PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Cell Enlargement”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1986

Effects of NaCl and CaCl(2) on Cell Enlargement and Cell Production in Cotton Roots.

In many crop species, supplemental Ca(2+) alleviates the inhibition of growth typical of exposure to salt stress. In hydroponically grown cotton seedlings (Gossypium hirsutum L. cv Acala SJ-2), both length and weight of the primary root were enhanced by moderate salinities (25 to 100 millimolar NaCl) in the presence of 10 millimolar Ca(2+), but the roots became thinner. Anatomical analysis showed that the cortical cells of these roots were longer and narrower than those of the control plants, while cortical cells of roots grown at the same salinities but in the presence of only 0.4 millimolar Ca(2+) became shorter and more nearly isodiametrical. Cell volume, however, was not affected by salinities up to 200 millimolar NaCl at either 0.4 or 10 millimolar Ca(2+). Our observations suggest Ca(2+)-dependent effects of salinity on the cytoskeleton. The rate of cell production declined with increasing salinity at 0.4 millimolar Ca(2+) but at 10 millimolar Ca(2+) was not affected by salinities up to 150 millimolar NaCl.

Journal Article↗
PubMed1984

Ly-2+ T cell enlargement and null cell proliferation occur at the onset of splenomegaly and autoantibody production in New Zealand Black mice.

Splenic T and B lymphocyte and null cell populations were analyzed in NZB mice as autoimmune disease developed during the first year of life. In the B lymphocytes, a progressive shift occurred from the surface IgD bright subset to the surface IgM bright subset. There was a slight increase in the ratio of Ly-2- to Ly-2+ T cells. Splenomegaly was not detected until after 40 wk of age and was primarily due to an increase in the number of null cells. This change was accompanied by an increase in the size, as determined by narrow-angle forward light scatter, of the Ly-2+ but not the Ly-2- T cells, an elevation of IgG-containing plasma cells, and the appearance of anti-erythrocyte autoantibody. The splenic B cell subset distribution and the enlargement of the Ly-2+ T cells were reflected in the peripheral blood, whereas the T cell subset ratio was not. The B cell subset alteration did not correlate with any of the other changes observed. Statistical associations were found between the ratios of T cell subsets, the enlargement of the Ly-2+ T cells, and the increased number of null cells, suggesting a linkage among those late changes that immediately precede the development of overt autoimmune disease.

Aging↗
PubMed1992

Role of septal fibrosis in development of hepatic circulatory disturbance in the presence of liver cell enlargement.

The effect of septal fibrosis on hepatic circulation was examined in rats with enlarged liver cells. Septal fibrosis was produced by horse serum injections and liver cell enlargement by a choline-deficient diet. Septal fibrosis alone did not induce any disturbance of hepatic circulation. In fatty livers, a slight increase in sinusoidal vascular resistance and a slight elevation of portal vein pressure were found. However, in fatty livers with septal fibrosis, portal hypertension and sinusoidal vascular resistance were higher than in fatty livers without septal fibrosis. These experimental data clearly demonstrate that septal fibrosis alone has no effect on hepatic circulation, but septal fibrosis in the presence of liver cell enlargement markedly affects sinusoidal circulation and induces portal hypertension. The augmentation of sinusoidal vascular resistance by septal fibrosis in the presence of liver cell enlargement might be due to the severe deformation of the sinusoids by enlarged liver cells in the limited spaces surrounded by septal fibrous bands.

Animals↗
PubMed2004

Histological, ultrastructural, and in situ hybridization study on enlarged cells in grouper Epinephelus hybrids infected by grouper iridovirus in Taiwan (TGIV).

Grouper iridovirus in Taiwan (TGIV) infection in the Epinephelus hybrid is a major problem in the grouper industry. ATPase gene sequences indicate that this virus is closely related to cell hypertrophy iridoviruses. Histologically, the appearance of basophilic or eosinophilic enlarged cells in internal organs is the most characteristic feature of this disease. These cells are acid-phosphatase positive and are able to phagocytose injected carbon particles. In our study, TGIV infection inhibited normal phagocytic ability in these cells in vivo after 4 d post-infection (p.i.) but not before 2 d p.i. Their staining properties and phagocytic ability suggested a monocyte origin of enlarged cells, which appeared in high numbers in the trunk kidney, head kidney, spleen and gill. After infection, the enlarged cells first appeared in the spleen, with an abundance peak at 64 h p.i. (Peak 1); at 120 h p.i., a second peak (Peak 2) occurred in the spleen, head kidney, trunk kidney and gill. Lower numbers of enlarged cells were observed in the liver, muscle, heart, eye, intestine, but no enlarged cells were found in the brain. A TGIV-specific DNA probe labeled most of the basophilic but not eosinophilic enlarged cells. Nuclei of infected cells were labeled during an early stage of the infection; at later stages, both nuclei and cytoplasms were labeled. Ultrastructurally, heterochromatins of the infected cells were marginated or aggregated to one side of the nuclei during the early stages of infection. Damage and rupture of the nuclear membrane started before formation of the viromatrix. Capsids were assembled in ring-shaped or disc-shaped structures. Bullet-shaped electron-dense material was present near the incomplete virus particles, and is speculated to be inserted into the capsids later.

Adenosine Triphosphatases↗
PubMedDate not supplied

Soybean cell enlargement oscillates with a temperature-compensated period length of ca. 24 min.

Rate of enlargement of epidermal cells from soybean, when measured at intervals of 1 min using a light microscope equipped with a video measurement system, oscillated with a period length of about 24 min. This oscillation parallels the 24-min periodicity observed for the oxidation of NADH by the external plasma membrane NADH oxidase. The increase in length was not only non-linear, but intervals of rapid increase in area alternated with intervals of rapid decrease in area. The length of the period was temperature compensated, and was approximately the same when measured at 14, 24 and 34 degrees C even though the rate of cell enlargement varied over this same range of temperatures. These observations represent the first demonstration of an oscillatory growth behavior correlated with a biochemical activity where the period length of both is independent of temperature (temperature compensated) as is the hallmark of clock-related biological phenomena.

Cell Size↗
PubMed1968

Studies on the role of RNA synthesis in auxin induction of cell enlargement.

Selective inhibitors were used to study the connection between nucleic acid synthesis and indoleacetic acid (IAA) induction of cell enlargement. Actinomycin D (act D) and azaguanine (azaG) almost completely inhibit IAA-induced growth in aged artichoke tuber disks when they are added simultaneously with IAA. In contrast, when they are added 24 hours after the hormone, these inhibitors have little or no effect on the induced growth which continues for 48 hours or more with little or no inhibition. Inhibitors of protein synthesis still stop growth when applied 24 hours after the IAA, thus protein synthesis and presumably supporting metabolism are still essential.In corn coleoptile sections auxin-induced growth did not show any pronounced tendency to become less sensitive to act D as the IAA treatment progressed. Act D did not completely inhibit the response to IAA unless the sections were pretreated with act D for 6 hours. In contrast to act D, cordycepin produced almost complete inhibition of IAA-induced growth when added with the IAA.Although IAA has a very large and very rapid stimulatory effect (within 10 min) on incorporation of (32)P-orthophosphate into RNA in disks, it did not cause a detectable change in the base composition of the RNA synthesized. Furthermore, the promotive effect could be accounted for through increased uptake of the (32)P. That much of the RNA synthesis in these tissues is not necessary for auxin action is indicated by the results with fluorouracil (FU). FU strongly inhibits RNA synthesis, probably acting preferentially on ribosomal RNA synthesis, without inhibiting auxin-induced growth in the disks or coleoptile sections. FU also strongly inhibited respiration in auxin-treated disks indicating that the large promotion of respiration by auxin likewise may not be entirely necessary for growth.At least in the artichoke disks, RNA synthesis is required for auxin induction of cell enlargement and not for cell enlargement itself.The possible relationships of auxin induction of cell enlargement and RNA synthesis are discussed.

Journal Article↗
PubMed1980

Decreased density in membrane localized macromolecules in cells enlarged after X-irradiation or polyploidization.

Cytophotometric measurements of DNA, dry mass (total proteins) and surface localized IgM and Ia were performed on individual cells of a Burkitt lymphoma derived cell line after X-irradiation and after polyploidization. Blockage of cell division was achieved with 250 r, and an arrest in G2 was found 48 hr after irradiation. The cells unable to divide increased in volume and total protein content. Cell enlargement was also achieved by polyploidization. The amount of surface localized IgM and Ia did not keep up pace with the increase in total proteins, thus their density decreased. This was reflected in decreased sensitivity of the enlarged cells to the cytotoxic effect of specific antisera.

Cell Line↗
PubMed1997

The ROOT HAIR DEFECTIVE3 gene encodes an evolutionarily conserved protein with GTP-binding motifs and is required for regulated cell enlargement in Arabidopsis.

In plants, morphogenesis is largely determined by the orientation and extent of cell enlargement. To define the molecular mechanisms regulating plant cell enlargement, we have conducted a molecular genetic analysis of the ROOT HAIR DEFECTIVE3 (RHD3) gene of Arabidopsis thaliana. Mutations affecting the RHD3 gene were found to alter cell size, but not cell number, in tissues throughout the plant. Genetic and physiological analyses suggest that the RHD3 gene is not required for proper cell type specification, and it is likely to act downstream of the hormones auxin and ethylene. The RHD3 gene was cloned by a T-DNA tagging method and confirmed by the molecular complementation of the rhd3 mutant phenotype and by the analyses of six rhd3 mutant alleles. Consistent with the global effects of the rhd3 mutations, the RHD3 gene is expressed in all major plant organs. The deduced RHD3 product is a novel 89-kD polypeptide with putative GTP-binding motifs near the amino terminus. RHD3-like genes were identified from a protozoan (Entamoeba histolytica), a fungus (Saccharomyces cerevisiae), and another plant species (Oryza sativa), with the sequence identity including the putative GTP-binding motifs. These results imply that the RHD3 protein is a member of a new class of GTP-binding proteins that is widespread in eukaryotes and required for regulated cell enlargement.

Alleles↗
PubMed1990

The probability of G1 cells to enter into S increases with their size while S length decreases with cell enlargement in Allium cepa.

The distribution of cell surface area projection (cell size) has been measured at birth and at initiation of DNA synthesis in steady-state populations of Allium cepa root meristems. The conditional probability, P(I/G1), that initiation occurs given that the event of being in G1 also occurs has been estimated from these data. P(I/G1) was found to increase when cells became larger. The distribution of G1 duration has been constructed from indicated cell size distributions. The absolute frequencies of G1 times showed a maximum in the zone of cells with short G1 periods; about 14% of cells appear to enter into S with G1 congruent to 1 h. These results suggest that the increase of P(I/G1) was due to cell enlargement and not to cell aging. By comparing the cell size distribution at initiation of S and at the end of this period, a drastic reduction of cell size variability during DNA replication was observed and both curves were seen as rather similar in shape although they obviously had different modal points. These observations support that there is a negative correlation between the initiation size and the duration of genome duplication, and that cells which initiate DNA synthesis with the same size have a similar replication time. From this hypothesis, a plot of S duration versus cell size at initiation of this period was constructed by comparing the distributions of cell size at start and end of replication; this plot was also consistent with the existence of a negative correlation between cell initiation size and S length.

Allium↗
PubMedDate not supplied

Cell enlargement of plant tissue explants oscillates with a temperature-compensated period of ca. 24 min.

Rate of plant cell enlargement, measured at intervals of 3 min using a sensitive linear transducer, oscillates with a minimum period of about 24 min that parallels the 24-min periodicity observed with the oxidation of NADH by the external plasma membrane NADH oxidase and of single cells measured previously by video-enhanced light microscopy. Also exhibiting 24-min oscillations is the steady-state rate of cell enlargement induced by the addition of the auxin herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) or the natural auxin indole-3-acetic acid (IAA). Immediately following 2,4-D addition, a very complex pattern of oscillations is frequently observed. However, after several hours a dominant 24-min period emerges. The length of the 24-min period is temperature compensated and remains constant at 24 min when measured at 15, 25 or 35 degrees C, despite the fact that the rate of cell enlargement approximately doubles for each 10 degree C rise over this same range of temperatures.

2,4-Dichlorophenoxyacetic Acid↗
PubMedDate not supplied

Liver cell enlargement in rats given hydroxymethyl pyrroles analogous to pyrrolizidine alkaloid metabolites, followed later by the hepatotoxin dimethylnitrosamine.

Male rats aged 4-5 weeks were given single doses of pyrrolic alcohols having alkylating properties similar to those of pyrrolizidine alkaloid metabolites, followed several days later by one of the hepatotoxins dimethylnitrosamine (DMN), thioacetamide (TA) or carbon tetrachloride. After 24-32 days the livers of animals given the pyrroles 1-methyl-2,3-bishydroxymethylpyrrole (II) or 1-phenyl-5-methyl-2,3-bishydroxymethylpyrrole (V) and then DMN, contained enlarged parenchymal cells (megalocytes) similar to those seen in chronic pyrrolizidine alkaloid poisoning. At this time such abnormal cells were not found in rats given any of the other pyrroles followed by DMN, or compound II and then TA or CCl4.

Animals↗
PubMed1989

Association of collagenase and tissue inhibitor of metalloproteinases (TIMP) with hypertrophic cell enlargement in the growth plate.

In the transition from proliferating to hypertrophic cell zones in the growth plate, there is an increased in chondrocyte cell volume and a corresponding decrease in collagen content to allow for cell enlargement. To substantiate our hypothesis that collagenase is responsible for these changes, growth plates from rats treated with bisphosphonate (HEBP) were compared histologically and biochemically with growth plates from normal and vitamin D and phosphate deficient (-VDP) rats. HEBP-treated rats developed an expanded hypertrophic cell zone (HCZ) characterized by the presence of two distinct populations of hypertrophic cells. The proximal hypertrophic cells were only 2-fold enlarged compared to the proliferating cells, whereas 1/6 of the distal hypertrophic cells were enlarged almost 5-fold and appeared morphologically identical with hypertrophic cells from normal and -VDP rats. The HEBP growth plates were divided into cross-sectional thirds and analyzed for active and latent collagenase. The juxta-metaphyseal (lower 1/3) cartilage contained 100% of the fully enlarged hypertrophic cells and appeared identical to those found in normal and -VDP growth plates, along with 81% of the active and 77% of the total collagenase. Collagenase and tissue inhibitor of metalloproteinases (TIMP) were measured in extracts of similarly divided tissues. The presence of true collagenas was confirmed by using [3H]-telopeptide-free collagen. TIMP levels were inversely related to the presence of active collagenase and cellular hypertrophy. Substantial levels of latent collagenase were found in the extracellular fluid at sites of active collagenolysis, but not in the fluid phase surrounding the 2-fold enlarged hypertrophic cells. It is postulated that increased amounts of active collagenase and insufficient levels of TIMP may account for the reduced collagen content seen in the lower HCZ of both -VDP and HEBP rickets. Unlike active collagenase, which remains localized by binding to collagen, latent enzyme is probably restricted in its mobility throughout the extracellular space by diffusion, itself, or the interstices of the extracellular matrix.

Animals↗
PubMed1999

The mitotic inhibitor ccs52 is required for endoreduplication and ploidy-dependent cell enlargement in plants.

Plant organs develop mostly post-embryonically from persistent or newly formed meristems. After cell division arrest, differentiation frequently involves endoreduplication and cell enlargement. Factors controlling transition from mitotic cycles to differentiation programmes have not been identified yet in plants. Here we describe ccs52, a plant homologue of APC activators involved in mitotic cyclin degradation. The ccs52 cDNA clones were isolated from Medicago sativa root nodules, which exhibit the highest degree of endopolyploidy in this plant. ccs52 represents a small multigenic family and appears to be conserved in plants. Overexpression of ccs52 in yeast triggered mitotic cyclin degradation, cell division arrest, endoreduplication and cell enlargement. In Medicago, enhanced expression of ccs52 was found in differentiating cells undergoing endoreduplication. In transgenic M.truncatula plants, overexpression of the ccs52 gene in the antisense orientation resulted in partial suppression of ccs52 expression and decreased the number of endocycles and the volume of the largest cells. Thus, the ccs52 product may switch proliferating cells to differentiation programmes which, in the case of endocycles, result in cell size increments.

Amino Acid Sequence↗
PubMed1989

Perisinusoidal cells (Ito-cells) enlargement in a family with myotonic dystrophy.

Two cases are reported, a daughter and her mother who both have myotonic dystrophy with abnormalities of liver function tests and an important perisinusoidal cell enlargement without other pathologic features. In both cases, the myotonic dystrophy was clinically obvious and confirmed by electromyography. No other causes of perisinusoidal cell enlargement were found including vitamin A intake, psoriasis, viral disease or alcoholism. These observations suggest a genetic linkage and that serum test abnormalities could be associated with a perisinusoidal cell change.

Adolescent↗
PubMed1966

Action of inhibitors of RNA and protein synthesis on cell enlargement.

Further studies with inhibitors of protein synthesis are presented to support the conclusion, drawn from work with chloramphenicol, that protein synthesis is a critical limiting factor in auxin-induced cell expansion. The indoleacetic acid-induced elongation of oat coleoptile sections was strongly inhibited by dl-p-fluorophenylalanine, and the inhibition is antagonized by phenylalanine. Puromycin at 10(-4)m very strongly inhibited the indoleacetic acid-induced growth of oat coleoptile and artichoke tuber sections and exerted a less powerful effect on pea stem sections. As found earlier with chloramphenicol, concentrations of puromycin effective in inhibiting the growth of coleoptile sections had quantitatively similar effects on protein synthesis, as measured by the incorporation of C(14)-leucine into protein of the coleoptile tissue. Several analogues of RNA bases were also tested, but while 8-azaguanine very strongly inhibited growth of artichoke tuber disks, 6-azauracil was the only one of this group clearly inhibitory to growth in coleoptile or pea stem sections. Actinomycin D actively inhibited both elongation and the incorporation of C(14)-leucine into protein in oat coleoptile sections. Inhibition of the 2 processes went closely parallel. Actinomycin D also powerfully inhibited growth of artichoke tuber disks. All the compounds effective in inhibiting growth generally inhibited the uptake of leucine as well. The possibility that auxin causes cell enlargement in plants by inducing the synthesis of a messenger RNA and of one or more new but unstable enzymes, is discussed. Possible but less favored alternative explanations are: A) that auxin induces synthesis of a wall protein, or B) that the continued synthesis of some other unstable protein (by a process independent of auxin) may be a prerequisite for cell enlargement.

Antimetabolites↗
PubMed1972

Regulation of cell division and cell enlargement by turgor pressure.

Isolated radish (Raphanus sativus L., var. Red Prince) cotyledons were incubated in growth medium plus graded concentrations of mannitol (-1 to -16 bars) for 28 hours. At the end of the incubation period, turgor pressures were measured using thermocouple psychrometers. Cell division, as measured by DNA increase, was greatly stimulated by increasing turgor from 5 to 6 bars. Cell enlargement was stimulated as turgor increased above 3 bars. The critical turgor pressure for increased cell division thus appeared significantly greater than that for increased cell enlargement.

Journal Article↗
PubMed2006

Neuromuscular abundance of RB1CC1 contributes to the non-proliferating enlarged cell phenotype through both RB1 maintenance and TSC1 degradation.

RB1-inducible coiled-coil 1 (RB1CC1) is a novel tumor suppressor implicated in the regulation of RB1 expression. It is abundant in post-mitotic neuromuscular cells, which are matured and enlarged, but scarce in smaller leukocytes, indicating an association between RB1CC1 status and cell size. To clarify whether RB1CC1 is involved in cell size control, we investigated the contribution of RB1CC1 to the TSC-mTOR pathway, which plays an important role in the control through translational regulation. RNAi-mediated knockdown of RB1CC1 reduced the activation of mTOR and S6K as well as the size of HEK293 and C2C12 cells. Such knockdown also suppressed RB1 expression and the population of G1-phase cells. Exogenous expression of RB1CC1 maintained S6K activity and cell size, and decreased TSC1/hamartin contents under nutritionally starved conditions, which usually inhibit the mTOR-S6K pathway. Furthermore, RB1CC1 interfered with and degraded TSC1 through the ubiquitin-proteasomal pathway. A lentiviral RNAi for RB1CC1 reduced the size of mouse leg muscles. These findings suggest that RB1CC1 is required to maintain both RB1 expression and mTOR activity. The activity of mTOR was supported by RB1CC1 through TSC1 degradation. RB1CC1 preserved cell size without cell cycle progression especially in neuromuscular tissues, and the abundance contributed to the non-proliferating enlarged cell phenotype.

Animals↗