CA I antibody labeled blood BFU-E-derived colonies as early as day 6 of culture, whereas in similar experiments with the anti-glycophorin A antibodies, they were stained three or four days later. No labeling was observed in CFU-GM- or CFU-MK-derived colonies. The phenotype of the day 6 cells expressing CA I was similar to that of erythroid progenitors (CFU-E or BFU-E): negative for glycophorin A and hemoglobin, and positive for HLA-DR antigen, the antigen identified by FA6 152, and blood group A antigen. Among the cell lines tested, only HEL cells expressed CA I, while K562 was unlabeled by the anti-CA I antibody. In contrast, HEL and K562 cells expressed CA II as detected by a biochemical technique. Synthesis of CA I, as with other erythroid markers such as glycophorin A and hemoglobin, was almost abolished after 12-O-tetradecanoyl-phorbol-13 acetate treatment of HEL cells. In conclusion, CA I appears to be an early specific marker of the erythroid differentiation, expressed by a cell with a similar phenotype as an erythroid progenitor.

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