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Results for “cellular proliferation”

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At least 19 recordsLinked to original sources

PubMed1979

Cellular proliferation, cellular death and atherosclerosis.

The multipotential smooth muscle cell (SMC) is the predominant cell in arterial media and intima, and the major cell type involved in proliferative lesions. Studies using a precursor of DNA, namely [3H] thymidine, and autoradiography have shown that proliferation of SMC is an important and early response to atherogenic stimuli, such as cholesterol feeding, surgically induced hypertension or endothelial injury. Cultures of aortic SMC offer excellent in vitro models to study the reactivity of these cells to recognized or suspected risk factors. Pure SMC cultures are obtained by placing small fragments of aortic media in a defined culture medium and their response evaluated by thymidine incorporation and/or increase in size of the outgrowing cell colony. Factors essential for adequate growth include normal serum constitutents, including the lipoproteins and a platelet derived factor. Replacing the normal serum with dietarily induced hyperlipemic serum results in greatly increased proliferation. The serum fraction largely responsible for this phenomenon is the low density lipoprotein. Simultaneous addition of high density lipoproteins partly suppress this reaction. Serum from diabetic or hypertensive--but normolipemic--animals similarly stimulates these cells to increased proliferation.

Animals↗

PubMed1992

Calories, fat, fibers, and cellular proliferation in Swiss Webster mice.

Increased cellular proliferation has been associated with the enhanced expression of several key stages in carcinogenesis. A standard protocol was used to investigate the effect of specific dietary regimens on cellular proliferation. Young adult Swiss Webster mice were fed for 30 days with modified AIN-76A semi-purified diets designed to illustrate the effects of the levels of dietary or calorie restriction, different fibers and bulking agents, and different fats on cellular proliferation. Female mice were used for the restriction and fat studies, males for the fiber and bulking agent studies. Vaginal smears were taken from females from treatment day 15, and the mice killed 2 days following the first estrus following 30 days feeding; males were killed on the 30th day. One hour before death, mice were injected ip with 0.25 micro Ci/g 3[H]-thymidine. Slides were prepared for radioautography and histopathology. Both dietary and calorie restriction led to reduced 3[H]-thymidine labeling indices in each of the seven tissues studied, the mammary gland being the most severely affected. Different fibers and bulking agents, in specific cases, reduced labeling in the duodenum but not to a consistent statistically significant extent in the colon or colo-rectal region. In the duodenum, oat bran and oat gum were the most effective while wood cellulose (alphacel) had no effect. Investigations on the effects of different fats is continuing. High levels of lard, menhaden oil, or cod liver oil as the fat component of the AIN-76A diet, led to much higher levels of labeled cells in the mammary gland or colo-rectal region than did fat components rich in vegetable oils. The labeling indices appeared to be inversely correlated with the level of linoleic acid in the diet, a presumption that has been confirmed by investigating a series of diets containing different levels of this acid. Anti-oxidants were not used in any of these fat-modified diets. The overall results obtained in these studies clearly indicate the utility of cellular proliferation studies in investigating the effects of dietary modifications.

Animals↗

PubMed1991

Early indicators of potential neoplasia produced in the rat forestomach by non-genotoxic agents: the importance of induced cellular proliferation.

Forestomach neoplasia induced by the apparently non-genotoxic carcinogens, butylated hydroxyanisole and propionic acid, appears to arise by way of sustained high levels of cellular proliferation. Several other inducers of enhanced cellular proliferation, or the consequential incidence of hyperplastic lesions, have been identified in the rodent forestomach but the requisite carcinogenicity bioassays remain undone. In other tissues, such as the male rat kidney, the rodent thyroid follicular cell and the bladder epithelium, there is also evidence supporting the concept that sustained enhanced cellular proliferation may be an important early marker for non-genotoxic carcinogens. This reaction is, however, not likely to be the only marker necessary for the identification of non-genotoxic carcinogens.

Acrylates↗

PubMed1992

Effect of the dietary fibre content of lifelong diet on colonic cellular proliferation in the rat.

The effect of the fibre content of lifelong (18 months) diets on proximal and distal colonic cellular proliferation and short chain fatty acid (SCFA) content was investigated in 40 rats. Rats were fed a low fibre diet (17 g/kg non-starch polysaccharides NSP) or the stock diet (133 g/kg NSP). The higher fibre fed rats had increased caecal and colonic total contents (p < 0.001) and SCFAs than the low fibre fed rats (caecal SCFAs: higher fibre rats 96.4 (6.8) mumol/g wet weight v low fibre 22.7 (3.0): p < 0.001, colonic SCFAs: higher fibre 52.3 (3.1) mumol/g wet weight v low fibre 6.9 (2.2) mumol/g wet weight: p < 0.001). Cellular proliferation was increased in the proximal colon (bromodeoxyuridine labelling index, higher fibre 9.3 v low fibre 8.4 p < 0.05; flow cytometry, % cells in S phase higher fibre diet 7.9 v low fibre 6.9; p < 0.01) and there was a shift of proliferating cells to a higher region in each crypt. There was no significant difference in the percentage of cells in S phase in the distal colon of rats in both diet groups. The proliferative zone, however, was expanded in the distal colon of the higher fibre diet fed rats. This study indicates that long term higher fibre intake in rats is associated with a modest increase in cellular proliferation in the proximal colon but not the distal colon.

Animals↗

PubMed1975

Cellular proliferation and renewal in the various zones of the hamster epididymis after colchicine administration.

Cellular proliferation was examined in the various regions of the excurrent ducts of the reproductive system of the male golden hamster after colchicine administration. Each of the two zones of the ductuli efferentes displayed only infrequent mitotic figures. Similarly, the basal cell population of the epididymis as well as the epithelium of the vas deferens exhibited too few mitotic figures to allow meaningful evaluation of cellular proliferation. The following observations were reported. 1. The principal cells of the entire epididymis are characterized by a singular diurnal cycle of proliferative activity reaching its maximum about 3 P.M. and its nadir about 9 A.M. 2. A circadian rhythm of cell division is also found in the principal cells of each of the six zones of the epididymis, although the time of maximal activity may vary from zone to zone. 3. The most actively proliferating region of the excurrent duct system is zone 3 of the epididymis, whereas the least active region is the ductuli efferentes. 4. The renewal rates of the principal cells vary considerably at various points along the excurrent duct system, ranging from cells which renew themselves as many as 10 times to cells which fail to renew themselves at all during the normal life-span of the animal.

Animals↗

PubMed1992

Effects of high glucose on cellular proliferation and fibronectin production by cultured human mesangial cells.

Diabetic glomerulosclerosis is characterized by the accumulation of the matrix protein fibronectin in the glomerular mesangium and could result from increased mesangial cell fibronectin synthesis induced by hyperglycemia. To test this hypothesis, we cultured human mesangial cells for up to 14 days in media containing normal (5 mM) or high glucose (20 to 115 mM) concentrations and assessed cellular proliferation and fibronectin synthesis. When compared to 5 mM glucose, high glucose levels significantly inhibited cellular proliferation in a dose dependent fashion, as assessed by direct cell counting and thymidine incorporation. After eight days in culture, tissue culture supernatant fibronectin levels, as assessed by ELISA, were significantly higher from cells cultured under high glucose conditions than cells exposed to normal glucose levels. After 14 days and when compared to 5 mM glucose, matrix fibronectin levels and fibronectin mRNA expression (by Northern analysis) were also increased by 20 mM glucose. To control for the osmotic effects of high glucose, mesangial cells were also cultured in the presence of 20 mM or 50 mM mannitol. Mannitol had no effect on cellular proliferation but significantly increased tissue culture supernatant fibronectin levels and fibronectin gene expression. These studies demonstrate that, in vitro, high glucose suppresses human mesangial cell proliferation and stimulates fibronectin synthesis. The increase in fibronectin synthesis may in part result from changes in osmolality induced by high glucose. These data suggest that increased mesangial cell fibronectin synthesis may play a role in the accumulation of glomerular fibronectin common to diabetic glomerulosclerosis.

Cell Division↗

PubMed1990

Regulation of IL-4 lymphokine gene expression and cellular proliferation in murine T helper type II cells.

Activation of T cells results in the production of lymphokines and cellular proliferation. Protein kinase C (PKC) plays a key role in this process. It has been shown that this enzyme is essential to elicit a response to Con A or specific antigen in CD4+ T helper type 1 (Th 1) cells that secrete IL-2. We have now explored the signal transduction pathway that leads to transcription of the IL-4 gene and proliferation in murine CD4+ T helper type 2 (Th 2) cells. Surprisingly, we have found in two independently derived Th 2 clones that neither cellular proliferation nor IL-4 lymphokine production is affected by blocking or depletion of PKC. This differential mechanism of signal transmission leading to cellular activation implies a new distinction between murine Th 1 and Th 2 cells.

Animals↗

PubMed1992

Measurement of cellular proliferation within the vitreous during experimental proliferative vitreoretinopathy.

Cellular proliferation is an important component in the pathogenesis of complex retinal detachments caused by proliferative vitreoretinopathy (PVR). We used flow cytometry to measure the proliferation of cells recovered from the vitreous cavity in an experimental model of tractional retinal detachment induced by homologous fibroblast injection. Two distinct populations of cells were detected. One population comprised smaller, dense cells representing mostly leukocytes. A second population of larger cells contained not only the injected fibroblasts but also high concentrations of host-derived cells with significant proliferative activity, whose number increased for 3 days following injection. Flow cytometry was useful for analysis of the recovered cells for concentration, morphologic features and proliferation. This technique may be applicable in the identification of patients at high risk for the development of PVR.

Animals↗

PubMed1977

Effects of antiinflammatory agents on mouse skin tumor promotion, epidermal DNA synthesis, phorbol ester-induced cellular proliferation, and production of plasminogen activator.

The antinflammatory ateroids fluocinoine acetonide, fluocinonide, and fluclorolone acetonide were found to be very effectiveinhibitory agents of mouse skin tumor promotion. These steroids also drastically inhibited epidermal DNA synthesis and epidermal cellular proliferation induced by a phorbal ester tumor promoter. In addition, these compounds were potent inhibitors, of plasminogen activator production in tumor cell cultures. The clinically used non-steroidal antiinflammatory agents oxyphenbutazone, indomethacin, and Seclazone also inhibite tumor promotion but were much less effective. Although these agents are useful against inflammatory disorders in general when given p.o., in our studies they had little effect on inflammation and epidermal cellular proliferation induced by a phorbol ester tumor promoter when given topically. The afore mentioned nonsteroidal antiinflammatory agents also had little effect on epidermal DNA synthesis. Oxyphenbutazone and indomethacin were less potent inhibitors of plasminogen activator production in tumor cells than were the antiinflammatory steroids, and Seclazone produced a negligible inhibition. There is, therefore, a general correlation in the potencies of a series of steroidal antiinflammatory agents for inhibition of tumor promotion and their ability to inhibit plasminogen activator production by tumor cell cultures and epidermal DNA synthesis.

Animals↗

PubMed1991

The effects of histamine H2 receptor antagonists on melanogenesis and cellular proliferation in melanoma cells in culture.

B16-C3 murine melanoma, A375P human melanotic melanoma, and C32 human amelanotic melanoma cells were incubated in the presence of (0-4 mM) H2-antagonists, ranitidine and cimetidine. Cell proliferation, tyrosinase activity and melanin content were monitored. H2-antagonists stimulated tyrosinase activity and melanin accumulation in B16-C3 cells in a dose- and time-dependent manner. Stimulation of enzyme activity and pigment production was accompanied by inhibition of cellular proliferation in B16-C3 cells. The inhibitory concentration of cimetidine was approximately 2-fold higher than that of ranitidine. H2-antagonists failed to stimulate melanogenesis in A375P or C32 cells, but inhibited cellular proliferation in both cell lines. These results are the first demonstration of H2-antagonist induced phenotypic changes in malignant melanoma cells in vitro, and represent a novel mechanism for the previously described in vivo antitumor effects of these agents.

Animals↗

PubMed1992

Inhibition of cellular proliferation after experimental balloon angioplasty by low-molecular-weight heparin.

BACKGROUND: The proliferative response induced by balloon angioplasty is known to be an important factor in the development of restenosis after successful coronary angioplasty. METHODS AND RESULTS: To study the effects of low-molecular-weight heparin (LMWH) on cellular proliferation after experimental balloon angioplasty, LMWH (3.9 kd, 400 anti-Xa units/kg/day) was given to 20 male New Zealand White rabbits. After an intimal fibromuscular plaque was induced by electrical stimulation in the right carotid artery, LMWH was applied during the 7 days after balloon dilatation. As the control group, 20 other rabbits underwent balloon angioplasty without application of LMWH. The vessels were excised 3, 7, 14, and 28 days after balloon treatment. During the final 18 hours before the rabbits were killed, bromodeoxyuridine was applied. Intimal wall thickness increased from 13 +/- 5 cell layers (preangioplasty control group) to 20 +/- 6 cell layers in the LMWH-treated group at 28 days (p less than 0.05). In contrast, histological examination of control animals 28 days after angioplasty revealed a significant increase to 35 +/- 15 cell layers (p less than 0.01). Immunohistological quantification showed a significant increase (p less than 0.001) of cells undergoing DNA synthesis at 3 (10.2 +/- 4.2%) and 7 (7.7 +/- 4.8%) days after balloon dilatation in control animals. In contrast, at 3 and 7 days after balloon treatment, the percentage of cells undergoing DNA synthesis in LMWH-treated rabbits was lower (3 days, 2.7 +/- 1.8%; 7 days, 1.9 +/- 0.3%) than the corresponding untreated controls but showed a significant increase (p less than 0.01) compared with the preangioplasty controls. The differences between the two groups were statistically significant, however (3 days, p less than 0.01; 7 days, p less than 0.05). As early as 14 days after angioplasty, the extent of cellular proliferation was normalized and was comparable to the preintervention levels in both groups. CONCLUSIONS: Our data indicate that the proliferative response after balloon angioplasty can be reduced in vivo by early treatment with LMWH and thus encourage further clinical investigations.

Angioplasty, Balloon↗

PubMed1978

Patterns of cellular proliferation during thyroid organogenesis.

The changes in rate and location of cellular proliferation were analyzed to determine if localized areas of cell division were influencing shape changes in the chick thyroid. Pulse labeling with tritiated thymidine indicates that the gland's labeling index declines throughout its development. Initially, the thyroid placode has a lower labeling index than the neighboring pharyngeal epithelium. An evaluation of the positions of pulse-labeled cells reveals that the evaginating thyroid grows by annexing cells from the pharyngeal epithelium. The older evaginated regions of the gland exhibit the lowest labeling indices. The newly acquired regions still maintain higher labeling indices.

Animals↗

PubMed1992

Detection of cellular proliferation during compensatory renal growth using flow cytometry.

Compensatory renal growth (CRG) consists of cellular enlargement and a small but consistent increase in DNA content. It has been assumed that the increase in total renal DNA content was due to new cell formation, however, the possibility of nuclear polyploidy remained an alternative explanation. To test the hypothesis whether cellular hyperplasia is the cause of the increase in DNA content during compensatory growth after renal deprivation, we performed cell cycle analysis using flow cytometry. Following unilateral nephrectomy, the amount of cortical cells in the S phase increased by 12% at 10 h while the number of cells in the G2M phase increased by 7% at 120 h. Medullary cells entering the S phase increased by 26% at 24 h and those in G2M increased by 12% at 168 h. DNA synthesis and replication occurs during CRG following unilateral nephrectomy as evidenced by an increase in cells entering both the S and G2M phases of the cell cycle. The increase in DNA content during CRG is a result of cellular proliferation and not polyploidy.

Animals↗

PubMed1977

Relationship of cellular proliferation and the generation of cytotoxic cells in an in vitro secondary immune response to syngeneic rat lymphoma cells.

The role of cellular proliferation for the generation of cytotoxic activity in an in vitro secondary immune response to syngeneic lymphoma cells was investigated. Spleen cells from W/Fu rats immunized with the syngeneic (C58NT)D tumor proliferate and generate cytotoxic potential for tumor targets after exposure to mitomycin C-treated (C58NT)D cells in vitro. Elimination of proliferating cells by exposure to high specific activity 3H thymidine at approximate intervals impaired the generation of cytotoxic activity. Elimination of cells proliferating to either syngeneic lymphoma or BN rat alloantigens allowed the remaining cells to generate cytotoxic potential to the second set of antigens. Elimination of proliferating cells also abrogated the ability of the in vitro generated cells to adoptively confer anti-tumor protection on nonimmune recipients. These results demonstrate that cellular division is required for the generation of cells which are cytotoxic in vitro and can adoptively confer anti-tumor protection in vivo.

Animals↗

PubMed1992

Cellular proliferation and genetic events involved in the genesis of Burkitt lymphoma (BL) in immune compromised patients.

A mathematical model simulating lymphomagenesis based on the two-hit theory of carcinogenesis is presented by contrasting the biologic variables responsible for a high risk of developing Burkitt lymphoma (BL) in three immunosuppressed groups with that of nonendemic BL. In this model, the pro-B lymphocyte is considered to be the target for BL-specific translocations such as t(8;14). With repeated mitosis, the target cell pool expands in the high-risk individual, and, thereby, the opportunities for a spontaneous translocation to arise are increased. The chromosomal translocation endows the target cell with survival advantages, and, hence, lymphoma develops. Modeling results demonstrate that this increased cell proliferation is sufficient in accounting entirely for the increase in tumor prevalence. Preventing enhanced cellular proliferation by obviating immune deficiency and treating patients with agents that restore immunity or have antiviral and antiproliferative properties prior to conversion from polyclonal B-cell proliferation to monoclonal malignancy could obviate the development of BL.

B-Lymphocytes↗

PubMed1975

Role of cellular proliferation in the stimulation of MPS phagocytic activity.

Administration of agents such as stilboestrol, endotoxin, C. parvum and zymosan, which enhance the phagocytic activity of the mononuclear phagocyte system, also stimulated cellular proliferation in the liver and spleen as assessed by [13H] thymidine incorporation into these organs, and by autoradiography and the number of mitoses in the liver. Sublethal whole body irradiation abolished the proliferative response to stimulation and also reduced or prevented the increase in phagocytic activity. This latter effect depended on the stimulatory agent used, dose of radiation and time of irradiation with respect to stimulation. The results indicate that cell proliferation is important for the increase in phagocytic activity after administration of C. parvum, zymosan and stilboestrol. Endotoxin, however, appears to act primarily by increasing the capacity of existing cells while at the same time causing cell proliferation. The population of cells responding to zymosan by increased phagocytic activity through proliferation was shown to be resident in the liver.

Animals↗

PubMed1991

Inhibition of cellular proliferation in human T lyophotropic virus type I (HTLV-I)-infected T cells from patients with HAM by steroid hormones and cyclosporin A.

The effects of steroid hormones and Cyclosporin A (CsA) on de novo DNA synthesis in four human T lymphotropic virus type I (HTLV-I)-infected T cell lines from patients with HTLV-I-associated myelopathy (HAM) were investigated. These T cell lines were characterized by helper/inducer phenotypes and expressed IL-2-receptor (Tac) and HLA-DR antigen in high percentages. Three of the four cell lines had their de novo DNA synthesis inhibited by steroid hormones (dexamethasone and 1,25-dihydroxyvitamin D3 (1,25 (OH)2D3)) and CsA in a dose dependent manner. The inhibitory effects arose 24 hours after initiation of incubation with either steroid hormones or CsA. The forth cell line was not inhibited by these reagents. It also revealed through the use of an in vitro assay utilizing the human IL-2 dependent cell line, Sez 627, that none of these T cell lines secrete IL-2 in detectable volumes. In order to clarify the mechanism of the inhibitory effects of steroid hormones and CsA, among these 4 cell lines H-89-59, insensitive to the reagents, and H-109, sensitive to them, were used for northern blotting analysis. C-myc gene expression was demonstrated both in H-89-59 and H-109. 1,25(OH)2D3 and CsA suppressed c-myc expression in H-109 as well as cell proliferation. In H-89-59, however, neither expression of c-myc nor cell proliferation was suppressed. On the other hand, the level of HTLV-I gene transcripts was not changed by these agents. Hence, inhibition of cellular proliferation by these reagents was not caused by the inhibition of HTLV-I p40(x) gene but by inhibition of transcriptional factors such as c-myc products.

Calcitriol↗

PubMed1991

Kinetics of cellular proliferation and hormonal receptors in EVSA-T breast cancer cell line.

The hormone-independent human breast cancer cell line EVSA-T, originally described as negative estrogen and progesterone receptors is shown to become positive hormone receptors when the cellular proliferation rate is slowed down. The experimental procedure included the following steps: 1) EVSA-T cells were seeded in minimum essential medium supplemented with 10% fetal bovine serum and kept undisturbed for 2 days; 2) culture medium was replaced with Dulbecco's solution and Ham's F-12 and cells were incubated in serum-free media for another 24 h; 3) then, cells were "rescued" with 10% FBS supplemented medium and estrogen (ER) and progesterone receptors (PgR) were measured immediately, time 0, and 6, 12, 18, 24 and 30 h after the media were changed. Cell yield was quantified at the same times. Experimental data indicate that changing the proliferation kinetics makes it possible to detect estradiol and progesterone receptors on EVSA-T cells. Estrogen receptor appeared at 18 h after rescue, 6 hours before progesterone receptor could be detected. Immunohistochemical analysis of ER content confirmed this observation, showing maximal positive stain at 18 h. Furthermore, ER disappeared when cells recovered their normal proliferation rate.

Breast Neoplasms↗