共查询到20条相似文献,搜索用时 15 毫秒
1.
C Nadal 《Cell and tissue kinetics》1987,20(3):331-341
The activity of a glycopeptide prepared from rat serum by treatment with trypsin and ultrafiltration was investigated in several in vivo proliferation systems. In baby rat hepatocytes synchronized by a subcutaneous injection of casein solution it caused a G1-S block, stopping cells at the end of the G1 phase and sending them back to the G0 phase. The glycopeptide also caused a G1-S block in young adult rats during the first semi-synchronized wave of proliferation that followed partial hepatectomy. Inhibition of hepatocyte proliferation by the glycopeptide was suppressed by blood proteins from normal rats but not from acute phase rats. Alpha 1-acid glycoprotein, an acute phase protein, increased this inhibition and reversed the antagonistic effect of normal blood proteins. In normal baby rats a G1-S block of non-synchronously proliferating hepatocytes was produced in two situations in which the antagonistic effect of normal blood proteins was eliminated: after treatment of the glycopeptide with leucine-aminopeptidase, and after mixing it with alpha 1-acid glycoprotein. The glycopeptide did not inhibit cell proliferation in kidney, submaxillary gland, or tongue epithelium. It seems to be the active component of a system that inhibits the proliferation of hepatocytes, probably by reducing their sensitivity to various mitogenic stimuli. 相似文献
2.
C. Nadal 《Cell proliferation》1973,6(5):437-446
The subcutaneous injection of irritating substances to baby rats results in a very reproducible wave of synchronized S phase DNA synthesis in hepatic cell involving 20% of the total population. Use has been made of this reaction to detect factors affecting DNA synthesis in hepatic cells. It enables substances to be tested during precise periods of the cell cycle. Two activities which were detected in normal adult rat serum, could not be found in the serum of the baby rat or of the partially hepatectomized adult rat: an activity inhibiting the progression of hepatocytes through the cell cycle in the late G1 phase, and an activity inducing the production of binucleate hepatocytes, effective in the late G1 and in the S phase. 相似文献
3.
Abstract. The physiologically active form of vitamin D3 , 1,25-dihydroxy-vitamin D3 , (1,25(OH)2 , D3 ), induces differentiation of several types of myeloid leukaemia cells. The acquisition of monocyte-like phenotype is accompanied by slower progression through the cell cycle, and G1 , block has been reported to be the basis of this effect. It is shown here that human promyelocytic leukaemia HL60 cells treated with analogues of vitamin D3 , which are potent inducers of monocytic differentiation, have an additional cell cycle block. Exposure to 10-7 m 1,25(OH)2 , D3 , or 1,25-(OH)2 ,-16-ene-D3 resulted in monocytic differentiation and the expected G1 , block evident at approximately 48 h in a rapidly differentiating variant of HL60 cells (HL60-G), and at 96 h in the more slowly differentiating HL60-240 cells. In addition, a G2 ,+M block was noted at approximately 72 h in HL60-G and HL60-240 cells. Exposure to vitamin D3 , analogues also markedly increased the number of dikaryons, suggesting that cytokinesis was impaired more than karyokinesis. Treatment with a third analogue 25-hydroxy-16,23-diene-D3 , produced little differentiation and had minimal effects on the cell cycle parameters. These findings indicate that vitamin D3 , analogues regulate cell proliferation by control of the transition of G1 , and G2 ,+M phases, reminiscent of the cdc2/CDK2 type of cell cycle control. 相似文献
4.
Pertussis Toxin-Insensitive Signaling of the ORL1 Receptor: Coupling to Gz and G16 Proteins 总被引:1,自引:1,他引:0
Joy S. C. Chan Lisa Y. Yung Jonathan W. M. Lee Ya-Lan Wu Gang Pei Yung H. Wong 《Journal of neurochemistry》1998,71(5):2203-2210
Abstract: Nociceptin/OFQ is the endogenous ligand for the G protein-coupled opioid receptor-like (ORL1 ) receptor. To elucidate the cellular functions of the ORL1 receptor, we examined its ability to interact with Gz and G16 , two pertussis toxin (PTX)-insensitive G proteins that are known molecular partners for the opioid receptors. In HEK 293 cells transiently expressing the ORL1 and dopamine D1 receptors, nociceptin/OFQ dose-dependently inhibited dopamine-stimulated cyclic AMP (cAMP) accumulation in a PTX-sensitive manner. However, PTX failed to block the nociceptin/OFQ-induced inhibition of dopamine-stimulated cAMP accumulation in HEK 293 cells co-expressing the α-subunit of Gz . This result indicates functional interaction between the ORL1 receptor and Gz . A similar result was obtained with retinoic acid-differentiated SH-SY5Y cells, which endogenously express both the ORL1 receptor and Gz . When the ORL1 receptor was transiently co-expressed in COS-7 cells with the α-subunit of G16 , nociceptin/OFQ dose-dependently stimulated the formation of inositol phosphates. Nociceptin-induced stimulation of phospholipase C was absolutely dependent on the co-expression of α16 and exhibited the appropriate ligand selectivity. In terms of its ability to interact with PTX-insensitive G proteins, the ORL1 receptor behaves very much like the opioid receptors. 相似文献
5.
Jonathan W. M. Lee Sushma Joshi Joy S. C. Chan Yung H. Wong 《Journal of neurochemistry》1998,70(5):2203-2211
Abstract: The μ-opioid receptor has recently been shown to stimulate phosphoinositide-specific phospholipase C via the pertussis toxin-sensitive G16 protein. Given the promiscuous nature of G16 and the high degree of resemblance of signaling properties of the three opioid receptors, both δ- and κ-opioid receptors are likely to activate G16 . Interactions of δ- and κ-opioid receptors with G16 were examined by coexpressing the opioid receptors and Gα16 in COS-7 cells. The δ-selective agonist [ d -Pen2 , d -Pen5 ]enkephalin potently stimulated the formation of inositol phosphates in cells coexpressing the δ-opioid receptor and Gα16 . The δ-opioid receptor-mediated stimulation of phospholipase C was absolutely dependent on the coexpression of simeter for quality control of blood units and irradiators. 13. Transfusion 1993 ; 33 : 898 – 901 . [PubMed link] 14. Butson MJ , Yu PK , Cheung T , et al . Dosimetry of blood irradiation with radiochromic film. Transfus Med 1999 ; 9 : 205 – 8 . [PubMed link] 15. Nath R , Biggs PJ , Ling CC , et al . AAPM code of practice for radiotherapy accelerators: Report of AAPM Radiation Therapy Task Group No. 45. Med Phys 相似文献
6.
S. K. Lahiri 《Cell proliferation》1973,6(5):509-514
A short-term in vitro method was employed to study the Mitomycin-C sensitivity of normal mouse bone marrow CFU without triggering the G0 -phase cells into the proliferative cycle. Comparison was made of the toxicities of the drug against cells in different phases of the cell cycle including G0 . Mitomycin-c killed CFU both in and out of the S-phase. No significant difference could be found between its toxicities against normal and proliferating CFU; along the exponential part of the survival curve 1·6 μg/ml concentration of the drug reduced survival to 10%. Although in the normal bone marrow only a few CFU are in the S-phase and are killed by the agent, presence of the sensitive G0 cells produce a significant amount of non-S-phase mortality. Among the proliferating CFU population the non-S-phase lethality is less due to the absence of G0 cells. About 75% of the S-phase cells are killed after incubation with 1 μg/ml drug; outside the S-phase, the lethality is about 40–50%. The studies indicate that the G0 cells which are situated near the G1 -S boundary are almost as sensitive to the drug as other non-S-phase cells like G1 cells. The clinical significance of the findings is discussed. 相似文献
7.
Abstract. The synthetic molecule N-Acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), corresponding to the low molecular weight inhibitory factor preventing in vivo haematopoietic stem cell (CFU-S) entry into DNA synthesis, was tested in two heterologous systems in vivo: adult regenerating rat liver and 10-day-old rat hepatocytes synchronized by an irritating trigger. In both systems, it was shown that doses of 2–8 μg kg-1 of tetrapeptide inhibited 50–70% of the hepatocyte G1 -S transitions. 相似文献
8.
Abstract. From the 20th day to the 30th day of life, the mitotic rhythm is progressively induced by a reduction in nocturnal values, while diurnal rhythms remain unchanged. Mitotic peaks emerge at 10.00 hours.
A labelling index wave occurs 8 hr before the corresponding mitotic wave, with a peak at 02.00 hours and a minimum in the evening, coincidental with the acrophase of plasma corticosterone level (activity phase).
Labelled mitoses curves and metaphase accumulation after colchicin injection show that the duration of the S, G2 and M phases remain approximately constant and that the circadian variation is due to a variation in the rate of cells that enter these successive phases. During the synchronization period (from day 20 to 30), the growth fraction decreases progressively. Adrenalectomy at this time is followed by a higher cell proliferation and all rhythms disappear after 2 days.
Corticosterone injected before the triggering of the rhythmic activity in 17-day-old rats immediately reduces the labelling index, while the mitotic index is decreased 10 hr later; this delay is equal to the S + G2 duration.
The results are discussed. They favour the hypothesis that the circadian variation of corticosterone is responsible for the induction of a circadian variation in developmental cell proliferation by inhibition of the G1 -S transition when it is higher in the evening.
The circadian rhythm of hepatic cell proliferation in rats appears on the 20th day of life, when the hypothalamo-adrenal axis is mature enough for circadian activity to occur. 相似文献
A labelling index wave occurs 8 hr before the corresponding mitotic wave, with a peak at 02.00 hours and a minimum in the evening, coincidental with the acrophase of plasma corticosterone level (activity phase).
Labelled mitoses curves and metaphase accumulation after colchicin injection show that the duration of the S, G
Corticosterone injected before the triggering of the rhythmic activity in 17-day-old rats immediately reduces the labelling index, while the mitotic index is decreased 10 hr later; this delay is equal to the S + G
The results are discussed. They favour the hypothesis that the circadian variation of corticosterone is responsible for the induction of a circadian variation in developmental cell proliferation by inhibition of the G
The circadian rhythm of hepatic cell proliferation in rats appears on the 20th day of life, when the hypothalamo-adrenal axis is mature enough for circadian activity to occur. 相似文献
9.
Naoto Ohnishi Hiroaki Kodania Satoshi Ando Atsushi Komamine 《Physiologia plantarum》1990,80(1):95-101
The effects of inhibition of the synthesis of protein, mRNA or rRNA on the progression of the cell cycle have been analyzed in cultures of Catharanthus roseus in which cells were induced to divide in synchrony by the double phosphate starvation method. The partial inhibition of protein synthesis at the G1 phase by anisoniycio or cycloheximide caused the arrest of cells in the G1 phase or delayed the entry of cells into the S phase. When protein synthesis was partially inhibited at the S phase, cell division occurred to about the same extent as in the control. When asynchronously dividing cells were treated with cycloheximide, cells accumulated in the G1 phase, as shown by flow-cytometric analysis. The partial inhibition of mRNA synthesis by α-amanitin at the G1 phase caused the arrest of cells in the G1 phase, although partial inhibition of mRNA synthesis at the S phase had little effect on cell division. In the case of inhibition of synthesis of rRNA by actinomycin D at the G1 phase, initiation of DNA synthesis was observed, but no subsequent DNA synthesis or the division of cells occurred. However, the addition of actinomycin D during the S phase had no effect on cell division. These results suggest that specific protein(s), required for the progression of the cell cycle, are synthesized in the G1 phase, and that the mRNA(s) that encode these proteins are also synthesized at the G1 phase. 相似文献
10.
11.
Abstract. Cellular uptake of [3 H]thymidine ([3 H]TdR) and incorporation into DNA of Ehrlich ascites tumour cells were studied in relation to the cell cycle by measuring the activity in the acid-soluble and insoluble parts of the cell material. Cells were synchronized at various stages of the cell cycle using centrifugal elutriation. The degree of synchrony of the various cell fractions was measured by flow-cytofluorometric DNA analysis. From the cellular uptake, the TdR triphosphate (dTTP) concentration of a mean cell in an unseparated cell population was calculated to be 20 × 10-18 mol/cell. The pool activity of G1 cells was unmeasurable but rose to maximum values at the border of the G1 -S phase. It decreased again during G2 . The [3 H]TdR incorporation into DNA was low during early S phase, reached a maximum value at two-thirds of the S phase and decreased again during late S phase. These changes in DNA synthesis were not due to changes in the dTTP pool being a limiting factor. During maximum DNA synthesis, 10%× min-1 of the dTTP pool was utilized, at which time the pool size also decreased by about 30%. Changes in pool size during the cell cycle have to be taken into account when the results of incorporation of radioactive TdR into DNA are discussed. 相似文献
12.
Actinomycin D (0.5 μg/ml) did not prevent M stage cells from entering G1 stage, but blocked their progress from G1 to S stage. The position of the block was approximately 1.4 hr before S stage or just after the beginning of G1 stage. Actinomycin D in this concentration also significantly depressed uridine-3 H uptake into G1 stage cells, but did not suppress leucine-3 H uptake by M and G1 cells. This suggests that some proteins may be synthesized in M and G1 stage cells by messenger RNA left over from the previous cell cycle. However, entry of G1 cells into S stage would require synthesis of new messenger RNA near the beginning of G1 stage. Puromycin (10 μg/ml) did not prevent M cells from entering G1 stage, but blocked their progress from G1 to S stage. The site of blockage was about 0.7 hr before S stage or in the first two-third of G1 stage. This might be the site where the cells synthesize new G1 proteins necessary for entry to S stage.
Comparison of sensitivities of G1 and G2 stages to the two antibiotics reveals that the puromycin sensitivity of G1 cells was similar to that of G2 cells, but the actinomycin D sensitivity of G1 was greater than that of G2 cells. 相似文献
Comparison of sensitivities of G
13.
Induction of replicative senescence by 5-azacytidine: fundamental cell kinetic differences between human diploid fibroblasts and NIH-3T3 cells 总被引:5,自引:0,他引:5
Abstract. To analyse the putative role of methylation of cytosine residues in the nuclear DNA as a regulatory step during cellular ageing, we incubated ageing human amniotic fluid derived fibroblast-like cells and non-ageing NIH-3T3 cells with 5-azacytidine. BrdUrd/Hoechst and acridine orange (AO) flow cytometry was used to compare the effects of the base analogue on cell proliferation and cell differentiation. In NIH-3T3 cultures, 96 h exposures to 4 μM 5-azacytidine caused diminished cell proliferation due to cell arrest in the G1 compartments of the second and third cell cycles of serum stimulated cells. The exit from the G0 /G1 compartment was not affected. The 5-azacytidine induced cell kinetic disturbances were unstable in NIH-3T3 cultures, such that pre-treated cells reverted to normal cell cycle transit within 2–3 days after termination of treatment. In contrast, 5-azacytidine pre-treated amniotic fluid derived fibroblast-like cell cultures showed persistently elevated G2 phase arrests and delayed G0 /G1 phase exit kinetics, which explain the premature cessation of proliferation observed in these primary cultures. In both cell systems, 5-azacytidine exposed cultures showed elevated numbers of G1 phase cells with increased RNA content as revealed by AO flow cytometry. Again, this effect was reversible in NIH-3T3 cells but not in amniotic fluid derived fibroblast-like cells. These contrasting responses to 5-azacytidine are likely to reflect intrinsic differences in methylation patterns or de novo methylase activity between ageing cell strains and non-ageing cell lines. 相似文献
14.
Regulation of α2A -Adrenergic Receptor Expression by Epinephrine in Cultured Astroglia from Rat Brain
Abstract: Epinephrine (Epi) mediates various physiological effects via α2A -adrenergic receptors (α2A -ARs). Studies in mice with a point mutation in the gene for α2A -AR have shown that these receptors are responsible for the centrally mediated depressor effects of α2 -AR agonists. These studies underscore the importance of understanding the basic cellular mechanisms involved in the expression of α2A -ARs, of which little is known. We use astroglia cultured from the hypothalamus and brainstem of adult Sprague-Dawley rats as a model system in which to study factors that regulate α2A -AR expression. These cells contain α2 -ARs, which are predominately of the α2A -AR subtype. Our studies have shown that Epi causes a dose- and time-dependent decrease in steady-state levels of α2A -AR mRNA and number of α2A -ARs, effects that are mediated via α1 - and β-adrenergic receptors (α1 -ARs and β-ARs). These effects of Epi on α2A -AR mRNA and α2A -AR number are mimicked by activation of protein kinase C or increases in cellular cyclic AMP, which are intracellular messengers activated by α1 -ARs and β-ARs, respectively. Taken together, these results indicate that expression of α2A -ARs is regulated in a heterologous manner by Epi, via α1 -AR- and β-AR-mediated intracellular pathways. 相似文献
15.
Cytophotometric determination of single-cell DNA after repeated 3 H-thymidine labelling of the JB-1 ascites tumour in the plateau phase of growth showed a massive accumulation of unlabelled cells with both G1 and G2 content. Autoradiography combined with cytophotometry or colcemid block demonstrated that some of these unlabelled cells were rapidly triggered into the cell cycle when plateau tumours were transferred to new hosts. This indicated that tumour cells may be held up in non-cycling stages corresponding to both the G1 and the G2 phase of the cell cycle. 相似文献
16.
Structure and Functional Characterization of a Novel Human Low-Voltage
Activated Calcium Channel 总被引:7,自引:0,他引:7
Mark E. Williams Mark S. Washburn Michael Hans Arturo Urrutia Paul F. Brust Patricia Prodanovich Michael M. Harpold & Kenneth A. Stauderman 《Journal of neurochemistry》1999,72(2):791-799
Abstract : We have isolated and characterized overlapping cDNAs encoding a novel, voltage-gated Ca2+ channel α1 subunit, α1H , from a human medullary thyroid carcinoma cell line. The α1H subunit is structurally similar to previously described α1 subunits. Northern blot analysis indicates that α1H mRNA is expressed throughout the brain, primarily in the amygdala, caudate nucleus, and putamen, as well as in several nonneuronal tissues, with relatively high levels in the liver, kidney, and heart. Ba2+ currents recorded from human embryonic kidney 293 cells transiently expressing α1H activated at relatively hyperpolarized potentials (-50 mV), rapidly inactivated (τ = 17 ms), and slowly deactivated. Similar results were observed in Xenopus oocytes expressing α1H . Singlechannel measurements in human embryonic kidney 293 cells revealed a single-channel conductance of ~9 pS. These channels are blocked by Ni2+ (IC50 = 6.6 μ M ) and the T-type channel antagonists mibefradil (~50% block at 1 μ M ) and amiloride (IC50 = 167 μ M ). Thus, α1H -containing channels exhibit biophysical and pharmacological properties characteristic of low voltage-activated, or T-type, Ca2+ channels. 相似文献
17.
M. Ffrench † J. P. Magaud‡ M. Arzounian C. Souchier C. Charrin† P. A. Bryon 《Cell proliferation》1990,23(4):251-260
Abstract. In some cases of acute lymphoblastic leukaemia (ALL) the percentage of cells in G2 + M is higher than anticipated when compared with the percentage in S phase. This increase in G2 + M, as detected by flow cytometry measurement of DNA content, may be due to an accumulation of cells, either in G 2 or during the end of S phase; it may also be related to the existence of small tetraploid clones generally ignored by cytogeneticists. In order to identify possible subpopulations of cells with a DNA index ≥ 2-0, we have compared the results of a cytogenetic analysis to the G2 + M values. We have also studied the distribution of S phase cells in 24 cases of ALL by incorporating 5-bromodeoxyuridine, labelling the cells by indirect immunofluorescence, and analysing them by flow cytometry after propidium iodide staining. The distribution of cells during S phase was quantified: no accumulation of cells was ever observed at the end of S phase. The question of the existence of small tetraploid clones, G2 arrested cells or cells with a G2 elongation remains open. However, we feel that it is more probable that, in this pathology, an elongation of the duration of G2 occurs. 相似文献
18.
19.
Cell-cycle dependence of a ganglioside glycosyltransferase activity and its inhibition by enkephalin in a neurotumor cell line 总被引:3,自引:3,他引:0
Abstract: Rat glioma mouse neuroblastoma hybrid neurotumor cells (NG108-15), synchronized by amino acid deprivation, showed a cell-cycle-dependent peak of activity of a ganglioside N-acetylgalactosaminyl transferase 14-24 h following release from the cell cycle block (S/G2 phase). Maximal expression of two typical lysosomal hydrolases, N-acetyl-β-hexosaminidase and β-galactosidase, occurred between 18 and 21 h following release (S phase), declining to G1 phase levels during the peak of N-acetylgalactosamine (GalNAc) transferase activity. In addition, glycosyltransferase activity in G2 phase cells showed an increase in apparent Vmax (suggesting the presence of more enzyme/mg of cell protein) and apparent binding affinity for uridine diphosphate N-acetylgalactosamine (UDP-GalNAc) (32 versus 14 M) when compared to transferase activity in the G1 phase. However, the opioid peptide enkephalin [D-Ala2 , o-Leu5 ], which inhibits ganglioside GalNAc transferase activity in unsynchronized NG108-15 cultures, was much more inhibitory in whole cells 8 h after release from the cell cycle block (G1 phase) than in cells 20 h after release (G, phase), with 50% inhibition occurring at 2 ± 10-9 M and 2 ± 10-7 M, respectively. These results suggest that the GalNAc transferase activity is regulated in more than one way during the cell cycle, since both Vmax and Km changes are observed, and that the cyclic AMP-dependent mechanism by which opiates reduce transferase activity is receptor mediated and cell cycle dependent. 相似文献
20.
F. Nicoletti M. L. Barbaccia M. J. Iadarola O. Pozzi H. E. Laird II 《Journal of neurochemistry》1986,46(1):270-273
Abstract: We found that the binding of [3 H]prazosin, a selective ligand for α1 -adrenergic recognition sites, is significantly lower in the frontal cortex of the genetically epilepsy-prone rats (GEPRs), as compared with normal Sprague-Dawley rats. Scatchard analysis reveals a decrease in the B max of [3 H]prazosin binding with no change in the apparent K D , suggesting that there are fewer α1 -adrenergic recognition sites in the frontal cortex of the GEPR. This abnormality is associated with a reduced capacity of norepinephrine (NE) to stimulate [3 H]inositol monophosphate ([3 H]IP1 ) formation in frontal cortex slices prelabeled with [3 H]inositol. No significant differences in [3 H]prazosin binding as well as NE-stimulated [3 H]IP1 formation have been observed in other brain regions including hippocampus, corpus striatum, and inferior colliculus. These results indicate that a deficit in the α1 -adrenergic receptor system in the frontal cortex may play a role in the seizure process in the GEPR. 相似文献