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Results for “proliferation”

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PubMed1978

Factors influencing endothelial cell proliferation in vitro.

The relative roles of blood cell products and plasma factors on endothelial cell proliferation were evaluated by studying the proliferative response of human umbilical vein endothelial cells to cell free plasma derived serum (CFPDS), whole blood serum (WBS), platelet released factors, fibroblast growth factor and macrophage conditioned medium in vitro. Human adult arterial smooth muscle cells were treated in a similar manner for comparison. The rate of endothelial cell proliferation was directly related to the concentrations of both WBS and CFPDS. Grwoth rate in WBS was marginally greater than that observed in CFPDS during early culture, however, similar confluent densities were achieved. The addition of platelet released factors to CFPDS did not further stimulate endothelial cell proliferation. In contrast smooth muscle cells were quiescent in CFPDS despite increasing serum concentrations, but proliferated actively in response to platelet released factors. Both human macrophage conditioned medium and fibroblast growth factor increased endothelial cell proliferation significantly when compared with CFPDS alone. It is concluded that endothelial cell proliferation in preconfluent cultures is dependent on plasma factors while human vascular smooth muscle cells also require cell derived mitogens such as platelet growth factor to proliferate. The release of a substance by human macrophages mitogenic for endothelial cells may be involved in endothelial cell proliferation in vivo.

Blood↗

PubMed1978

Gradients of proliferation of ciliary basal bodies and the determination of the position of the oral primordium in Tetrahymena.

The pattern of proliferation of new basal bodies in ciliary rows (somatic proliferation) in Tetrahymena was observed. Starved and refed cells were used, because proliferation in these cells is more pronounced than that under other circumstances. The formation of new basal bodies is locally determined by the position of "old" pre-existing basal body (short range determination). However, the probability of proliferation associated with any given "old" basal body differs very much. This probability is determined by the spatial coordinates of the particular region of the cell (long range determination); however some randomness in this process was also observed. Two different gradients of proliferation were found. The first gradient is circumferential with a maximum number of new basal bodies added in ciliary rows n, 1, 2 and 3 and the minimum number added in ciliary rows 7, 8 and 9. The second is an antero-posterior gradient with the highest number of new basal bodies added in the midbody region. Moreover, at least in some cases, new oral primordia first appear, as a random proliferation of new basal bodies adjacent to a few old cilia of ciliary row No. 1, resembling somatic proliferation. Then 2,3 or even more clumps of basal bodies appear, each having one old cilium posteriorly. These clumps, however, are not linear groups within the ciliary row but instead they form small fields of basal bodies. These findings suggest, that the same two-gradient system for new basal body addition operates during somatic proliferation and also determines the position of the new oral primordium as the site of the highest gradient value at the intersection of two gradients.

Animals↗

PubMed1977

The influence of adrenoceptor activity on cell proliferation in colonic crypt ipithelium and in colonic adenocarcinomata.

The effects of chemical sympathectomy and of the injection of amines or amine-receptor blocking drugs on cell proliferation in colonic crypts and in dimethylhydrazine-induced colonic carcinomata is examined in rats using a stathmokinetic technique. In animals which had been chemically sympathectomized by injection of 6-hydroxydopamine cell proliferation essentially ceased in the colonic crypts but continued at a normal rate in the tumours. Stimulation of alpha-adrenoceptors by metaraminol, a drug with properties similar to noradrenaline, caused acceleration of cell proliferation in colonic crypts but not in tumours. Conversely, blockade of alpha-adrenoceptors by phentolamine inhibited cell proliferation in crypts but not in tumours. Injection of adrenaline, predominantly a beta-adrenergic agonist, inhibited cell proliferation in the tumours but not in colonic crypts whereas blockade of beta-adrenoceptors by propranolol accelerated cell proliferation in tumours but not in colonic crypts. It is postulated that cell proliferation in the crypts of Lieberkühn in rat colon resembles that in rat jejunum in being controlled by the autonomic nervous system. However, tumour cell proliferation does not appear to be subject to such regulation.

Adenocarcinoma↗

PubMed1976

Cell proliferation in the descending colon of dimethylhydrazine treated rats and in dimethylhydrazine induced adenocarcinomata.

A stathmokinetic technique which has estimable precision has been used to estimate mitotic rates in the crypts of Lieberkühn in the descending colon of normal, and of dimethylhydrazine (DMH)-treated rats, as well as in DMH-induced adenocarcinomata. Estimates of the mean number of proliferating and of non-proliferating cells per crypt of Lieberkühn were also made in normal and in DMH-treated rats. In normal rats, epithelial cell proliferation was found to be relatively slow in the basal one-fifth of the crypts of Lieberkühn and to be most rapid in the second one-fifth of the crypt. In DMH-treated rats the number of cells around the circumference of transversely sectioned crypts was significantly increased, as was the number of proliferating cells present in longitudinally sectioned crypts. The region of relatively slow cell proliferation in the base of the crypts was expanded to occupy the lower two-fifths of the crypt in DMH-treated rats whilst the region of most rapid cell proliferation was displaced upwards to occupy the third one-fifth of the crypt. In DMH-induced adenocarcinomata cell proliferation occurred at a rate similar to that in the relatively quiescent zone at the bases of the colinic crypts in normal animals. However, tumour cell proliferation was substantially slower than that in the second one-fifth of the crypt in normal animals.

Adenocarcinoma↗

PubMed1979

Experimental double-perforating injury of the posterior segment in rabbit eyes: the natural history of intraocular proliferation.

A reproducible model of double perforating injury of the posterior segment of the rabbit eye was developed. Immediately after injury, a viterous condensation was visible between wounds. The scleral exit wound was sealed by fibroblastic proliferation of probable episcleral origin by the fourth day and the entrance similarly by the seventh day. Cellular proliferations originating in the wounds crossed the vitreous cavity following the vitreous injury tract or condensed vitreous to the disc or to the vitreous base. The earliest intraocular proliferations, composed of spindle-shaped, fibroblast-like cells, were seen at day 4. Occasional pigment epithelia were present in and on these proliferations. Other proliferations occurred directly on the retinal surface adjacent to the wounds. The transvitreous proliferations employed the vitreous as a scaffold, while the surface proliferations used the retinal surface for contact guidance.

Animals↗

PubMed1977

The proliferation of chondrocytes and pannus in adjuvant arthritis.

Cell proliferation in the pannus formation of adjuvant arthritis was studied by autoradiography. It was found that after day 9 an increased cell proliferation starts in the joint capsule recessus and synovial villi on the injected side. From these proliferating cells a pannus, which during the first phase frequently consists only of few cell layers, extends over the cartilage surface. With advancing disease the thickness of the pannus increases and further centripetal growth may cause the entire cartilage surface to be covered. This proliferating pannus tissue may invade the cartilage and destroy it. Since in this area of destruction labelled cells are frequently present, it may be assumed that proliferating cells with a high enzyme content are particularly responsible for the immediate degradation of cartilage. No involvement of chondrocytes in pannus formation was confirmed by the methods employed. There was neither increased proliferation of surface chondrocytes nor increased proliferation of chondrocytes in the depth of cartilage.

Animals↗

PubMed1979

Effect of risk factors and antirheumatic drugs on the proliferation of aortic wall cells.

The proliferation of aortic smooth muscle cells (ASMC) of Wistar rats, impaired by risk factors such as arterial hypertension, diabetes mellitus, atherogenic diet and staphylolysin injections and of normal Wistar rats treated with antirheumatic drugs such as prednisolone and acetylsalicylic acid was investigated. The cells of these animals were cultivated, subcultivated, and in the 2nd subcultures the cell numbers/5 ml medium were counted by means of Coulter Counter, and the cells were incubated with [3H]thymidine and the percentage of labelling in 100 or 1000 counted cells was stated. The effect of risk factors such as LDL and staphylolysin and of antirheumatic drugs such as prednisolone, acetylsalicylic acid, D-penicillamine and chloroquine added to the 2nd subcultures of cultivated ASMC of normal minipigs was investigated by the same method. The proliferation of cultivated ASMC of rats impaired by risk factors was accelerated. The proliferation of cultivated ASMC of rats treated with antirheumatic drugs was inhibited. The proliferation of ASMC of minipigs in the 2nd subcultures was activated by addition of risk factors and inhibited by addition of antirheumatic drugs. Antirheumatic drugs given to the rats and added to the medium of the 2nd subcultures of ASMC of normal minipigs inhibit the acceleration of ASMC proliferation induced by simultaneously given risk factors. The proposal to augment up our arsenal of the hitherto existing preventive and therapeutical measures by the application of antirheumatic drugs based on the experimental models referred to is supported by the result of a limited prospective double-blind-study of a sample of 133 male patients after myocardial infarction. The most remarkable result that the acceleration of the ASMC proliferation, the real pathologic process of arteriosclerosis, is inhibited by the application of antirheumatic drugs, at exactly the same time as the acceleration of the fibroblast proliferation, the real pathologic process in rheumatic diseases--ASMC and fibroblast, both being mesenchymal cells--recommends the use of these drugs in the prevention and therapy of human arteriosclerosis. The surprising result of our in-vivo experiments, that the acceleration of the growth of the ASMC induced by risk factors and the inhibition of the growth induced by antirheumatic drugs persist in the subcultures, is explained by the "selection theory" that there are dissimilar kinds of ASMC in normal arteries and that they react differently.

Animals↗

PubMed1977

Effect of hydroxyurea and vinblastine on the proliferation of the pluripotential stem cells.

The population of the pluripotential hemopoietic stem cells in mice, i. e. those cells forming colonies in the spleens of lethally irradiated mice (colony forming cells CFc) is proliferating relatively slowly. After a partial damage the population regenerates which is achieved by means of the increased proliferation rate. The effect of damage caused by different doses of hydroxyurea or vinblastine on the proliferation of the CFc has been investigated. CFc population was measured in femur bone marrow after grafting the sample of the bone marrow into the lethally irradiated mice recipients (spleen colony method). The proliferation rate was estimated either according to the magnitude of the fraction of cells synthesizing DNA in the S phase of the cell cycle, or according to the sensitivity of the population to the repeated injections of vinblastine. Data showed that even after very minute damage caused by hydroxyurea the stem cells started to proliferate intensively. The effect was dose dependent. The comparable damage caused by vinblastine had a significantly weaker effect on the proliferation of the stem cells. From the results it is concluded that the proliferation response of the pluripotential stem cells depends on two factors: one being the extent of the damage caused to the hemopoietic tissue and the second the position of the killed cells in the cell cycle.

Animals↗

PubMed2026

Transcriptomic insights into temperature regulation of proliferation and differentiation in skeletal muscle cells of Nibea albiflora.

Myogenesis involves sequential stages of muscle satellite cell activation, myoblast proliferation, differentiation, and fusion into multinucleated myotubes. Teleost muscle exhibits indeterminate growth and is highly sensitive to environmental temperature, yet the underlying mechanisms by which temperature regulate proliferation and differentiation remain poorly understood. In this study, we established a primary skeletal muscle cell culture from the yellow drum (Nibea albiflora), an economically important marine fish, and integrated morphological observations with comparative transcriptomics analysis to characterize cellular and molecular responses at 28 °C and 20 °C during both proliferation and differentiation stages. Phenotypic analysis revealed that 28 °C significantly enhanced both myoblast proliferation and myogenic differentiation ability compared with 20 °C. Transcriptomic profiling revealed that at 28 °C, differentiation upregulated extracellular matrix(ECM) organization, calcium signaling, and sarcomere assembly, while proliferation enhanced focal adhesion, growth factor signaling, and lipid metabolism. At 20 °C, differentiation was characterized by glutathione metabolism, and ferroptosis, while proliferation involved cytokine-cytokine receptor interaction and negative regulation of signal transduction. Core myogenic regulatory factors (MRFs), particularly myogenin, were strongly upregulated at 28 °C during the differentiation stage, serving as an internal control. Based on these findings, we propose a testable model that elevated temperature coordinates Ca2+-dependent MRF activation with ECM-integrin signaling to drive sarcomere assembly and muscle growth. Key differentially expressed genes (DEGs) regulating myogenesis in N. albiflora were also identified. This study provides a mechanistic framework for temperature adaptation in teleost skeletal muscle and identifies candidate genes for functional validation and marker-assisted selection, as well as a rationale for temperature management strategies to improve aquaculture yield of N. albiflora.

Animals↗

PubMed2026

PIEZO1 Mediates Myoblast Proliferation Under Simulated Microgravity.

Skeletal muscle atrophy is a major health risk of prolonged spaceflight, yet how microgravity reshapes muscle cells through mechanotransduction remains poorly understood. Here, we examined the mechanosensitive cation channel PIEZO1 in myoblast proliferation under simulated microgravity. Using a two-dimensional clinostat combined with Hi-C-based 3D genomics, transcriptomics, and functional assays, we found that simulated microgravity promotes C2C12 myoblast proliferation and upregulates Piezo1. Piezo1 mRNA knockdown reduced both proliferation and depolarization-induced Ca2 + influx, each partially restored under simulated microgravity, consistent with PIEZO1 being a central mediator of the response. Simulated microgravity also drove extensive 3D genome reorganization alongside changes in proliferation-related gene expression. Integrating chromatin architecture with transcriptomics, we found that PIEZO1 inhibition increased Elavl2 mRNA expression, PIEZO1 activation suppressed Elavl2 mRNA expression, and Elavl2 mRNA knockdown enhanced cell proliferation. These findings define a PIEZO1-ELAVL2 mechanotransduction axis, coupled to 3D chromatin remodeling, that regulates myoblast proliferation under simulated microgravity, and thus may be a target for countering spaceflight-associated muscle dysfunction.

Cell Proliferation↗

PubMed1977

Serum-stimulated phosphate uptake and initiation of fibroblast proliferation.

Previous studies have shown that initiation of proliferation of density-inhibited fibroblasts by fresh serum is accompanied by a rapid increase in phosphate uptake. This increase might be a key event in the initiation of DNA synthesis. The present studies examined this possibility. Mouse 3T3, secondary chick embryo, or human diploid foreskin cultures were grown to quiescence in medium containing varying levels of serum. When proliferation of the cultures was initiated by addition of fresh serum, the changes in phosphate uptake were inversely related to the final increases in cell number. Additional experiments showed that the change in phosphate uptake following serum addition was determined by the level of phosphate uptake prior to serum addition. Addition of dexamethasone to quiescent 3T3 cultures caused them to proliferate but did not increase phosphate uptake. Similarly, trypsin or insulin stimulated proliferation of quiescent secondary chick embryo cultures, but caused little or no change in phosphate uptake. Quiescent 3T3 cultures switched to medium containing fresh serum and reduced levels of phosphate showed a decrease in both phosphate uptake and intracellular phosphate pool size. Cell proliferation in these cultures, however, was stimulated to the same degree as cultures switched to medium containing fresh serum and the normal amount of phosphate. In addition, quiescent secondary chick embryo cultures switched to medium containing fresh serum and no phosphate showed a decrease in the intracellular phosphate pool size. Thymidine incorporation and final cell number in these cultures, however, was stimulated to the same or higher degree than in cultures switched to medium containing fresh serum and the normal amount of phosphate. These results demonstrate that the rapid increase in phosphate uptake following addition of fresh serum to quiescent fibroblasts is not a necessary event for the initiation of proliferation.

Animals↗

PubMed1976

Re-entry of resting leukaemic blood cells into proliferation in human acute leukaemia during diffusion chamber culture.

From 17 patients with different forms of acute leukaemia, mononuclear blood cells were cultured in diffusion chambers (DC) implanted intraperitoneally into pre-irradiated mice. In 14 patients, growth of blast cells could be observed during the culture period of up to 21 days. To question whether this growth of blast cells was due only to proliferation of the initially proliferating fraction or whether a re-entry of resting leukaemic cells into proliferation was involved, various 3H-thymidine (3H-TdR) labelling studies were carried out. The absolute increase of blast cells in EC showed no correlation with the fraction of leukaemic blast cells in DNA-synthesis in the implanted cell suspension as measured by 3H-TdR labelling in vitro. Furthermore, in 2 patients where the kinetic behaviour of initially labelled leukaemic blast cells was followed during DC culture, the increase in total blast cells could only be attributed to a small extent to proliferation of those cells initially in the cell cycle. Lastly, "in vivo" labelling during the culture period showed that in one case 25% and in another case 60% of the blast cells in DC were proliferating. The conclusion is that, owing to the stimulation of the diffusion chamber milieu and possibly also due to removal of an in vivo inhibition, in most cases of acute leukaemia resting leukaemic blast cells can apparently re-enter the active cell cycle. This has relevance for an understanding of the self-maintenance of the leukaemic cell population and may also be a reason for relapse of leukaemia after the usual cytostatic drug treatment which affects mainly the proliferating leukaemic cells.

Acute Disease↗

PubMed1978

Hormonal regulation of ovarian cellular proliferation.

The steroid hormone estradiol, and the glycoprotein hormones follicle-stimulating hormone (FSH) and luteinizing hormone (LH), are known to be essential for the growth and differentiation of follicles in the ovary. The present study was conducted to determine quantitatively the effects of estradiol, FSH and LH on proliferation of different ovarian cell types (granulosa and theca cells). The immature female hypophysectomized rate sequentially primed with estradiol, FSH and LH was used as the experimental model. Proliferation was assessed by examining changes in total DNA, incorporation of 3H-thymidine into DNA and labeling index in specific cell types. Estradiol and FSH each acted on follicles at different stages of development to stimulate proliferative activity of both granulosa and theca cells. Continued administration of either hormone caused a decrease in the proliferative activity of both cell types. These observations have been interpreted to indicate that estradiol and FSH can each alter the length of the specific phases of the cell cycle. A luteinizing dose of LH caused a cessation of proliferation in luteinizing granulosa cells while stimulating a limited proliferation of theca cells. Absence of the appropriate hormonal stimulus caused both granulosa and theca cells to stop proliferating and the follicles to undergo atresia. These results indicate that, depending upon the state of differentiation of granulosa and theca cells, estradiol, FSH and LH can stimulate or inhibit the ability of these cells to proliferate.

Cell Division↗

PubMed1977

Vitamin A-induced density-dependent inhibition of L-cell proliferation.

Retinoic acid, the acid form of vitamin A, was found to have an inhibitory effect on the proliferation of L-929 mouse cells. Cultures treated with retinoic acid (5.0 mug/ml) were shown to cease proliferation at cell densities corresponding to confluent monolayers (10.0+/-1.0 X 10(4) cells/cm2). Control cultures, however, continued to proliferate and consistently reach densities two to four times higher than those of treated cultures. Viability was determined by trypan blue exclusion, and the results (80-90 percent viable) excluded cytotoxicity as an explanation of decreased proliferation. Replenishing the medium on confluent retinoic acid-treated cultures failed to stimulate further proliferation, while control cells continued to grow exponentially with each medium change. Therefore, the cessation of cell proliferation at confluence did not result from medium depletion. Studies of cell growth after seeding at relatively low cell densities have indicated that retinoic acid-treated cultures had greater nutritional requirements than did control cultures. Cell-cloning experiments have shown that DNA synthesis was not blocked, since clones formed by cells seeded with retinoic acid contained an average of 27 cells after 9 days of incubation (indicating between four and five cell divisions). However, clones developing from treated cells had fewer cells per clone (27 vs. 54) and were less dense than control clones. These data suggested the restoration of contact inhibition (topoinhibition) to L-929 cells treated with retinoic acid.

Antineoplastic Agents↗

PubMed1976

Proliferation rate of haemopoietic stem cells after damage by several cytostatic agents.

The haemopoietic tissue of mice was damaged by different cell-cycle-stage specific and cell-cycle-stage non-specific cytostatic agents. The proliferation rate among the surviving pluripotential stem cells, i.e. those cells forming colonies in spleens of lethally irradiated mice (CFUs), was then investigated. The results suggest that, at least in the CFUs population, the cells which synthesize DNA in the S phase of the cell cycle inhibit the entry of the non-proliferating GO cells into cell cycle. This evidence was based on the ability of three cytostatic agents, hydroxyurea, cytosine arabinoside and methotrexate, which are toxic specifically to the S phase cells to increase the proliferation in the CFUs population. This increase was quite out of proportion to the small amount of damage they caused to the population. Colchicine, which kills cells in mitosis, and ionizing irradiation, damaging cells in all stages, proved to be much weaker stimulators of proliferation. It has been suggested that a mechanism for the control of cellular proliferation might be based on the negative feedback in the cell cycle. In this feedback control loop the cells which are preparing for cell division in the S phase of the cell cycle inhibit the entry of the non-proliferating GO cells into cell cycle.

Animals↗

PubMed1976

A localized region of basal body proliferation in growing cells of Dileptus visscheri (ciliata, gymnostomate).

In the ciliate Dileptus organisms are completely organized at the time of excystation. They grow intensively, increasing in volume several times, before they reach the trophic cell size. The growth includes both the somatic part of the body as well as the oral parts, consisting of the cytostomal field and the ventral band of the proboscis. From the time of excystation, during the growth of the cell, the oral apparatus is able to capture and ingest food. Growth of an oral apparatus while functioning has not previously been reported in cilates. The proliferation of new oral kinetosomes in the growing oral apparatus occurs only in the cytostomal field. There is no proliferation of ciliature in the oral kineties of the growing proboscis. In those regions of the somatic kineties bordering the cytostomal field an extensive proliferation of somatic ciliature takes place. The zone of proliferation common to the oral and somatic ciliature supplies new kinetosomes for the elongating proboscis, the growing oral apparatus and the growth of the rest of the body. The mode of proliferation of the oral kinetosomes differs from that of the somatic kinetosomes. The oral kinetosomes form randomly in large numbers, appearing similar to an anarchic field such as is found in other ciliates. The somatic kinetosomes always arise singly and in a defined position in relation to the mature kinetosome. The proliferation of basal bodies in a defined area in Dileptus suggests the existence of a growth zone localized around the cytostomal field.

Ciliophora↗

PubMed1978

Steroidal control mechanism of cell proliferation in mouse uterine epithelium.

The percentage of labeled cells in the uterine luminal epithelium of cycling mice showed the different zonal distributions at each stage of estrous cycle after cumulative labeling with 3H-thymidine for 36 hr. It was estimated that the proliferating fraction in the epithelium at proestrus, estrus, metestrus, and diestrus was 100%, 100%, 40% and 5%, respectively. The percentage of labeled cells in the uterine luminal epithelium of cycling mice treated with progesterone remained below 10% level for at least 20 hr after injections of progesterone. Total labeling was attained in the uterine epithelium of castrated mice by the administration of estradiol-17beta. On the other hand, the cell proliferation in the uterine epithelium of castrated mice treated with estradiol and progesterone was markedly suppressed and the percentage of labeled cells remained approximately at 35%. The remaining cell population, however, still showed the mitotic potency when mice received estradiol. It is suggested from this study that the effect of progesterone is to suppress the epithelial cell proliferation and transfer cells into resting cell fraction which is still evoked to proliferate as the effect of estradiol and that a key factor controlling epithelial proliferation in mouse uterus during the estrous cycle is proliferating fraction rather than cell cycle time.

Animals↗

PubMed1975

The requirement for macrophage-lymphocyte interaction in T lymphocyte proliferation induced by generation of aldehydes on cell membranes.

Guinea pig T lymphocyte proliferation induced by sodium periodate (NaIO4) or neuraminidase-galactose oxidase (NG) occurs when lymphocytes and macrophages are cultured together after treatment of either purified T lymphocytes or macrophages with these agents. Regardless of which cell initially bears the modified surface carbohydrate, lymphocyte proliferation requires the presence of viable homologous macrophages and fails to occur when they are replaced with fibroblasts, erythrocytes, L2C leukemia cells, thymocytes, PMN, line I hepatoma cells, or murine macrophages. Lymphocyte proliferation resulting from NaIO4 or NG treatment of lymphocytes is diminished when these cells are treated with proteolytic enzymes or aged in in vitro culture for 48 hr. By contrast, proteolytic enzyme treatment or in vitro aging has no effect on the ability of NaIO4 or NG-treated macrophages to induce lymphocyte proliferation. The requirement for macrophage-lymphocyte interaction in NaIO4 or NG-induced lymphocyte proliferation is indicative of a central role for the macrophage in the initiation of T lymphocyte proliferation.

Aldehydes↗