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At least 19 recordsLinked to original sources
PubMed1979

[Cell proliferation and migration in the roof of the mesencephalon (tectum) in Xenopus laevis tadpoles and adult frogs normally and in brain injury. II. Cell proliferation and differentiation of the tectum in frogs].

The proliferation and directions of cell differentiation in tectum opticum were studied in the young frogs under the conditions of normal development and upon brain trauma by means of 3H-thymidine autoradiography. The same types of cells were shown to be able of proliferation in both the cases: cells of the ventricle zone and glioblasts (gliocytes) in all other tectum layers. A study of directions of the tectum proliferating cells' differentiation in the frogs has shown that the proliferating cells differentiate mainly in the ependyme tanicytes in the ventricle layer 1 and gliocytes in the other tectum layers. The trauma did not change the direction of proliferating cells' differentiation towards the formation of neurons. The complete regeneration is observed in the tectum layer 1 only.

Animals↗
PubMed1979

[Arterial intimal proliferation in the rat : nature and origin of the proliferating cells].

This study had two objectives: 1) Identification of the type of cell involved in intimal proliferation (endothelial cells, smooth muscle fibres or fibroblasts). 2) Determination of the origin. For this purpose a model was used which consisted of implantation in the rat of femoral arterial segments in the interstitial tissue. Sequential examination of tissue collected on days 1, 2, 3, 4, 5, 6, 7 revealed that proliferation was more marked if not solely present at the extremities of the segments. The proliferating cells were also in continuity with the extravascular granulation tissue, which would appear to indicate that the intimal proliferation in this model came from the cells of the granulation tissue and "muscular" differentiation occurred in contact with the endothelium.

Animals↗
PubMed1979

T-antigen expression in proliferating and non-proliferating simian virus 40-transformed mouse cells.

Previous studies with simian virus 40-transformed mouse 3T3 cells which are temperature sensitive for the expression of the transformed phenotype (ts SV3T3 cells) have shown that T-antigen expression and viral DNA transcription are under cell cycle control. Using these ts SV3T3 cells, we studied the expression of the viral genome under proliferating and non-proliferating conditions, in the presence and absence of inhibitors of macromolecular synthesis and of the tumor promoter phorbol myristate acetate. ts SV3TE cells which are growth arrested at 39 degrees C by low serum concentration or saturation density accumulated in G1 and did not express T-antigen. When these cells were induced to proliferate, at either 32 or 39 degrees C, T-antigen synthesis preceded the entry of the cells into the S-phase and was not coupled to DNA replication. G1-arrested ts SV3T3 cells were induced to synthesize T-antigen by phorbol myristate acetate treatment, but T-antigen alone was not sufficient to induce cellular DNA synthesis. Isoleucine deprivation arrested growth of ts SV3T3 cells, but these cells, as well as normal 3T3, did not accumulate in G1 and continued to express T-antigen. The temperature-sensitive expression of the transformed phenotype in the ts SV3T3 cells does not appear to be due to a lack of transcription of specific regions of the integrated simian virus 40 genome at 39 degrees C.

Animals↗
PubMed1977

T cells which proliferate in response to concanavalin A include cells which proliferate in mixed leucocyte reactions.

Selection in long-term culture of alloreactive T cells, by successive in vitro restimulation with semi-allogeneic cells, results in primed responder cell populations which maintain full proliferative reactivity to allogeneic cells as well as to the T cell mitogens concanavalin A (Con A) and phytohemagglutinin (PHA) but are depleted of cells which can effect target cell destruction in either a specific or nonspecific manner. Con A-induced T cell blasts (selected by velocity sedimentation) can revert to small resting lymphocytes in the presence of inert "filler" cells. Con A blasts which have reverted, readily proliferate in response to Con A or allogeneic stimulator cells but are largely depleted of effector killer cells and PHA-responsive cells.

Animals↗
PubMed1977

Glial cell proliferation in human retinal detachment with massive periretinal proliferation.

By transmission electron microscopy we studied 38 epiretinal membranes obtained from human eyes by vitrectomy operation in rhegmatogenous retinal detachment. Two of the membranes were composed of closely packed glial cell processes. The cytoplasm of the glial cell processes in both membranes contained little besides loosely packed filaments and microtubules. Microvilli protruded from the cells at the vitreal surface of one of the membranes. Junctional complexes were present between the cells only at the vitreal surface. In the other glial membrane, microvilli extended into a duct-like structure with junctional complexes sealing the lumen. A discontinuous basal lamina was laid down by cell processes at the retinal side of the membranes. Similar glial membranes, formed by migration and proliferation of astrocytes from the retina, were seen in owl monkeys with experimental and naturally occurring retinal detachment. A new epiretinal membrane (reformed in one of the eyes from which a dense glial membrane had been removed three weeks previously), was composed primarily of single large cells with extensively developed rough endoplasmic reticulum. The new cells were surrounded by collagen, fine fibrillar material, and fibrin. The new membrane also contained free pigment granules and pigment-containing macrophages. Additionally, we observed spicule-like crystals between the cells in the glial membrane specimens, identified as calcium phosphates by energy-dispersive x-ray analysis.

Animals↗
PubMed1979

Separation of non-proliferating from proliferating thymic lymphocytes based on light scatter analysis.

Two populations of thymic lymphocytes from eight-week-old mice were separated based on the light scatter intensity they generated while passing through a flow cell analyser. The two populations were subsequently studied morphologically and analysed for the relative amount of DNA present in each cell. Cells having a low light scatter intensity had a high nuclear:cytoplasmic ratio, a heterochromatic nucleus, and a proliferative index (S + G2 + M) of only 23%. Cells with a high light scatter intensity had a low nuclear:cytoplasmic ratio, dispersed chromatin, frequently a uropod with budding microvilli and a proliferative index of 71%. The low light scatter cells resemble small cortical thymocytes or lymphocytes from the thoracic duct described by others. The highest light scatter cells resemble medium lymphocytes shown by others to be proliferative.

Animals↗
PubMed1978

F1-hybrid anti-parental-strain reactivity. II. Proliferation of C3H X CBA hybrid lymphocytes in the spleens of irradiated CBA mice.

Experiments were conducted to explore whether C3H X CBA lymphocytes can react by proliferation when they meet parental CBA spleen cells. MLC tests could not detect such a reaction, but infusion of C3H X CBA lymph node cells into irradiated CBA hosts resulted in rapid cell proliferation in the host's spleen. Such a cell proliferation was also observed after infusion of T-cell-enriched lymph node cell preparations or thymic cells from C3H X CBA donors. Upon transfer to new irradiated mice these proliferating cells continued to proliferate in CBA mice but not in C3H X CBA mice. Further evidence that the injected T-cells were the proliferating emerged from experiments where AKR X CBA lymphocytes were found to proliferate in spleens of irradiated CBA mice and that most of these cells posessed the theta antigen determined by AKR. Proliferation of F1-hybrid lymphocytes in the spleens of its irradiated parental strains was found not to be a general phenomenon and is probably restricted to some Mls-antigen-compatible strain combinations. The possibility that the C3H X CBA hybrid lymphocytes are stimulated to proliferations by CBA lymphocytes reactive against the C3H-determined Mls antigen is discussed.

Animals↗
PubMed1979

Mechanisms of haemopoietic stem cell proliferation control.

The control of stem cell (CFU-S) proliferation is mediated by short-range acting factors which can be detected by the proliferation modifying activities present in media conditioned by haemopoietic cells. A specific inhibitor of stem cell proliferation is obtained from haemopoietic tissue containing minimally proliferating CFU-S, whilst stimulatory material is obtained from cell suspensions containing rapidly proliferating CFU-S. Used competitively, these factors, which are detected in different molecular weight range fractions, manipulate the rate of CFU-S proliferation in a manner compatible with a physiological control mechanism. In addition, a long-term bone marrow culture system has been shown to provide an in vitro model of stem cell control. Fractionation of cell populations from haemopoietic tissues reveals marked concentration differences of the CFU-S proliferation modifying activities depending on the proliferative state of the CFU-S. However, irrespective of whether the tissue contains stem cells that are actively or minimally proliferating, both stimulatory and inhibitory activities are detected. From dose-response studies it is concluded that stem cell proliferation is controlled by an appropriate balance of stimulatory and inhibitory factors which, however, are not produced by the stem cells themselves.

Animals↗
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↗
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↗
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↗