Showing papers on "Cell growth published in 1971"
TL;DR: Addition of thyrotropin releasing hormone to the medium of 2 clonal strains of functional rat pituitary cells stimulated the production of prolactin and inhibited growth hormone production and there was no effect on cell growth.
411 citations
233 citations
TL;DR: The dorsal funiculus in cervical spinal cords of rats from 3 to 120 days postnatal was studied in order to document and quantitate glial cell development and axonal growth as related to the initiation and progress of central myelination.
Abstract: The dorsal funiculus in cervical spinal cords of rats from 3 to 120 days postnatal was studied in order to document and quantitate glial cell development and axonal growth as related to the initiation and progress of central myelination. Within the dorsal funiculus are three major and distinct tracts, each having distinct developmental trends and adult characteristics in terms of fiber sizes and amount of myelin. These tracts are the cuneate and gracile fasciculi and the cortico-spinal tracts.
Glial cell counts and cross-sectional surface area determinations of each tract at increasing ages show that the initial rate of glial population increase is similar. However, each tract is unique in terms of the age at which a maximum population density is reached and the rate at which the expected population dilution takes place. An electron-microscopic examination indicates that oligodendrocytes constitute over 85% of the total glial population throughout the development period surveyed. As such, these cells are primarily responsible for the population density changes.
The diameters of unmyelixgnated fibers, promyelin fibers and some myelinated fibers in these tracts were measured at 5, 10, 15, 20 and 120 days postnatal. This was done both for the purpose of relating glial population density changes with the initiation and decline of active myelination, and for determining whether or not a critical diameter for myelination exists in the CNS as was found in peripheral nerves (Matthews, '68). For each tract there is a characteristic sequence of events involving not only myelination, but also changes in diameter distribution just prior to the appearance of myelin and during the period of active myelin formation. These events coincide with the concentration and dilution of the glial population, but it is also evident that there is no critical and constant diameter in the CNS above which all axons are myelinated and below which all are unmyelinated. Myelin appears first on larger axons, but as the animal matures, it is found on progressively smaller axons until between 20 and 120 days, axons 0.2–0.4 μ in diameter acquire myelin. Thus, myelination begins with axons destined to be large and then extends down to those which enlarge very little prior to acquiring myelin and remain very small even in adult animals.
Finally, from the determination, in adult rats, of the number of axons and oligodendrocytes in a defined volume of each tract and an estimation of internode length, the ratio of internodes to oligodendrocytes was calculated. The specific values obtained could vary by as much as ±50% and are only meant to serve as indicators of a trend. However, it is suggested that the number of internodes per oligodendrocyte may be inversely proportional to the length of the internode.
225 citations
TL;DR: Evidence is summarized which indicates that treatment with T3 affects cell formation rather than cell destruction, resulting in a 30–40% reduction in the number of cells formed after birth, which suggests that the sensitivity of the tissue to thyroid hormone depends on the developmental state of the cells.
206 citations
TL;DR: During late larval stages of Xenopus laevis the neural retina increases in area in concert with the increase in diameter of the eye and there is an increase in thickness of the inner nuclear layer over the whole expanse of the retina.
142 citations
TL;DR: Wounding experiments showed that pH affected cell migration in a manner similar to its effects on cell multiplication, but those cells which migrated into the denuded region multiplied as rapidly at low pH as at high pH.
Abstract: Sparse and dense cultures of chick embryo cells were affected differently by pH. The rates of cell multiplication and of thymidine-3H incorporation into DNA of dense cultures were increased as the pH was increased from 6.6 to 7.6. At pH higher than 7.6 the rate of multiplication decreased slightly in the dense cultures, but the rate of thymidine-3H incorporation continued to increase. The discrepancy was due in part to cell death and detachment at very high pH, and in part to a more rapid uptake of thymidine-3H at very high pH. Sparse cultures were much less sensitive to pH reduction and, when a suitably conditioned medium was used to minimize cell damage, very sparse cultures grew almost as well at pH 6.7 as at higher pH. The rates of cell multiplication and thymidine-3H incorporation at low pH decreased in the initially sparse cultures before they reached confluent cell densities. There was no microscope evidence of direct contact between plasma membranes of cells at these densities although the parallel orientation indicated that the cells were influencing locally each other's behavior. Even at much higher cell densities, electron microscopy revealed large intercellular gaps partly filled with a fragmentary electron-opaque material suspected to be glycoprotein. Wounding experiments showed that pH affected cell migration in a manner similar to its effects on cell multiplication. Low pH inhibited cell migration, but those cells which migrated into the denuded region multiplied as rapidly at low pH as at high pH. The effects of pH on growth were correlated with effects on the uptake of 2-deoxyglucose-3H. Dense populations of cells inhibited by low pH were stimulated to incorporate thymidine-3H by the addition of small amounts of diethylaminoethyl-dextran. Rous sarcoma cells at high cell density were less sensitive to pH than were normal cells at the same density, but were more sensitive than sparse normal cultures. The results suggest that cell growth is inhibited through the combined effects of both lowered pH and high cell density on cell surface permeability.
127 citations
TL;DR: The wide range of tumour doubling times seems largely to be due to differences in the proportions of proliferating cells (growth fraction) and rates of cell loss, and the slowing down of the growth rate of a solid tumour depends on these two parameters.
Abstract: The radiosensitivity of a cell varies throughout the cell cycle, and the effects of a course of radiotherapy depend therefore on the distribution of the proliferating cells into the various phases of the cell cycle and on the proportion and characteristics of the quiescent cells. This is true not only of the first dose of radiation, but also applies when the subsequent doses are delivered. The difference in cell cycle durations between normal and malignant tissues and between different experimental and human tumour types is relatively small. It cannot be evoked to explain the wide range of tumour doubling times, which seems largely to be due to differences in the proportions of proliferating cells (growth fraction) and rates of cell loss. The slowing down of the growth rate of a solid tumour depends on these two parameters. In solid tumours, these parameters may vary from the centre of the tumour to its periphery and appear to be influenced by environmental factors. At least four types of factors...
124 citations
TL;DR: During the first ten minutes after the beginning of a continuous exposure of rat thymocyte populations (maintained in vitro) to epinephrine, there is an increase in the cellular concentration of cyclic AMP.
Abstract: : During the first ten minutes after the beginning of a continuous exposure of rat thymocyte populations (maintained in vitro) to epinephrine, there is an increase in the cellular concentration of cyclic AMP. The hormone also increases the activity of a crude preparation of the thymocyte's cyclic AMP-forming enzyme, adenyl cyclase. Between 30 and 45 minutes after the beginning of exposure to epinephrine, an additional part of the cell population begins to synthesize deoxyribonucleic acid (DNA). These changes are finally followed two to four hours later by an increase of the flow of cells into mitosis. Since cyclic AMP itself is known to stimulate both the initiation of DNA synthesis and thymocyte proliferation, and since the mitogenic action of epinephrine is shown to be potentiated by caffeine and inhibited by imidazole, it is concluded that the mitogenic action of this hormone is mediated by the cyclic nucleotide. (Author)
111 citations
TL;DR: This chapter discusses the fate of sex steroid hormones in their target tissues and their interaction with the molecule(s) of primary importance for the physiological response and special emphasis has been given to the idea that there is a classification of binding proteins involved in steroid action at the cellular level.
Abstract: Publisher Summary This chapter discusses the fate of sex steroid hormones in their target tissues and their interaction(s) with the molecule(s) of primary importance for the physiological response(s). Sex steroids, in particular androgens, are involved in differentiation processes, especially in the irreversible determination and organization of secondary sex organs. Hormone activity on already differentiated secondary sex organs concerns functional activity—secretion, mobility—and growth, which depend on cell size and cell number, an excess leading to hypertrophy and hyperplasia. The effects of hormones are generally not limited to a single parameter of the responsive tissue but may affect cell development, secretion, and replication in an automatic, coordinated manner. Many aspects of the response of secondary sex organs to hormones injected in vivo have been studied, such as constitutive proteins, enzymes, phospholipids, and nucleic acids. The only in vitro system for which the specific response is established involves progesterone and utilizes cultured oviduct cells of estrogenized chicken. Special emphasis has been given to the idea that there is a classification of binding proteins involved in steroid action at the cellular level.
105 citations
TL;DR: It was, therefore, somewhat surprising to find that the enhancing effect of the carrier-primed cells, once they had been generated, is not inhibited by x-irradiation.
Abstract: The in vitro primary response of mouse spleen cell suspensions to 2,4,6-trinitrophenyl(Tnp)-erythrocytes has been studied. The number of anti-Tnp plaque-forming cells that arise after antigenic stimulation in vitro is greatly enhanced by prior immunization in vivo with the carrier erythrocyte. The enhancement is antigen specific. The priming for an enhanced response can be elicited with very low antigen doses and is often apparent 24 hr after immunization. It is marked from day 3 to day 14. Spleen cells from carrier-primed mice will enhance the anti-Tnp response of normal cells when mixed cultures of the two cell populations are challenged with Tnp-erythrocytes in vitro. The carrier-primed cells mediating this enhancing effect are thymus derived.
The development of the thymus-derived, carrier-specific cell population has been generally assumed to involve the antigenic stimulation of cell proliferation. It was, therefore, somewhat surprising to find that the enhancing effect of the carrier-primed cells, once they had been generated, is not inhibited by x-irradiation.
94 citations
TL;DR: Prostaglandin A 1 and E 1, but not F 1 α or F 2 α, stimulate thymic lymphocyte adenylate cyclase with resultant increases in the intracellular level of cyclic AMP and the rate of cell proliferation.
TL;DR: The cultured skin fibroblast from both the homozygous affected individual and the heterozygous parents can be distinguished from normals by decreased cell growth in culture.
Abstract: Progeria is an autosomal recessive disorder showing precocious senility. The cultured skin fibroblast from both the homozygous affected individual and the heterozygous parents can be distinguished from normals by decreased cell growth in culture. Mitotic activity, DNA synthesis, and cloning efficiency are markedly reduced.
TL;DR: Findings suggest that Ewing's tumor is a neoplasm of myelogenous origin with a manner of growth and spread analogous to plasma cell myeloma.
Abstract: A typical Ewing's tumor was grown in tissue culture for a prolonged period of time. The pattern of growth was that of a malignant mesenchymal tumor. Cell growth, in vitro, was accompanied by accumulation of glycogen and acquisition of hydrolytic enzyme activity, and some clones developed ultrastructural features characteristic of developing myelocytes. These findings suggest that Ewing's tumor is a neoplasm of myelogenous origin with a manner of growth and spread analogous to plasma cell myeloma.
TL;DR: The different repair-replication abilities of cells from different species of mammals suggest that mammalian cells may express different levels of host-cell reactivation, confirmed using u.v.-irradiated herpes simplex virus assayed in mouse, rat, monkey, and human cells.
Abstract: SummaryThe different repair-replication abilities of cells from different species of mammals suggest that mammalian cells may express different levels of host-cell reactivation. This was confirmed using u.v.-irradiated herpes simplex virus assayed in mouse, rat, monkey, and human cells. The survival curves usually had two components, the slopes of both varying among the different cells. The slopes of the first, sensitive components varied considerably (factor of 4), implying that there are different amounts of host-cell reactivation in this component. The slopes of the second, resistant components also varied, implying different extents of host-cell reactivation there also. That the HCR of the first component apparently varied independently of that of the second component among the different host cells suggested that different mechanisms were responsible for the two HCR's. At the virus concentrations used, multiplicity reactivation was not found. The known cellular radiation recovery mechanisms, repair re...
TL;DR: Results indicate that the inability to lyse the cells in the presence of specific anti-viral antibody and complement during the logarithmic phase of cell growth is not due to the lack of expression of Moloney virus antigen on the cell surface, inaccessibility of this surface antigen to antibody, or failure to activate the complement effector system.
Abstract: The expression of Moloney leukemia virus on the surface of a viral-induced lymphoma cell, availability of the virus to anti-viral antibody, and the nature and extent of activation of the complement system during the cell cycle were studied in vitro. Viral antigen was present on the cell surface, accessible to antibody, and was able to activate complement in the presence of antibody throughout all cellular growth phases, while cytotoxicity was confined to the G1 phase of cell growth. In addition, when cells were arrested in metaphase, viral antigen could be demonstrated on the cell surface by immunofluorescence, and budding virus was seen by electron microscopy. All nine components of complement were activated on the addition of antibody throughout the cell cycle. Additional experiments indicated that in the presence of antibody, C3 and/or C4 were immunospecifically bound to viral-induced lymphoma cells throughout the cell cycle as a result of complement activation. These results indicate that the inability to lyse the cells in the presence of specific anti-viral antibody and complement during the logarithmic phase of cell growth is not due to the lack of expression of Moloney virus antigen(s) on the cell surface, inaccessibility of this surface antigen(s) to antibody, or failure to activate the complement effector system.
TL;DR: It is postulated that adenylate cyclase activity may be enhanced by cell to surface contact or cell to cell interaction and that this phenomenon may represent a form of self regulation or modulation of hormonal response by a tissue.
Abstract: HeLa S3 cells, a clonal strain adapted for growth in suspension culture, contain adenylate cyclase activity that is stimulated by glucagon, prostaglandin E1, and epinephrine. Total enzymatic activity and response to hormones is increased as a result of these cells being in stationary culture for several days. The parental strain of HeLa cells normally grown in stationary culture shows even greater adenylate cyclase activity. Hepatoma (HTC) cells grown in suspension culture have no detectable adenylate cyclase activity, but when grown in stationary culture they contain low, but detectable, amounts of adenylate cyclase, which is stimulated by glucagon, epinephrine, or prostaglandins. Chang's liver cells, both suspension and stationary culture, contain relatively high levels of adenylate cyclase that is stimulated by epinephrine or prostaglandin E1, with differences in activity depending upon culture conditions. Adenylate cyclase of 3T3 and L929 mouse fibroblasts respond to catecholamines, as well as to prostaglandin E1, but not to glucagon. Characteristic increases in basal activity of adenylate cyclase and in activity in the presence of hormone occurred as cell density increased during stationary culture of certain cell lines, but do not occur with fluoride ion present. In addition to the influence of growth conditions and rate or phase of cell growth on cyclase activity and hormonal response, the cultured cell lines frequently showed marked differences in activity from one another; malignant cells generally exhibited less activity. It is postulated that adenylate cyclase activity may be enhanced by cell to surface contact or cell to cell interaction and that this phenomenon may represent a form of self regulation or modulation of hormonal response by a tissue.
TL;DR: Evidence is presented for the first time demonstrating the incorporation of 2-DG into yeast cell wall material and showing that S. cerevisiae grown in the presence of 1-deoxy-d-glucose formed weakened cell walls responsible for the osmotic fragility.
Abstract: The growth inhibition and the lysis of Saccharomyces cerevisiae caused by 2-deoxy-d-glucose (2-DG) were shown to be a consequence of unbalanced cellular growth and division. The lysis, but not the repression of growth and osmotic fragility of cells, could be suppressed by the addition of mannitol as an osmotic stabilizer. This result, as well as the morphological changes observed in the cells and changes in the chemical composition of the cell walls, showed that S. cerevisiae grown in the presence of 2-DG formed weakened cell walls responsible for the osmotic fragility. Evidence is presented for the first time demonstrating the incorporation of 2-DG into yeast cell wall material. Other data suggest that the inhibition of yeast growth by 2-DG results from an interference of phosphorylated metabolites of 2-DG with metabolic processes of glucose and mannose involved in the synthesis of structural cell wall polysaccharides.
TL;DR: Differential susceptibility to acute cyto-intoxication by AMD, or other inhibitors of RNA synthesis, among different types of cultured cells is analogous to that observed in vivo in certain tissues and tumors, and cannot be accounted for by differences in the effect of AMD on RNA, DNA, or protein syntheses.
Abstract: Actinomycin D (AMD) at concentrations that inhibit cellular RNA synthesis by 85% or more causes an acute phase of lethal cell degeneration in HeLa cultures beginning as early as 3 hr after drug exposure, resulting in the nearly complete loss of viable cells by 12 hr. The loss of cells during this acute phase of lethality is closely dose dependent. Vero, WI38, or L cells are not susceptible to this early acute cyto-intoxication by AMD, and may begin to die only after 1–2 days. Differential susceptibility to acute cyto-intoxication by AMD, or other inhibitors of RNA synthesis (daunomycin or nogalamycin), among different types of cultured cells is analogous to that observed in vivo in certain tissues and tumors, and cannot be accounted for by differences in the effect of AMD on RNA, DNA, or protein syntheses, or by the over-all loss of preformed RNA. Actinomycin D in a dose that inhibits RNA synthesis causes an equivalent loss of the prelabeled RNA in all the cell types studied. Inhibition of protein synthesis with streptovitacin A or of DNA synthesis with hydroxyurea does not cause acute lethal injury in HeLa cells as does inhibition of RNA synthesis. Furthermore, since Vero or L cells divide at about the same rate as HeLa cells, no correlation can be drawn between the rate of cell proliferation and susceptibility to the cytotoxicity of AMD. Susceptibile cells are most vulnerable to intoxication by AMD in the G1-S interphase or early S phase. Inhibition of protein synthesis (which protects cells against damage by other agents affecting DNA) does not protect against AMD-induced injury. Although HeLa cells bind more AMD at a given dose than Vero or L cells, the latter cell types, given higher doses, can be made to bind proportionally more AMD without succumbing to acute cyto-intoxication. It is suggested that the differential susceptibility of these cell types to acute poisoning by AMD may reflect differences among various cells in the function or stability of certain RNA species not directly involved in translation whose presence is vital to cells. In HeLa cells, these critical species of RNA are presumed to have a short half-life.
TL;DR: There are indications that the rate of initiation of mitosis is less closely associated with the rates of protein synthesis than is the rateof initiation of DNA synthesis, and there is evidence that at least 40% of the cells remained in the cycle well into the decline period, and no evidence that any cells left thecycle.
TL;DR: In mouse cell lines after transformation with SV40 or polyoma virus there was shown to be a reduction in the content of higher ganglioside homologs and in the activity of an enzyme necessary for the synthesis of the highergangliosides.
TL;DR: In growing 3T6 and “old” human fibroblast lines, omission of serum inhibits non-collagen protein synthesis more strongly than collagen synthesis, so that a higher percentage of the protein synthesized is collagen.
TL;DR: The results of experiments designed to test each of the possibilities for the inhibitory effect of interferon on the division cycle of L1210 cells are presented.
Abstract: We have previously described the inhibitory effect of interferon preparations on the multiplication of L1210 cells in vitro and presented the experimental results suggesting that interferon itself was the responsible factor (3, 4, 6) . This inhibition could be due to a decrease in the number of cells capable of dividing, to a prolongation of the cell generation time, to a decrease in the doubling potential of each cell between subcultivation and the stationary phase, or to a combination of these effects . We present here the results of experiments designed to test each of these possibilities by analyzing the effect of interferon on the division cycle of L1210 cells .
TL;DR: The sensitizing action of the halogenated compound was not ascribed to an overall increase of base damage but to qualitatively different lesions in BU-DNA, viz.
Abstract: SummaryPhotochemical damage produced by u.v.-irradiation was studied in normal and 5-bromouracil-substituted DNA (BU-DNA) of mammalian cells in relation to repair processes known to occur in these cells. The main photoproduct of incorporated bromouracil was identified as uracil, accompanied by a single-strand break in the DNA chain. Uracil was excised from the DNA and the break was rejoined at a rate much faster than the excision of pyrimidine dimers from unsubstituted DNA. Therefore, the sensitizing action of the halogenated compound was not ascribed to an overall increase of base damage but to qualitatively different lesions in BU-DNA, viz. Double strand breaks and DNA-protein crosslinks.
TL;DR: Cell growth, mitotic frequency and thymidine-H 3 incorporation were all decreased by the presence of mimosine or 3,4-dihydroxypyridine and the toxic effects of these compounds were decreased bythe presence of Al 3+.
TL;DR: It is found that adrenaline alone reduced epidermal mitotic activity in mouse ears by about 50% in vitro and this action was augmented by adrenaline.
Abstract: CATECHOLAMINES probably influence cell proliferation by delaying cells in the premitotic phase1,2. Bullough and Laurence found that crude skin extracts contained a tissue-specific protein (chalone) which inhibited epidermal cell proliferation and that the action of this extract was augmented by adrenaline3. They later found that adrenaline alone (0.00025 µg/ml.) reduced epidermal mitotic activity in mouse ears by about 50% in vitro4.
TL;DR: The specific activity of mouse neuroblastoma choline-O-acetyltransferase and thymidylate synthetase increased when the rate of cell division was restricted and when nondividing cells again entered the logarithmic phase of cell growth, respectively.
Abstract: The specific activity of mouse neuroblastoma choline-O-acetyltransferase (EC 2.3.1.6.) increased 5.7-fold when the rate of cell division was restricted (as compared to cells kept rapidly dividing for 9 days); the specific activity of mouse neuroblastoma thymidylate synthetase increased 2.4-fold when nondividing cells again entered the logarithmic phase of cell growth. The highest specific activities for choline-O-acetyltransferase and lowest specific activities for thymidylate synthetase were obtained from cultures where cell division was restricted; the opposite result was observed when the cells were growing rapidly. Thus, the regulation of these two enzymes is out of phase with respect to each other and is dependent on the rate of cell division. The inverse relationship for the regulation of these two enzymes is discussed in relation to the needs of mitotic versus differentiated neuroblastoma cells.