Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heat-killed Lactobacillus casei YIT9018 (LC9018), when administered intravenously to normal mice, induced increase in Mac-1+ cells and Mac-2+ cells but not in Mac-3+ cells in spleen. The number of both populations changed in the same time course and was maximal 14 d after the administration. To know the effect of LC9018 on hematopoietic progenitor level, we examined the number of macrophage colony-forming cells (M-CFC), granulocyte-macrophage CFC (GM-CFC), and colony-forming units in spleen (CFU-S) in bone marrow 3 d after the administration. LC9018 stimulated the proliferation of M-CFC but not that of GM-CFC and CFU-S. LC9018-induced M-CFC were similar to normal M-CFC in dependence on macrophage colony-stimulating factor (M-CSF) and buoyant density. M-CFC-derived macrophages cultured in the presence of M-CSF expressed Mac-1 and Mac-2 but not Mac-3. They showed cytotoxic activity against syngenic tumor cells, Meth A, via direct contact, when assayed by using an in vitro colony inhibition assay or an in vivo Winn test. These results indicate that LC9018 stimulates the proliferation of cytotoxic macrophage progenitors in bone marrow and induces their differentiation in spleen. These effects may be one of the ways in which LC9018 suppresses tumor growth.
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PMID:Increased production of cytotoxic macrophage progenitors by Lactobacillus casei in mice. 250 42

Myeloid progenitor cells and macrophages derived from bone marrow and spleen were efficiently transformed in vitro by infection with Moloney-based retroviral vectors carrying a human c-myc gene. Infected cells were plated in agar in the presence of combinations of the murine lymphokines CSF-1, IL-3, GM-CSF and IL-1. Between 20% and 100% of the colony-forming cells in the initial bone marrow or spleen population could be infected and gave rise to drug-resistant colonies. A large fraction of the infected cells showed continued proliferation after transfer to liquid media and we have derived over 200 growth factor-dependent cell lines. These include adherent and non-adherent CSF-1 or GM-CSF dependent macrophages and macrophage precursors and cell lines which require complex combinations of growth factors for optimal growth. Each of the cell lines displays a unique pattern of expression of surface markers specific for the myeloid lineage including the Mac-1, Mac-2, Mac-3, Ser-4 and F4/80 antigens. Surface markers not specifically associated with the myeloid lineage such as the MHC class II antigens and the Fc-receptor; and surface markers normally associated with the B-cell and T-cell lineages such as B220, L3T4 and Thy1.2 are also found on these cell lines.
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PMID:Transformation of growth factor-dependent myeloid stem cells with retroviral vectors carrying c-myc. 266 72

An accessory cell line, designated line A, was generated from bone marrow stem cells which differentiated in vitro in response to colony-stimulating factor (CSF) in substratum cultures. The cells were found to constitutively secrete large amounts of CSF, the activity of which was neutralized by anti-CSF-1 antibodies. Cells of line A and its supernatants potentiate the suboptimal response of thymocytes to PHA, manifesting an interleukin-1 (IL-1)-like activity. Culture fluids of this line also reconstitute the response to T cell mitogens of spleen cells depleted of adherent accessory cells. It was also found that cells of line A bear low levels of surface Ia, and they efficiently present soluble antigen to proliferating memory T cells. Constitutive prostaglandin secretion, which sometimes masks antigen-presenting capacity, was also demonstrated. Cells of line A are poorly phagocytic, do not secrete lysozyme, and lack Fc and complement receptors. However, they manifest strong cytoplasmic nonspecific esterase staining and an ectoenzyme profile resembling that of elicited inflammatory macrophages. In addition, the cell surface antigen Mac-2 was demonstrated, while stainings with anti-Mac-1 and anti-Mac-3 were negative. Thus, line A may represent a unique subpopulation of immunoregulatory accessory cells, the features of which are discussed.
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PMID:Establishment and characterization of a novel bone-marrow-derived macrophage-like accessory cell line. 348 60

In the present study, we have constructed a subtraction cDNA library to identify novel genes induced by IFN-gamma in GM-CSF-derived bone marrow macrophage (m phi). M theta were treated with 50 U/ml IFN-gamma for 40, 70 and 140 min to induce expression of early genes regulated by IFN-gamma, and the M phi were pooled. Poly(A)+RNA was prepared from both unactivated and IFN-gamma-stimulated m theta, and cDNA libraries were constructed in lambda ZAP. Genes expressed in common by both m theta populations were removed by subtraction using biotin-avidin precipitation of hybrid complexes. Further selection was performed by differential screening using cDNA prepared from mRNA of unactivated m phi as a probe, followed by colony hybridization to remove sister clones. Of 17 clones from which sequence information was obtained, two appeared to be identical with the murine genes, C10 (clone GM2B1) and Mac-2 (clone GM2C4) and an additional two clones had high similarity to human cDNAs encoding proteins of unknown function. cDNAs containing sequences which did not match published sequences were used to probe Northern blots prepared from both unstimulated and IFN-gamma-activated GM-CSF- and CSF-1-derived m phi. Five clones (GM1A2, GM1B4, GM1F2, GM2A12 and GM2B8) showed enhanced transcript levels following IFN-gamma treatment of GM-CSF-derived m phi, but demonstrated high constitutive transcript levels in CSF-l-derived m phi. In addition, C10 transcripts were constitutively expressed by GM-CSF-derived m phi, but not by CSF-1-derived m phi, even after activation by IFN-gamma. These data suggest that much of the functional heterogeneity of GM-CSF- and CSF-1-derived m phi resides in the differential expression of early genes specifically induced by IFN-gamma.
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PMID:Differential expression of novel genes by bone marrow-derived macrophage populations. 765 99

Osteoclast deficiency in op/op mice is cured by a single injection of 5 micrograms recombinant human macrophage colony-stimulating factor (rhM-CSF). In this study, we found that mouse osteoclasts are positive for Mac-2 antigen, but not for F4/80, MOMA-2, Mac-1, or BM8 antigen. By using F4/80 and MOMA-2 monoclonal antibodies, we confirmed the absence of mature macrophages in the femora of op/op mice and found that multiple injections of rhM-CSF are required for the recruitment of macrophages in the bones. After a single rhM-CSF injection, we found Mac-2 positive mononuclear cells in the femora of op/op mice. The time course of the appearance of Mac-2-positive cells was very similar to that of tartrate-resistant acid phosphatase (TRAP)-positive cells. In bone sections prepared from the mutant mice that received rhM-CSF 3 days earlier, 91% of the TRAP-positive mononuclear cells were also positive for Mac-2 antigen. These results demonstrate the expression of Mac-2 antigen in preosteoclasts. The antigen was detected on the plasma membrane of preosteoclasts, as well as in their cytoplasm and nucleus, and in the extracellular matrix in the space between the cells and bone. Since Mac-2 is a galactose-specific lectin, a potential role of the lectin in cell-cell and cell-matrix adhesion during osteoclast differentiation is suggested.
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PMID:Expression of Mac-2 antigen in the preosteoclast and osteoclast identified in the op/op mouse injected with macrophage colony-stimulating factor. 807 62

Twenty cases of histiocytic sarcoma in 15 female and five male (384 to 722 days of age) hybrid F1 (C57BL/6 x BALB/c) or F2 (F1 x F1) mice were studied for expression of mononuclear phagocyte and other antigens. Histiocytic sarcomas were found most often in liver, uterus, spleen, and lung. Tissues fixed in Bouin's fluid provided preservation of antigen immunoreactivity, using avidin biotin peroxidase complex immunohistochemistry, with monoclonal and polyclonal antibodies. The mononuclear phagocyte antigens, lysozyme and Mac-2 (a galactose-specific lectin that binds IgE), were found in 60-70% of the cases. The receptor for the macrophage colony-stimulating factor (CSF-1), c-fms, was expressed in 2/20 (10%) of the cases. Mouse immunoglobulins were not found in histiocytic sarcoma cells. In uterine histiocytic sarcomas, previously reported as Schwannomas because of their histologic appearance, S-100 protein was not expressed by tumor cells, although they usually expressed Mac-2 and lysozyme. Hyaline droplets were found in the renal tubules of only 2/19 cases. Our studies provide evidence that murine histiocytic sarcoma expresses antigens (Mac-2, lysozyme, c-fms) found in cells of the mononuclear phagocyte series, in contrast to the B-cell origin of many human histiocytic tumors.
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PMID:Expression of mononuclear phagocyte antigens in histiocytic sarcoma of mice. 811 50

Three major molecules have been recognized as IgE-binding structures on hematopoietic cells: the heterotrimeric high-affinity receptor for IgE (Fc epsilon RI), the low-affinity receptor for IgE (Fc epsilon RII/CD23) and the Mac-2/IgE-binding protein (epsilon BP). The latter has been shown to be expressed on polymorphonuclear neutrophils (PMN), where it regulates IgE-dependent activation. Experiments were undertaken to determine whether the IgE-binding capacity of PMN is mediated exclusively by this molecule. No detectable binding of human myeloma IgE to unstimulated PMN from normal volunteers could be evidenced. In contrast, PMN stimulated with granulocyte macrophage colony stimulating factor (GM-CSF) (500 U/ml) for 24 h displayed positive IgE binding. This binding was significantly inhibited in the presence of mAb directed against Mac-2/epsilon BP and also in the presence of anti-CD23 mAb, but not of anti-Fc epsilon RI mAb or isotype-matched controls. By flow cytometry, CD23 expression was detected on GM-CSF-primed PMN by several anti-CD23 mAb, including EBVCS-5, BB10 or Mab135, which recognize different epitopes. CD23 was also evidenced by immunocytochemistry in GM-CSF-primed PMN. By in situ hybridization, GM-CSF-treated PMN exhibited a hybridization signal for CD23 mRNA and the presence of the CD23b isoform-specific mRNA was detected by RT-PCR. These findings indicate that PMN can synthesize CD23 molecules under GM-CSF induction. This strong CD23 expression might be of physiopathological relevance in IgE-dependent activation during allergic processes.
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PMID:Granulocyte macrophage colony stimulating factor induces Fc epsilon RII/CD23 expression on normal human polymorphonuclear neutrophils. 872 38

Wallerian degeneration (WD) is the inflammatory response of peripheral nerves to injury. Evidence is provided that granulocyte macrophage colony stimulating factor (GM-CSF) contributes to the initiation and progression of WD by activating macrophages and Schwann, whereas IL-10 down-regulates WD by inhibiting GM-CSF production. A significant role of activated macrophages and Schwann for future regeneration is myelin removal by phagocytosis and degradation. We studied the timing and magnitude of GM-CSF and IL-10 production, macrophage and Schwann activation, and myelin degradation in C57BL/6NHSD and C57BL/6-WLD/OLA/NHSD mice that display normal rapid-WD and abnormal slow-WD, respectively. We observed the following events in rapid-WD. The onset of GM-CSF production is within 5 h after injury. Production is steadily augmented during the first 3 days, but is attenuated thereafter. The onset of production of the macrophage and Schwann activation marker Galectin-3/MAC-2 succeeds that of GM-CSF. Galectin-3/MAC-2 production is up-regulated during the first 6 days, but is down-regulated thereafter. The onset of myelin degradation succeeds that of Galectin-3/MAC-2, and is almost complete within 1 week. IL-10 production displays two phases. An immediate low followed by a high that begins on the fourth day, reaching highest levels on the seventh. The timing and magnitude of GM-CSF production thus enable the rapid activation of macrophages and Schwann that consequently phagocytose and degrade myelin. The timing and magnitude of IL-10 production suggest a role in down-regulating WD after myelin is removed. In contrast, slow-WD nerves produce low inefficient levels of GM-CSF and IL-10 throughout. Therefore, deficient IL-10 levels cannot account for inefficient GM-CSF production, whereas deficient GM-CSF levels may account, in part, for slow-WD.
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PMID:The cytokine network of wallerian degeneration: IL-10 and GM-CSF. 976

CSF-1 and GM-CSF have been implicated in the pathogenesis of rheumatoid arthritis. We report the effects of CSF-1 and GM-CSF in the development of an acute methylated bovine serum albumin (mBSA)-induced murine arthritis model. Examination of histopathological features revealed that the systemic administration of CSF-1 or GM-CSF following mBSA administration into the knee resulted in the exacerbation of arthritis. This included synovial hyperplasia and joint inflammation, most evident at 7 and 14 days post-mBSA administration, and the appearance of erosive pannus tissue. The exacerbation by CSF-1 and GM-CSF was not sustained but declined in incidence and severity by 21 days post-mBSA administration, similar to the effects of IL-1beta in this model, reported here and previously. Macrophages expressing Mac-2 and F4/80 were a prominent feature of the pathology observed, particularly the infiltration of Mac-2+ macrophages seen in all mice administered CSF-1, GM-CSF or IL-1beta. Present in inflamed knees was a locally dividing population of cells which included Mac-2+ and F4/80+ macrophages. These studies demonstrate that CSF-1 and GM-CSF can exacerbate and prolong the histopathology of acute inflammatory arthritis and lend support to monocytes/macrophages being a driving influence in the pathogenesis of inflammatory arthritis.
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PMID:Exacerbation of acute inflammatory arthritis by the colony-stimulating factors CSF-1 and granulocyte macrophage (GM)-CSF: evidence of macrophage infiltration and local proliferation. 1063 76

Here we report in vivo evidence of a neuroprotective role of proliferating microglial cells in cerebral ischemia. Using transgenic mice expressing a mutant thymidine kinase form of herpes simplex virus driven by myeloid-specific CD11b promoter and ganciclovir treatment as a tool, we selectively ablated proliferating (Mac-2 positive) microglia after transient middle cerebral artery occlusion. The series of experiments using green fluorescent protein-chimeric mice demonstrated that within the first 72 h after ischemic injury, the Mac-2 marker [unlike Iba1 (ionized calcium-binding adapter molecule 1)] was preferentially expressed by the resident microglia. Selective ablation of proliferating resident microglia was associated with a marked alteration in the temporal dynamics of proinflammatory cytokine expression, a significant increase in the size of infarction associated with a 2.7-fold increase in the number of apoptotic cells, predominantly neurons, and a 1.8-fold decrease in the levels of IGF-1. A double-immunofluorescence analysis revealed a approximately 100% colocalization between IGF-1 positive cells and Mac-2, a marker of activated/proliferating resident microglia. Conversely, stimulation of microglial proliferation after cerebral ischemia by M-CSF (macrophage colony stimulating factor) resulted in a 1.9-fold increase in IGF-1 levels and a significant increase of Mac2+ cells. Our findings suggest that a postischemic proliferation of the resident microglial cells may serve as an important modulator of a brain inflammatory response. More importantly, our results revealed a marked neuroprotective potential of proliferating microglia serving as an endogenous pool of neurotrophic molecules such as IGF-1, which may open new therapeutic avenues in the treatment of stroke and other neurological disorders.
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PMID:Selective ablation of proliferating microglial cells exacerbates ischemic injury in the brain. 1734 97


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