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Results for “cellular proliferation”

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PubMed2005

[Effect of ginsenoside on the cellular proliferation, apoptosis and cell cycles in LC A549 and HUVEC 304 cell lines].

OBJECTIVE: To determine the effect of ginsenoside on the cellular proliferation, apoptosis and cell cycles in LC A549 and HUVEC 304 cell lines. METHODS: A549 and HUVEC 304 cell lines were cultured with different concentrations of ginsenoside. Cellular proliferation was detected with MTT, apoptosis and cell cycles were checked with Flow Cytometer, and change of microstructure was observed by transmission electron microscope. RESULTS: The apoptosis rate was 29.8% in A549 cell lines after being interfered with ginsenoside at 3 x 10(-6) mol/L, significantly higher than that in the control group ( P < 0.05). No change was observed in the cell cycles after being interfered with ginsenoside. The inhibitive rate of ginsenoside was 12.53% for HUVEC 304 cell line at 1 x 10(-4) mol/L (P < 0.05 ). The cells induced by conditioned medium could be inhibited by ginsenoside, and apoptotic body could be found in cells induced by conditioned medium at 10(-6) mol/L. CONCLUSION: The proliferation of vascular endothelial cell could be inhibited by ginsenoside, and apoptosis could also be found in both tumor cells and cells induced by conditioned medium after being interfered with ginsenoside.

Adenocarcinoma↗

PubMed2006

Selective transcription and cellular proliferation induced by PDGF require histone deacetylase activity.

Histone deacetylases (HDACs) are key regulatory enzymes involved in the control of gene expression and their inhibition by specific drugs has been widely correlated to cell cycle arrest, terminal differentiation, and apoptosis. Here, we investigated whether HDAC activity was required for PDGF-dependent signal transduction and cellular proliferation. Exposure of PDGF-stimulated NIH3T3 fibroblasts to the HDAC inhibitor trichostatin A (TSA) potently repressed the expression of a group of genes correlated to PDGF-dependent cellular growth and pro-survival activity. Moreover, we show that TSA interfered with STAT3-dependent transcriptional activity induced by PDGF. Still, neither phosphorylation nor nuclear translocation and DNA-binding in vitro and in vivo of STAT3 were affected by using TSA to interfere with PDGF stimulation. Finally, TSA treatment resulted in the suppression of PDGF-dependent cellular proliferation without affecting cellular survival of NIH3T3 cells. Our data indicate that inhibition of HDAC activity antagonizes the mitogenic effect of PDGF, suggesting that these drugs may specifically act on the expression of STAT-dependent, PDGF-responsive genes.

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↗

PubMed1995

Assessing cellular proliferation: what's worth measuring?

The assessment of cellular proliferation is, in the main, carried out on histological material. Ideally, such methods should be applicable to routinely processed tissues, they should be relatively inexpensive and the results easily quantified and interpreted. A knowledge of what is 'normal' within the tissue from both a temporal and spatial point of view is essential. There is a burgeoning literature on novel markers of cell proliferation, usually these are immunohistochemically based, each method with its own unique set of conditions for optimal tissue processing. Some would argue this is simply a process of 'reinventing the wheel' since mitotic counting is a perfectly adequate indicator of proliferation, but we could justly counter that a labelling index (S-phase or growth fraction) is more likely to produce an accurate assessment when the sample size is small. In tumours, tissue heterogeneity is likely to render any single measurement meaningless. To date, there are no reliable validated immunohistochemical markers of the labelling index in animal tissues which visualise naturally occurring proliferation-associated molecules, though this may change shortly.

Animals↗

PubMed2002

Cellular proliferation of mucosa-associated lymphoid tissue with otitis media: a preliminary study.

Histopathologic and immunohistochemical analyses were used to investigate the cellular proliferation of mucosa-associated lymphoid tissue (MALT) in human temporal bones with and without evidence of otitis media (OM). Anti-proliferating cell nuclear antigen (PCNA) antibody (clone PC10) was applied after the antigen retrieval procedure. Positive PCNA expression was observed in temporal bones that had been stored for 10 to 31 years in 80% ethanol. In specimens with purulent OM, the MALT had faint germinal centers (GCs). Positive PCNA expression in the MALT was moderate and scattered. In specimens with mucous OM, the MALT had complete GCs. Positive PCNA expression in the MALT was moderate to strong, and the distribution of PCNA-positive cells was associated predominantly in the GCs, the mucosal epithelial layer, and/or the subepithelial layer. In specimens with serous OM, the MALT also had complete GCs. However, the PCNA expression was weak and scattered, and appeared to be similar to that of the MALT in the temporal bones without OM. These results indicate that the cellular proliferation of MALT in the temporal bone might reflect the activity that produces secretory IgA against invasion of foreign antigens. However, further studies are needed to elucidate whether the PCNA expression within MALT in the eustachian tube and middle ear is associated with a mucosal immune response to inflammation as in OM.

Autopsy↗

PubMed1994

Influence of luteinizing hormone-releasing hormone (LHRH) treatment on cellular proliferation in the rat anterior pituitary.

This study was designed to gain insight into the action of LHRH on the control of cellular proliferation in the anterior pituitary. The fraction of cells labelled with bromodeoxyuridine (S-phase cells) was studied in cytospin preparations of anterior pituitary cells taken from control male and female rats and from rats treated with daily doses of 2 micrograms/100 g body weight of LHRH (7 days), with doses of 40 micrograms of LHRH given on alternate days for 14 days (7 doses) or, finally, treated with daily doses of 50 ng of busereline acetate (14 days). Treatment with LHRH for 14 days resulted in a significant increase in the fraction of S-phase cells. However, neither the blockade of gonadotrophin secretion with busereline acetate nor its stimulation with LHRH for seven days resulted in a significant change in the proliferative activity of anterior pituitary cells. This action was independent of sex. No significant changes were seen in the proportions of pituitary gonadotrops of the different study groups. Regardless of the treatment-group very few cells doubly-immunostained for BrdU and LH were found. It is concluded that LHRH may stimulate cellular proliferation in the anterior pituitary, but further studies are needed to define which cells are involved in this action.

Animals↗

PubMed1996

Enhanced cellular proliferation in intact stenotic lesions derived from human arteriovenous fistulas and peripheral bypass grafts. Does it correlate with flow parameters?

BACKGROUND: Vascular interventions are often complicated by the development of intimal thickening, leading to stenosis. Cellular proliferation is a key event in stenosis formation in animals, but the role of cell proliferation in intimal thickening in humans is still unclear. Furthermore, the relation between proliferation in human stenotic lesions and flow parameters has not been established. METHODS AND RESULTS: We studied the proliferation patterns of 35 anatomically intact human stenotic lesions derived from either peripheral bypasses (normal flow) or hemodialysis AV fistulas (high flow) with the use of Ki-67, a cell proliferation marker. Local flow parameters were assessed with ultrasound. Proliferation patterns were similar in AV fistula and bypass stenoses. In the intima, proliferation was highest in the area just below the endothelium (AV fistulas, 3.6%; bypasses, 3.5%; P = NS). In adjacent nonstenotic vessel segments that were used as controls, proliferation rate in the intima was 0.3%. Double-labeling studies revealed that subendothelial-intimal proliferation consisted mainly (90%) of vascular smooth muscle cells, whereas proliferation in the other layers of the vessel wall also consisted of endothelial cells and macrophages. Blood flow velocity was negatively correlated with subendothelial-intimal proliferation (r = -.61, P < .05). The endothelial cell coverage of the lumen was positively correlated with proliferation (r = .85, P < .01). CONCLUSIONS: These data suggest enhanced cellular proliferation in human stenotic tissue derived from AV fistulas and peripheral bypass grafts. Furthermore, high proliferation rates seem to be associated with endothelial cell coverage of the lumen and low local flow velocities.

Adult↗

PubMed2005

Effect of hepatitis C virus core protein on modulation of cellular proliferation and apoptosis in hilar cholangiocarcinoma.

BACKGROUND: Hepatitis C virus (HCV) is believed to be an important human pathogen causing carcinoma. But the effect of HCV infection on the alteration of cellular proliferation and apoptosis and the relationship between the effect and the development of hilar cholangiocarcinoma are largely unknown. The aim of this study was to assess the effect of HCV core protein on proliferation and apoptosis of hilar cholangiocarcinoma. METHODS: HCV core protein (HCV C protein) was detected by peroxidase-antiperoxidase assay in surgical specimens from 48 patients with hilar cholangiocarcinoma. The apoptosis index (AI) and PCNA index (PI) in hilar cholangiocarcinoma were detected by in situ end labeling assay and streptavidin-biotin assay respectively. RESULTS: The expression of HCV C protein was observed in 32 (67.7%) of the 48 specimens of hilar cholangiocarcinoma. The mean+/-standard deviation for AI and PI was 3.52%+/-0.64% and 46.24%+/-11.46% respectively. The AI of hilar cholangiocarcinoma specimens with HCV C protein expression was significantly lower than that of HCV C protein negative specimens (P<0.01), whereas the PI of HCV C protein positive specimens was significantly higher than that of HCV C protein negative specimens (P<0.01). CONCLUSION: HCV C protein may promote the cellular proliferation of hilar cholangiocarcinoma and inhibit its cellular apoptosis.

Adult↗

PubMedDate not supplied

Mitomycin c influence on inhibition of cellular proliferation and subsequent synthesis of type I collagen and laminin in primary and recurrent pterygia.

The purpose was to investigate the biological effects of mitomycin C (MMC) on the inhibition of cellular proliferation and the subsequent synthesis of extracellular matrix like type I collagen (PIP) and laminin on primary and recurrent pterygia. The 3H-thymidine assay for cellular proliferation was consistent with the MMC dose and time response of both pterygia. The cellular inhibitory effect of MMC was greater on recurrent pterygial cells than primary ones. The inhibition of laminin by MMC followed the dose and time-response curves, with a stronger effect found in recurrent pterygial cells, but no significant difference between the two types concerning type I collagen synthesis. The inhibition of fibroblast proliferation and subsequent synthesis of laminin by MMC was more marked in recurrent pterygium than the primary one.

Adult↗

PubMed1996

Regulation of cellular proliferation and intimal formation following balloon injury in atherosclerotic rabbit arteries.

Injury to atherosclerotic arteries induces the expression of growth regulatory genes that stimulate cellular proliferation and intimal formation. Intimal expansion has been reduced in vivo in nonatherosclerotic balloon-injured arteries by transfer of genes that inhibit cell proliferation. It is not known, however, whether vascular cell proliferation can be inhibited after injury in more extensively diseased atherosclerotic arteries. Accordingly, the purpose of this study was to investigate whether expression of recombinant genes in atherosclerotic arteries after balloon injury could inhibit intimal cell proliferation. To test this hypothesis, we examined the response to balloon injury in atherosclerotic rabbit arteries after gene transfer of herpesvirus thymidine kinase gene (tk) and administration of ganciclovir. Smooth muscle cells from hyperlipidemic rabbit arteries infected with adenoviral vectors encoding tk were sensitive to ganciclovir, and bystander killing was observed in vitro. In atherosclerotic arteries, a human placental alkaline phosphatase reporter gene was expressed in intimal and medial smooth muscle cells and macrophages, identifying these cells as targets for gene transfer. Expression of tk in balloon-injured hyperlipidemic rabbit arteries followed by ganciclovir treatment resulted in a 64% reduction in intimal cell proliferation 7 d after gene transfer (P = 0.004), and a 35-49% reduction in internal area 21 d after gene transfer, compared with five different control groups (P < 0.05). Replication of smooth muscle cells and macrophages was inhibited by tk expression and ganciclovir treatment. These findings indicate that transfer of a gene that inhibits cellular proliferation limits the intimal area in balloon-injured atherosclerotic arteries. Molecular approaches to the inhibition of cell proliferation in atherosclerotic arteries constitute a possible treatment for vascular proliferative diseases.

Adenoviridae↗

PubMed1993

Comparison of five histopathologic methods to assess cellular proliferation in transitional cell carcinoma of the urinary bladder.

Transitional cell carcinomas of the urinary bladder vary in their biologic potential, which may be correlated with the grade and stage of the tumor. Cellular proliferation may prove to be another measure of predicting tumor biologic potential. We have compared five different methods to assess proliferation in 26 tumors and correlated these results with tumor grade and stage. A portion of each tumor was incubated in vitro with bromodeoxyuridine (BrdUrd). For each tumor this was compared with at least three of the following four other markers of proliferation: mitotic count, silver-stained nucleolar organizer regions, immunohistochemical staining with Ki67, and proliferating cell nuclear antigen. Statistical correlations were seen between tumor grade and stage and these markers. There were strong correlations between the BrdUrd labeling index (LI) and both the Ki67 LI and proliferating cell nuclear antigen LI. The correlation between the BrdUrd LI and mitotic count was more tenuous; no significant correlation was found between BrdUrd LI and silver-stained nucleolar organizer region count. The correlation between these measurements of proliferation and tumor grade and stage was less strong. Our data suggest that cellular proliferation of transitional cell carcinomas can be reliably assessed with several different markers and that most of these markers can be correlated with tumor grade but not with stage.

Bromodeoxyuridine↗

PubMed1994

Multiple myeloma: expression of nucleoside transporters on malignant plasma cells and their relationship to cellular proliferation.

The expression of nucleoside transporters is a limiting factor in the pharmacology of the nucleoside analogue, cytosine arabinoside (AraC) and is associated with cellular proliferation. We investigated the expression of nucleoside transporters on plasma cells from the bone marrow of 51 patients with multiple myeloma by 2-colour immunofluorescence flow cytometry, utilising 5-(SAENTA-x8)-fluorescein, a fluorescent ligand for the nucleoside transporter and anti-CD38 conjugated to phycoerythrin, as CD38 expression has unique characteristics on plasma cells. Mean nucleoside transporter expression on bone marrow plasma cells from patients with myeloma (1777 +/- 2181 transporters/plasma cell) was not significantly different from expression on plasma cells from normal bone marrow (997 +/- 1096 transporters/plasma cell). However, analysis of disease subgroups revealed a significant trend towards increased transporter expression in patients with progressive disease compared to those with stable disease (chi 2 = 4.0, p < 0.05). Nucleoside transporter expression correlated significantly with the plasma cell labeling index (LI) (r = 0.45, p < 0.01) and serum thymidine kinase levels (r = 0.66, p < 0.01), both markers of cellular proliferation but not with c-myc oncoprotein expression. These findings suggest that flow cytometric measurement of nucleoside transporter expression on plasma cells provides a rapid and convenient measurement of disease activity or quiescence in myeloma.

ADP-ribosyl Cyclase↗

PubMed1998

Effects of antisense-based folypoly-gamma-glutamate synthetase down-regulation on reduced folates and cellular proliferation in CCRF-CEM cells.

The effect of down-regulation of folylpoly-gamma-glutamate synthetase (FPGS) activity on intracellular reduced folate accumulation and cellular proliferation was examined, using an inducible antisense expression system in the human T-lymphoblastic leukemia cell line CCRF-CEM. FPGS catalyzes the addition of gamma-glutamyl residues to natural folates and classical antifolates, which results in their enhanced cellular retention and increased cytotoxicity. As such, this enzyme has become a focus as a potential anticancer drug target. However, direct evidence to support this concept has been elusive. Hence, a study was undertaken using an antisense-based expression system to down-regulate FPGS activity. This inducible expression system was used to demonstrate that lower FPGS activity can lead to substantially lower intracellular folate content, which coincides with suppression of thymidylate synthesis and inhibition of cellular proliferation.

DNA Primers↗

PubMed1988

Cellular proliferation in the lymphoid tissues of an inbred (RT1a) rat strain during the oestrous cycle.

Changes in body weight, uterine weight and tissue weight, cell content and cellular proliferation of the thymus and uterine regional and popliteal lymph nodes were examined at daily intervals during the oestrous cycle of the DA (RT1a) inbred rat strain. Thirty-nine sexually mature virgin animals, aged between 13 and 15 weeks were used in this investigation. During dioestrus body weight and uterine weight fell significantly, while intrathymic and intranodal cellular proliferation increased significantly. These findings are discussed in relation to ovarian hormone secretion and it is suggested that increased thymocyte and lymphocyte proliferation occurs in response to rising oestrogen levels. This proliferative response prepares the female for the immunological challenge with allogeneic spermatozoa should mating occur during the subsequent oestrous phase.

Animals↗

PubMed2004

Marrow stromal cell transplantation after traumatic brain injury promotes cellular proliferation within the brain.

OBJECTIVE: This study was designed to investigate the effects of intracerebral as well as intravenous administration of bone marrow stromal cells (MSCs) on endogenous cellular proliferation after traumatic brain injury (TBI). METHODS: Two experimental groups of Wistar rats were studied. One group received MSCs intracerebrally, and the other group received MSCs intravenously after injury by controlled cortical impact. MSCs were harvested from the bone marrow of male Wistar rats. For the intracerebral study, 24 male rats were divided into three groups (eight rats per group): rats injected with MSCs (1 x 10(6)) intracerebrally 1 day after TBI; 2) rats injected with phosphate-buffered saline intracerebrally 1 day after TBI; and 3) sham group not subjected to injury and not administered treatment. For the intravenous study, 10 female Wistar rats were injected 1 day after TBI with either MSCs (2 x 10(6)) (n = 5) or phosphate-buffered saline (n = 5) via the tail vein. Neurological function of the rats was evaluated with modified neurological severity scores and rotarod motor test. All rats were injected with bromodeoxyuridine intraperitoneally, to label the newly generating cells. Rats were killed 15 days after TBI, and coronal brain sections were stained immunohistochemically with diaminobenzidine to identify newly generating bromodeoxyuridine-positive cells. To study the differentiation of newly generating cells into neurons, sections were also double-stained for neuronal markers (Tuj1, doublecortin, NeuN) with fluorescein isothiocyanate. RESULTS: The data demonstrate that newly generating cells were mainly present in the subventricular zone, hippocampal formation, and boundary zone of contusion of both treated and control animals. Intracerebral MSC treatment significantly increased the progenitor cell proliferation in the subventricular zone and boundary zone compared with the controls, whereas intravenous MSC treatment enhanced this endogenous proliferation in subventricular zone, hippocampus, and boundary zone. In both groups, some of the new cells revealed positive staining for neuronal markers. A statistically significant functional improvement was observed in both the intracerebrally as well as intravenously treated groups. CONCLUSION: Intracerebral and intravenous MSC administration promotes endogenous cellular proliferation after TBI in rats. This may contribute to the functional improvement observed in these rats.

3,3'-Diaminobenzidine↗

PubMed2005

Ciglitazone induces early cellular proliferation and NF-kappaB transcriptional activity in colon cancer cells through p65 phosphorylation.

While it is well established that peroxisome proliferator activated receptor gamma (PPARgamma) ligands inhibit cell growth and induce apoptosis of colon cancer cells with a prolonged treatment (3-5 days), the early effects of PPARgamma exposure are less clear. In this report, we demonstrate that the PPARgamma ligand, ciglitazone, induces proliferation of HT-29 and Caco-2 colon cancer cells transiently (<48 h) prior to a decrease in cell proliferation (>72 h). Associated with this cellular proliferation phase, we observed an increase in NF-kappaB transcriptional activity. Ciglitazone exposure did not affect NF-kappaB DNA binding but rather, increased phosphorylation of p65 as well as the recruitment of the co-activator CBP. Pre-treatment of HT-29 cells with wortmannin, a phosphatidylinositol 3-kinase (PI3K) kinase inhibitor, inhibited ciglitazone-induced p65 phosphorylation, NF-kappaB transcriptional activity and cell proliferation. Interestingly, ciglitazone inhibited PPAR transcriptional activity, suggesting this early proliferative effect is PPRE independent. These data suggest that the early proliferative phase of PPARgamma ligand exposure is associated with activation of NF-kappaB by p65 phosphorylation and cofactor recruitment and not through increased DNA binding.

Blotting, Western↗

PubMed2005

Absence of caprin-1 results in defects in cellular proliferation.

Cytoplasmic activation/proliferation-associated protein-1 (Caprin-1) is a cytoplasmic phosphoprotein that is the prototype of a novel family of highly conserved proteins. Its levels, except in the brain, are tightly correlated with cellular proliferation. We disrupted caprin-1 alleles in the chicken B lymphocyte line DT40 using homologous recombination. We readily obtained clones with one disrupted allele (31% of transfectants), but upon transfection of heterozygous cells we obtained a 10-fold lower frequency of clones with disruption of the remaining allele. Clones of caprin-1-null DT40 cells exhibited marked reductions in their proliferation rate. To obviate the problem that we had selected for caprin-1-null clones with characteristics that partially compensated for the lack of Caprin-1, we generated clones of DT40 cells heterozygous for the caprin-1 gene in which, during disruption of the remaining wild-type allele of the chicken caprin-1 gene, the absence of endogenous Caprin-1 would be complemented by conditional expression of human Caprin-1. Suppression of expression of human Caprin-1 resulted in slowing of the proliferation rate, due to prolongation of the G1 phase of the cell cycle, formally demonstrating that Caprin-1 was essential for normal cellular proliferation.

Amino Acid Sequence↗

PubMed2004

p53, cellular proliferation, and apoptosis-related factors in thymic neuroendocrine tumors.

Thymic neuroendocrine tumors are biologically aggressive neoplasms with extensive local invasion and high mortality. Although various markers of cellular proliferation and apoptosis have correlated with degrees of tumor differentiation in pulmonary neuroendocrine neoplasms, they have not been systematically studied in thymic neuroendocrine tumors. We immunostained 21 cases of thymic neuroendocrine tumors for p53, MIB-1, and the apoptosis-related markers Bcl-2, Bcl-x, and Bax. By histological classification the cases were low-grade (nine cases), intermediate-grade (eight cases), and high-grade (four cases) thymic neuroendocrine tumors. p53 was expressed in five cases: 1/9 low grade, 3/8 intermediate grade, and 2/4 high grade. The mean cellular proliferation (MIB-1) was 7.1% (range 2-12%) in low-grade thymic neuroendocrine tumors, 6.1% (range 2-15%) in intermediate-grade thymic neuroendocrine tumors, and 34.2% (range 2-80%) in high-grade thymic neuroendocrine tumors. Bcl-2 was expressed in 16 cases: 7/9 low grade, 5/8 intermediate grade, and 4/4 high grade. Bcl-x was expressed in 16 cases: 7/9 low grade, 6/8 intermediate grade, and 3/4 high grade. Bax was expressed in 13 cases: 5/9 low grade, 4/8 intermediate grade, and 4/4 high grade. The presence of mutant p53 in the tumor was associated with a statistically significant decreased mean survival (P<0.05). In contrast, either by positive or negative staining or by the score technique (staining intensity x percentage of cells staining), the presence of Bcl-x was associated with an increased mean survival (P<0.05). Finally, a Bcl-x : Bax ratio >or=1 was also associated with an increased mean survival, as compared to a Bcl-x : Bax ratio >or=1 (P<0.05). Our study shows that p53 expression and certain apoptosis markers correlate with survival. The expression of these markers may account for differences in biological behavior.

Apoptosis↗