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M1 Cells (m1 + cell)

Distribution by Scientific Domains
Life Sciences80%

Selected Abstracts

Inhibition of the p38 pathway upregulates macrophage JNK and ERK activities, and the ERK, JNK, and p38 MAP kinase pathways are reprogrammed during differentiation of the murine myeloid M1 cell line

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 1 2002
J. Perry Hall
Abstract Mitogen-activated protein (MAP) kinases have been implicated as important mediators of the inflammatory response. Here we report that c-Jun NH2 -terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38 MAP kinase activities are reprogrammed during the IL-6 induced macrophage-like differentiation of the murine myeloid M1 cell line. Moreover, p38 inhibition upregulates JNK and ERK activity in M1 cells and in thioglycollate-elicited peritoneal exudate macrophages. IL-6-induced M1 differentiation also induces expression of the anti-inflammatory cytokine IL-10, and p38 inhibition potentiates this increase in IL-10 expression in an ERK-dependent manner. Thus, we speculate that during inflammatory conditions in vivo macrophage p38 may regulate JNK and ERK activity and inhibit IL-10 expression. These data highlight the importance of p38 in the molecular mechanisms of macrophage function. J. Cell. Biochem. 86: 1,11, 2002. © 2002 Wiley-Liss, Inc. [source]

The Binding Characteristics and Intracellular Localization of Temoporfin (mTHPC) in Myeloid Leukemia Cells: Phototoxicity and Mitochondrial Damage,

PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2000
J. Y. Chen
ABSTRACT The state of aggregation of the photosensitizer meso -tetrahydroxyphenylchlorin (mTHPC) in both cell free and intracellular environment was elucidated by comparing its absorption and excitation spectra. In methanol, mTHPC existed as monomers and strongly fluoresced. In aqueous solutions such as phosphate-buffered saline (PBS), mTHPC formed nonfluorescent aggregates. Some portion of mTHPC monomerized in the presence of 10% fetal calf serum PBS. In murine myeloid leukemia M1 and WEHI-3B (JCS) cells, cytoplasmic mTHPC were monomeric. By using organelle-specific fluorescent probes, it was found that mTHPC localized preferentially at the mitochondria and the perinuclear region. Photodynamic treatment of mTHPC-sensitized leukemia cells caused rapid appearance of the apoptogenic protein cytochrome c in the cytosol. Results from flow cytometric analysis showed that the release of cytochrome c was especially pronounced in JCS cells, and well correlated with the extent of apoptotic cell death as reported earlier. Electron microscopy revealed the loss of integrity of the mitochondrial membrane and the appearance of chromatin condensation as early as 1 h after light irradiation. We conclude that rapid release of cytochrome c from photodamaged mitochondria is responsible for the mTHPC-induced apoptosis in the myeloid leukemia JCS and M1 cells. [source]

Morphology and mosaics of melanopsin-expressing retinal ganglion cell types in mice

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 13 2010
David M. Berson
Abstract Melanopsin is the photopigment of intrinsically photosensitive retinal ganglion cells (ipRGCs). Melanopsin immunoreactivity reveals two dendritic plexuses within the inner plexiform layer (IPL) and morphologically heterogeneous retinal ganglion cells. Using enhanced immunohistochemistry, we provide a fuller description of murine cell types expressing melanopsin, their contribution to the plexuses of melanopsin dendrites, and mosaics formed by each type. M1 cells, corresponding to the originally described ganglion-cell photoreceptors, occupy the ganglion cell or inner nuclear layers. Their large, sparsely branched arbors (mean diameter 275 ,m) monostratify at the outer limit of the OFF sublayer. M2 cells also have large, monostratified dendritic arbors (mean diameter 310 ,m), but ramify in the inner third of the IPL, within the ON sublayer. There are ,900 M1 cells and 800 M2 cells per retina; each type comprises roughly 1,2% of all ganglion cells. The cell bodies of M1 cells are slightly smaller than those of M2 cells (mean diameters: 13 ,m for M1, 15 ,m for M2). Dendritic field overlap is extensive within each type (coverage factors ,3.8 for M1 and 2.5 for M2 cells). Rare bistratified cells deploy terminal dendrites within both melanopsin-immunoreactive plexuses. Because these are too sparsely distributed to permit complete retinal tiling, they lack a key feature of true ganglion cell types and may be anomalous hybrids of the M1 and M2 types. Finally, we observed weak melanopsin immunoreactivity in other ganglion cells, mostly with large somata, that may constitute one or more additional types of melanopsin-expressing cells. J. Comp. Neurol. 518:2405,2422, 2010. © 2010 Wiley-Liss, Inc. [source]

Morphology and mosaics of melanopsin-expressing retinal ganglion cell types in mice,

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 13 2010
David M. Berson
Abstract Melanopsin is the photopigment of intrinsically photosensitive retinal ganglion cells (ipRGCs). Melanopsin immunoreactivity reveals two dendritic plexuses within the inner plexiform layer (IPL) and morphologically heterogeneous retinal ganglion cells. Using enhanced immunohistochemistry, we provide a fuller description of murine cell types expressing melanopsin, their contribution to the plexuses of melanopsin dendrites, and mosaics formed by each type. M1 cells, corresponding to the originally described ganglion-cell photoreceptors, occupy the ganglion cell or inner nuclear layers. Their large, sparsely branched arbors (mean diameter 275 ,m) monostratify at the outer limit of the OFF sublayer. M2 cells also have large, monostratified dendritic arbors (mean diameter 310 ,m), but ramify in the inner third of the IPL, within the ON sublayer. There are ,900 M1 cells and 800 M2 cells per retina; each type comprises roughly 1,2% of all ganglion cells. The cell bodies of M1 cells are slightly smaller than those of M2 cells (mean diameters: 13 ,m for M1, 15 ,m for M2). Dendritic field overlap is extensive within each type (coverage factors ,3.8 for M1 and 4.6 for M2 cells). Rare bistratified cells deploy terminal dendrites within both melanopsin-immunoreactive plexuses. Because these are too sparsely distributed to permit complete retinal tiling, they lack a key feature of true ganglion cell types and may be anomalous hybrids of the M1 and M2 types. Finally, we observed weak melanopsin immunoreactivity in other ganglion cells, mostly with large somata, that may constitute one or more additional types of melanopsin-expressing cells. J. Comp. Neurol. 518:2405,2422, 2010. © 2010 Wiley-Liss, Inc. [source]

In vitro efficacy of l -asparaginase in childhood acute myeloid leukaemia

BRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2003
Shuichi Okada
Summary., To explore the potential efficacy of l -asparaginase treatment in acute myeloid leukaemia (AML) patients, we studied the in vitro resistance of French,American,British (FAB) subtypes of childhood AML to l -asparaginase using a methyl,thiazol,tetrazolium assay. We tested leukaemic cells obtained from 177 common acute lymphoblastic leukaemia (cALL) and 228 AML children at diagnosis. The median 70% lethal dose of l -asparaginase (LD70asp) (U/ml) was 0·46 in the cALL and 6·70 in the AML samples. The median LD70asp among each FAB subtype of AML was 0·76 (M0), 0·46 (M1), 10·00 (M2), 10·00 (M3), 1·18 (M4), 1·35 (M5) and 10·00 (M7). Type M3 samples had the highest LD70asp. The LD70asp of the M2 samples was significantly higher than that of the M1, M4 and M5 samples. When the LD70asp values were classified as low (0·016,0·159), intermediate (0·16,1·59) or high (1·6,10·00), the frequency of low, intermediate or high LD70asp among the M1 samples were similar to those among the cALL samples. In conclusion, cells from AML types M1, M4 and M5 were relatively sensitive to l -asparaginase, and M1 cells were as sensitive as those of cALL, suggesting that l -asparaginase treatment may be effective for these subtypes of AML. [source]