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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our preliminary study has shown that dimethyl sulfoxide (DMSO) has an inhibitory effect on the proliferation of cultured arterial smooth muscle cells and promotes phenotypic modulation from the synthetic state to the contractile state. In the present study we have examined the effect of DMSO with special attention to relationship between cell growth and cytoplasmic microtubules. DMSO inhibited DNA synthesis and cell division, and concomitantly promoted microtubule assembly. Initiation of DNA synthesis and cell division of nonproliferating cells by platelet-derived growth factor (PDGF) was also inhibited in the presence of 1% DMSO. A 12-hr incubation with 10(-6) M colchicine caused disruption of microtubules; however, pretreatment with 1% DMSO for 24 hr prevented the disruption, indicating that DMSO has a stabilizing action on microtubules. A 24-hr exposure to PDGF resulted in microtubule depolymerization, while the addition of 1% DMSO prevented the depolymerization. These results suggest that DMSO inhibits DNA synthesis of cultured smooth muscle cells by stabilizing cytoplasmic microtubules.
Exp Mol Pathol 1988 Feb
PMID:Inhibitory effect of dimethyl sulfoxide on the proliferation of cultured arterial smooth muscle cells: relationship to the cytoplasmic microtubules. 333 51

When cells of the HL-60 promyelocytic leukemia line are cultured with 1,25-dihydroxyvitamin D3 (calcitriol) they acquire a more highly differentiated, myelomonocytic phenotype. It was observed that the ability to ingest IgA-coated erythrocytes and to bind soluble dimeric IgA accompanied this maturation. Phagocytosis of IgA-coated erythrocytes was greater than 50% inhibited by 0.8 mg/ml free IgA, and not by IgG or IgM. Similarly, binding of dimeric IgA was not blocked by a 100-fold excess of IgG, IgM or IgE. Both IgA-mediated phagocytosis and IgA binding became apparent after two days of culture with calcitriol and increased with time in culture. The induction of functional IgA receptors was evident with 10(-11) M calcitriol and maximal levels of IgA binding and of numbers of cells capable of IgA mediated phagocytosis were induced by 10(-8)-10(-9) M calcitriol. 25-Hydroxyvitamin D3, which binds 100-1000-fold less avidly to the cytoplasmic D3 receptor than calcitriol, did not induce functional IgA receptors unless concns of 10(-7) M were used. Other compounds which induce differentiation of HL-60 cells, including retinoic acid and DMSO, produced similar results to calcitriol, whereas cells treated with gamma interferon expressed lower levels of IgA binding and did not ingest IgA-coated targets, suggesting that a critical density of IgA receptors must be reached to enable phagocytosis and/or that other cell activational events are required for IgA receptors to mediate killing. This model may provide useful insight into the function and regulation of IgA receptors on cells of the myeloid series.
Mol Immunol 1986 Jun
PMID:IgA-mediated effector function of HL-60 cells following treatment with calcitriol. 346 86

The effects of dimethyl sulfoxide (DMSO) on subsynaptic response and quantal release of transmitter have been studied at the mammalian neuromuscular junction. Subsynaptically, at low concentrations (up to 1% by volume), DMSO prolongs the time course of decay of miniature endplate currents, (MEPCs), with no significant effect on the amplitude of the currents, which is consistent with an action of DMSO to inhibit acetylcholinesterase. At higher concentrations of DMSO (in excess of 1% by volume) the amplitude of MEPCs and the steady state response to carbamoylcholine (carbachol) are significantly reduced, which suggests an additional action of DMSO other than pure anticholinesterase activity. After pretreatment of the preparation with a low concentration of paraoxon, higher concentrations of DMSO decrease MEPC height and cause highly variable changes in the decay time course of the MEPC. The results suggest that DMSO concentrations in excess of 1% by volume have two distinct and opposite actions on the subsynaptic response; a pure anticholinesterase activity to enhance the response and a depressant effect which is similar to that caused by d-tubocurarine. Presynaptically, DMSO increased both the spontaneous release (measured as the frequency of miniature endplate potentials, fMEPP) and the evoked release (measured as the quantal content of endplate potentials). Both types of release were increased as an exponential function, with the same slope, of the DMSO concentration, suggesting a common mode of action on these two types of release. This action appeared not to be due to an effect on the disposition or effectiveness of calcium ions inside the terminal but, rather, was due to a fusogenic or global effect. In addition, the increase in fMEPP with DMSO was the same when external calcium was replaced by barium. At the concentrations studied, up to 8% by volume, DMSO did not cause any substantial depolarization of the nerve terminal or any appreciable change in the nerve terminal action potential. In a few experiments facilitation was studied at the frog neuromuscular junction and was unchanged by DMSO at concentrations which considerably enhanced transmitter release.
Mol Pharmacol 1986 Dec
PMID:The actions of dimethyl sulfoxide on neuromuscular transmission. 378 40

Human carcinoma HEp-3 lost its tumorigenic and metastatic potential upon prolonged culture in vitro. This change was accompanied by a reduced production of plasminogen activator (PA) of the urokinase type (uPA), which is secreted by HEp-3 cells, a change in response to effectors that modulate uPA production, and an alteration of cell morphology. Similar but more rapid changes occurred when malignant HEp-3 cells were exposed to dimethyl sulfoxide (DMSO). uPA activity in the culture medium dropped below 50% of the control level within 6 h after the addition of DMSO and became undetectable after 24 h of treatment. This drop in uPA activity was not caused by an increased production of PA inhibitors. The cell-associated uPA decreased to 25 to 30% of the control level within 6 h of DMSO treatment and remained at this level for at least 96 h; the reduced uPA production was partially accounted for by a rapid decrease in the functional and chemical concentration of uPA mRNA. In contrast, the concentrations of most of the abundant mRNA species did not appear to be significantly affected, and cell growth was only slightly inhibited in the presence of DMSO. Malignant HEp-3 cells treated with DMSO responded to cholera toxin with an enhanced production of uPA, and their morphology became indistinguishable from that of nonmalignant HEp-3 cells grown in vitro for prolonged periods of time. All of the above changes were fully and rapidly reversible. The inhibitory effect of DMSO on PA production appears to be specific for uPA of human cell lines.
Mol Cell Biol 1985 Dec
PMID:Effect of dimethyl sulfoxide on human carcinoma cells, inhibition of plasminogen activator synthesis, change in cell morphology, and alteration of response to cholera toxin. 383 48

Reactive oxygen-derived free radicals form excessively during irradiation of biological structures, but also normally in many cellular oxidative processes, albeit in small amounts. Unless scavenged by protective mechanisms, such radicals may induce peroxidation of polyunsaturated fatty acids resulting in membrane damage. The process may be catalysed to a considerable extent by transitional metals with the capacity to form redox systems, such as Fe3+ in equilibrium Fe2+. In the present study, it is shown that radiation by X-rays and/or exposure to ionic iron (Fe3+) causes decreased survival in parallel with lysosomal labilization of cultured mouse peritoneal macrophages (MPMs). The latter event was demonstrated as a reduced capacity of lysosomes in living MPMs to retain acridine orange during photo-oxidative stress caused by continuous exposure to blue light of short wavelength. The effects of X-irradiation, and/or lysosomal iron-loading, could be counteracted by the addition of the .OH-scavenging drug dimethylsulfoxide (DMSO) to the cell culture medium. The findings suggest that X-irradiation may damage certain sensitive G0 cells, such as Kupffer cells, serous cells of salivary glands and old macrophages, which normally have substantial concentrations of metals within their vacuolar apparatus, possibly by lysosomal damage involving .OH-mediated lipid peroxidation.
Virchows Arch B Cell Pathol Incl Mol Pathol 1984
PMID:Dimethylsulfoxide increases the survival and lysosomal stability of mouse peritoneal macrophages exposed to low-LET ionizing radiation and/or ionic iron in culture. 615 May 76

Errors in chromosome segregation leading to numerical anomalies appear to be unusually frequent in Man and consequently a large proportion of conceptions in our species are aneuploid. Concern has been expressed that this frequency may be increased still further following exposure to inducing substances (trisomigens) present in the environment. We have been developing a fungal test system to screen for such trisomigens and in this paper we report its use in detecting induction following exposure to dimethylsulfoxide (DMSO). In our system DMSO induces segregational errors at both the first and second meiotic division. The results also show that increases in aneuploidy are proportional to the underlying spontaneous frequency. If this finding is generally true it will be especially important to avoid exposure to trisomigens as Man might be especially vulnerable to them.
Mol Gen Genet 1984
PMID:Dimethylsulfoxide induces aneuploidy in a fungal test system. 659 77

In mouse erythroleukemia cells (MELC) a lipophilic protein of apparent M.W. 9.5 kdaltons increases during differentiation. This increase is due either to an increase of biosynthesis or to a structural alteration impairing the capacity of the protein to form polymers of apparent high M.W. or favoring its extractability. The increases is related to differentiation and precedes hemoglobin synthesis by at least 1 day. It is not related to virus production because it occurs in cells (line F 4-1) which do not produce virus, but it does not occur in cells (TFA-II) in which dimethylsulfoxide (DMSO) causes an increase in virus production. As it occurs in cells treated with 4 different inducers, and as the increase is less marked when antagonists of the inducers are also present, it is unlikely that the increase of the 9.5 Kdalton protein is due to an effect of the inducers unrelated to differentiation.
Mol Biol Rep 1981 Aug 14
PMID:Modification of lipophilic proteins in Friend erythroleukemia cells during their differentiation. 694 77

Tissue injury that occurs as a result of ischemia and subsequent reperfusion is characterized by endothelial cell injury, edema formation, and the influx of inflammatory leukocytes. Two macrophage-derived proinflammatory cytokines which may play a critical role in cellular injury and leukocyte recruitment/activation that occurs in the setting of ischemia-reperfusion injury are tumor necrosis factor alpha (TNF) and macrophage inflammatory protein-1 alpha (MIP-1 alpha). To determine if modulation of ambient oxygen tensions in vitro alters the expression of proinflammatory cytokines from activated macrophages, murine alveolar macrophages (AMO) were cultured in various combinations of ambient oxygen concentrations, then the supernatant fluid and cell pellet assayed for the presence of TNF and MIP-1 alpha messenger RNA (mRNA) and protein. We demonstrated that conditions of anoxia (95% nitrogen/5% CO2) or hyperoxia (95% oxygen/5% CO2) independently resulted in the increased expression of both TNF and MIP-1 alpha mRNA and protein from lipopolysaccharide (LPS)-stimulated AMO, as compared with cells cultured in room air. The specific culture condition of anoxia (x 6 h) followed by hyperoxia (x 18 h) produced the greatest increases in both TNF and MIP-1 alpha, suggesting that when following a period of anoxic priming, oxygen stress results in exaggerated cytokine production. A period of at least 4.5 to 6 h of anoxia prior to hyperoxic exposure was found to be the minimal time required for anoxic priming. Furthermore, the coincubation of LPS-treated AMO with dimethyl sulfoxide (DMSO) attenuated the anoxia-hyperoxia-induced increases in TNF and MIP-1 alpha mRNA by 23% and 34%, respectively. These findings suggested that alterations in ambient oxygen tension can regulate the expression of TNF and MIP-1 alpha from activated AMO, and that oxidant-related cytokine production may represent an important mechanism by which inflammation occurs in the clinical settings of ischemia-reperfusion injury and hyperoxia.
Am J Respir Cell Mol Biol 1995 Oct
PMID:Alterations of ambient oxygen tension modulate the expression of tumor necrosis factor and macrophage inflammatory protein-1 alpha from murine alveolar macrophages. 754 69

A reduction of gap-junctional intercellular communication (GJIC) often accompanies neoplastic transformation. The present work demonstrates that transformation by the oncogenic human DNA virus, human papilloma virus 16(HPV16), also reduces GJIC between L6 rat myoblasts. HPVs are associated with anogenital cancers, the incidence of which is increasing in HIV positive patients of both sexes. Using videofluorescence imaging of Fura-2 loaded cells a lack of GJIC between transformed HPV16-L6 cells was first indicated by uncoordinated brief [Ca2+]i spikes in clusters of DMSO-treated HPV16-L6 cells instead of the synchronous, sustained [Ca2+]i surges in clusters of DMSO-treated L6 cells. Reduced GJIC between HPV16-L6 cells was demonstrated directly by a much reduced transfer of lucifer yellow dye from HPV16-L6 cells, which had been loaded with the dye through electroporation with an EPIZAP II in situ electroporator, to neighbouring nonelectroporated HPV16-L6 cells. One reason for this reduced GJIC between HPV16-L6 cells could have been their dramatically enhanced activity of membrane-associated PKC which is known to phosphorylate connexins and down-regulate gap junctions. However, the main reason was the viral-induced inhibition of the expression of a major gap junction component, Cx43 (Connexin 43), in the transformed myoblasts.
Cell Mol Biol (Noisy-le-grand) 1995 Jun
PMID:Alterations in cell-cell communication in human papillomavirus type 16 (HPV16) transformed rat myoblasts. 754 85

The activity of the octapeptide pyroGlu-Asp-Asp-Ser-Asp-Glu-Glu-Asn in the control of cell growth and differentiation of human myeloblastic leukemia cells HL-60 is reported. Treatment with peptide slightly slows down the rate of cellular proliferation and this effect becomes more evident in cells grown for several weeks in the presence of the effector. An enhanced effect (40-50% inhibition respect to the control) is found in reversibly permeabilized cells and after 1% DMSO is added to the medium. Moreover the presence of peptide markedly increases the percentage of cells differentiated by DMSO and RA. The effect in DMSO-induced cells is more evident than that observed in RA-induced cells. This in agreement with our hypothesis that DMSO facilitates the peptide entry and its effect is due to an intracellular action.
Cell Mol Biol (Noisy-le-grand) 1995 Jun
PMID:Synthetic octapeptide pyroGlu-Asp-Asp-Ser-Asp-Glu-Glu-Asn promotes differentiation in promyelocytic HL-60 cell line. 754 88


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