[Effect of titanium surfaces of various roughness on cell proliferation, cell differentiation and protein synthesis of human fetal osteoblasts (hFOB 1.19)].
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Cell Culture Techniques↗
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Results for “Cell Proliferation”
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Cell proliferation, cell death, E-cadherin, metalloproteinase expression and angiogenesis in gastric cancer precursors and early cancer of the intestinal type.
The aim of this study was to analyse the morphological, kinetic and molecular characteristics of low-grade (LGD) and high-grade dysplasias (HDG) in comparison with intestinal metaplasia type III (IM III) and normal mucosa (NM) as well as with early gastric cancer of the intestinal type (EGC). Based on this it was verified whether these categories are distinct, progressive proliferative steps from IM III to LGD, HGD and EGC, according to Correa's sequence of events. The morphology, mitotic index (MI), and the apoptotic index (AI) were assessed. The E-cadherin expression (E-Cad), matrix-metalloproteinase activity (MMP2), and the number of microvessels (NV) were also evaluated. Among the categories, MI increases from NM to IM III and LGD, and from LGD to HGD and EGC, while AI continues to increase also from HGD to EGC. E-cad decreases from NM to EGC, although not significantly from LGD to HGD; MMP2 is significantly more expressed only in EGC. Three groups are obtained by means of cluster analysis. The first group includes all the NMs and IM IIIs, all except 1 LGD, about half of HGDs, and 1 EGC. E-Cad is highly expressed, MMP2 and angiogenesis are low, the proliferative activity is low and mitoses are partly balanced by apoptoses. The second group includes some EGCs and HGDs and is characterised by a very high proliferative activity and cell death; there is an initial loss of cell adhesion, an increase of MMP2 and NV. The third group includes the majority of EGCs, but also 1 HGD: it has intermediate MI and AI, the lowest expression of E-Cad, the highest expression of MMP2 and the most numerous microvessels. These results underscore the necessity of evaluating each case individually within the same singular category of Correa's sequence. The use of kinetic and molecular parameters in addition to the morphological analysis may give important information on the behaviour of the various lesions.
Cadherins↗
Effects of fibres on cell proliferation, cell activation and gene expression.
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Animals↗
GnRH analogues and uterine leiomyomas. Effect of hormone replacement therapy on cell proliferation.
Cell proliferation in uterine leiomyomas treated preoperatively with either nafarelin (400 microg/day) for 3 months (7 patients) or nafarelin plus hormone (oestradiol + norethisterone) add-back therapy (6 patients) was investigated by automatic image analysis of frozen tissue sections using immunohistochemistry with anti-proliferating cell nuclear antigen antibody. GnRHa therapy decreased cell proliferation in leiomyomas to a level corresponding to the situation previously seen in postmenopausal leiomyomas. However, there was no consistent correlation between cell proliferation and shrinkage of leiomyomal size. The hormone add-back therapy moderated the influence of GnRHa on cell proliferation and completely blocked a decrease in size of leiomyomas in our patients.
Adult↗
Developmentally controlled farnesylation modulates AtNAP1;1 function in cell proliferation and cell expansion during Arabidopsis leaf development.
In multicellular organisms, organogenesis requires tight control and coordination of cell proliferation, cell expansion, and cell differentiation. We have identified Arabidopsis (Arabidopsis thaliana) nucleosome assembly protein 1 (AtNAP1;1) as a component of a regulatory mechanism that connects cell proliferation to cell growth and expansion during Arabidopsis leaf development. Molecular, biochemical, and kinetic studies of AtNAP1;1 gain- or loss-of-function mutants indicate that AtNAP1;1 promotes cell proliferation or cell expansion in a developmental context and as a function of the farnesylation status of the protein. AtNAP1;1 was farnesylated and localized to the nucleus during the cell proliferation phase of leaf development when it promotes cell division. Later in leaf development, nonfarnesylated AtNAP1;1 accumulates in the cytoplasm when it promotes cell expansion. Ectopic expression of nonfarnesylated AtNAP1;1, which localized to the cytoplasm, disrupts this developmental program by promoting unscheduled cell expansion during the proliferation phase.
Adenosine Triphosphatases↗
Activation of the phosphatidylinositol 3-kinase/protein kinase Akt pathway mediates CD151-induced endothelial cell proliferation and cell migration.
We previously reported that CD151 promotes neovascularization and improves blood perfusion in rat hind-limb ischemia model, but the precise mechanism is still unclear. Endothelial cell proliferation and cell migration play critical roles in angiogenesis. Many growth factors and hormones have been shown to regulate cell proliferation, cell migration and angiogenesis, including the activation of eNOS activity, via the PI3K/Akt signaling pathway. Whether CD151 induces cell proliferation and cell migration via PI3K/Akt signaling pathway is not known. Here we showed that CD151 promotes human umbilical vein endothelial cell (HUVEC) proliferation, migration and tube formation in vitro, accompanied by increased phosphorylation of Akt and eNOS, leading to increased eNOS activity and nitric oxide (NO) levels after rAAV-CD151 infection, whereas infection with rAAV-anti-CD151 attenuated the effects of CD151, which suggested that CD151 can activate PI3K/Akt pathway. Moreover, inhibitors of PI3K (LY294002) and eNOS (l-NAME) can attenuate CD151-induced cell proliferation and cell migration. The results suggested that activation of PI3K/Akt signaling pathway mediates CD151-induced cell proliferation and migration.
Antigens, CD↗
Voltage-gated K+ channels are associated with cell proliferation and cell cycle of ovarian cancer cell.
OBJECTIVES: To study the role of Voltage-gated potassium ion channels (Kv) in cell proliferation and cell cycle of ovarian cancer cell. METHODS: The effects of voltage-gate K+ channels on human ovarian cancer cell line (A2780 cell) proliferation and cell cycle were observed by means of MTT and flow cytometry. A variety of K+ channel blockers were used in order to differentiate the critical subtype of K+ channels involved. Mechanism of K+ channel in cell proliferation was explored by studying the relationship between the K+ channel and Ca2+ entry. Kv and L-type Ca2+ channel gene expressions were determined by RT-PCR. RESULTS: 4-Aminopyridine, an inhibitor of voltage-gated K+ channels, significantly inhibited the proliferation of A2780 cells as measured by MTT. 4-Aminopyridine also significantly affected the cell cycle, which increased the percentage of cells in G0/G1, and reduced the percentage of cells in S phase and G2/M phase. Non-selective K+ channel blockers tetrapentylammonium (TPeA) and verapamil had similar inhibitory effects on A2780 cell proliferation and cell cycle. In contrast, iberiotoxin, a selective inhibitor of KCa channels, and glibenclamide, a potent inhibitor of KATP channels, had no effect on the cell proliferation and cell cycle of A2780. Moreover K+ channels inhibitor, TPeA and verapamil, can blocked Ca2+ influx in these cells. CONCLUSION: Voltage-gated K+ channels play an important role in the proliferation and cell cycle of ovarian cancer cell. It is likely that the influence of Kv channels on A2780 cell proliferation and cell cycle is mediated by a Ca2+-dependent mechanism.
4-Aminopyridine↗
Short-term exposure of cancer cells to micromolar doses of paclitaxel, with or without hyperthermia, induces long-term inhibition of cell proliferation and cell death in vitro.
BACKGROUND: During intraoperative hyperthermic intraperitoneal chemotherapy for primary or secondary peritoneal malignancies, tumor cells are exposed to high drug concentrations for a relatively short period of time. We investigated in vitro the effect of paclitaxel and hyperthermia on cell proliferation, cell cycle kinetics and cell death under conditions resembling those during intraoperative hyperthermic intraperitoneal chemotherapy. METHODS: Human breast MCF-7, ovarian SKOV-3 and hepatocarcinoma HEpG2 cells were exposed to 10 and 20 microM paclitaxel at 37, 41.5 or 43 degrees C for 2 h. Cell proliferation, cell cycle kinetics, necrosis and apoptosis were evaluated. RESULTS: Hyperthermia exerted a cytostatic effect to all cell lines and at 43 degrees C a cytotoxic effect on MCF-7 cells. MCF-7 and SKOV-3 cells treated under normothermic conditions with paclitaxel were arrested at G2/M or M phase for at least 3 days. Most of MCF-7 cells and approximately half of SKOV-3 cells were in interphase and became multinucleated without properly completing cytokinesis. Hyperthermia at 41.5 degrees C altered cell cycle distribution and affected the paclitaxel-related effect on cell cycle kinetics of MCF-7 and SKOV-3 cells. Analysis of the mode of cell death showed that cell necrosis prevailed over apoptosis. Hyperthermia at 43 degrees C increased paclitaxel-mediated cytotoxicity in MCF-7 cells and to a lesser extent in SKOV-3 and HEpG2 cells. CONCLUSIONS: Short-time treatment of carcinoma cells with high (micromolar) concentrations of paclitaxel in normothermic and hyperthermic conditions is highly efficient for cell growth arrest and could be of clinical relevance in locoregional chemotherapy.
Antineoplastic Agents, Phytogenic↗
Evaluation of growth, cell proliferation, and cell death in bovine corpora lutea throughout the estrous cycle.
To evaluate the kinetics of luteal growth, bovine CL were obtained from four stages (stage I, Days 1-4; stage II, Days 5-10; stage III, Days 11-17; stage IV, Days 18-21) of the estrous cycle, and luteal fresh weight as well as DNA, protein, and progesterone contents was determined. To evaluate the relative rate of cell proliferation, proliferating cell nuclear antigen (PCNA; a specific marker for cell proliferation) was immunolocalized in paraffin-embedded luteal tissue sections. To evaluate the relative rate of cell death, nucleosomal fragmentation of DNA (a specific marker for apoptosis) was detected by agarose gel electrophoresis and also by histochemical localization in paraffin-embedded luteal tissue sections. Luteal fresh weight and DNA, protein, and progesterone contents increased (p < 0.01) from stage I to stage II, were similar between stages II and III, and then decreased (p < 0.01) from stage III to stage IV. The ratio of protein to DNA (an index of average cell size) was similar for stages I, II, and III and then decreased (p < 0.01) at stage IV. For stage I (corpora hemorrhagica), most proliferating (PCNA-positive) cells were located in or around the core of the tissue infoldings (presumably thecal-derived areas), whereas relatively few proliferating cells were located at the periphery of the tissue infoldings (presumably granulosa-derived areas). For stages II, III, and IV, the majority of proliferating cells appeared to be small cells (i.e., small parenchymal cells, fibroblasts, and endothelial cells). The labeling index (LI; percentage of cells that were PCNA-positive) was greatest at stage I (20.3 +/- 1.1%); it then decreased (p < 0.01) by stage II and was similar at stages II, III, and IV (3.4 +/- 1.1%). Apoptosis, as determined by evaluation of nucleosomal DNA fragmentation by agarose gel electrophoresis and in situ localization, was detectable only at stage IV. These data demonstrate that luteal growth from stage I to stage II resulted from cell proliferation as shown by a high LI at stage I, accompanied by increased luteal DNA content but no change in average cell size, and by similar protein: DNA ratios. Luteal regression from stage III to stage IV was primarily associated with cell deletion and decreased cell size as shown by a decrease in luteal DNA content and the appearance of apoptosis along with a decrease in the luteal protein: DNA ratio.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Expression of Nanog gene promotes NIH3T3 cell proliferation.
Cells are the functional elements in tissue engineering and regenerative medicine. A large number of cells are usually needed for these purposes. However, there are numbers of limitations for in vitro cell proliferation. Nanog is an important self-renewal determinant in embryonic stem cells. However, it remains unknown whether Nanog will influence the cell cycle and cell proliferation of mature cells. In this study, we expressed Nanog in NIH3T3 cells and showed that expression of Nanog in NIH3T3 promoted cells to enter into S phase and enhanced cell proliferation. This suggests that Nanog gene might function in a similar fashion in mature cells as in ES cells. In addition, it may provide an approach for in vitro cell expansion.
Animals↗
The HMX homeodomain protein MLS-2 regulates cleavage orientation, cell proliferation and cell fate specification in the C. elegans postembryonic mesoderm.
The proper formation of a complex multicellular organism requires the precise coordination of many cellular events, including cell proliferation, cell fate specification and differentiation. The C. elegans postembryonic mesodermal lineage, the M lineage, allows us to study mechanisms coordinating these events at single cell resolution. We have identified an HMX homeodomain protein MLS-2 in a screen for factors required for M lineage patterning. The MLS-2 protein is present in nuclei of undifferentiated cells in the early M lineage and in a subset of head neurons. In the M lineage, MLS-2 activity appears to be tightly regulated at the fourth round of cell division, coincident with the transition from proliferation to differentiation. A predicted null allele of mls-2, cc615, causes reduced cell proliferation in the M lineage, whereas a semi-dominant, gain-of-function allele, tm252, results in increased cell proliferation. Loss or overexpression of mls-2 also affects cleavage orientation and cell fate specification in the M lineage. We show that the increased cell proliferation in mls-2(tm252) mutants requires CYE-1, a G1 cell cycle regulator. Furthermore, the C. elegans Myod homolog HLH-1 acts downstream of mls-2 to specify M-derived coelomocyte cell fates. Thus MLS-2 functions in a cell type-specific manner to regulate both cell proliferation and cell fate specification.
Amino Acid Sequence↗
Cell surface changes in senescent and Werner's syndrome fibroblasts: their role in cell proliferation.
Cell surface is known to participate in the regulation of cell proliferation through interaction with adjacent cell surfaces or the extracellular matrix, or both. A clinical survey of the Werner syndrome suggests some disorders in glycosaminoglycan metabolism. Also, the skin fibroblasts derived from the patients with WS have a reduced proliferation capacity. We here examined, in vitro and in vivo, alterations of the cell-surface properties of WS cells and aging human fibroblasts. Cell-surface negative charges, examined by electrophoretic mobility of dispersed single cells in buffer, were seen to decline steadily as a function of cumulative population doublings. A strict linear relationship was found between electrophoretic mobility (micron/sec/V/cm) and number of cells harvested at each passage in all cell lines examined. The slope of this line in cells from donors of different ages indicated that WS fibroblasts resemble cells from much older normal controls. The same conclusion was drawn from our previous study of Con A-mediated red cell adsorption, which was confirmed as reflecting an alteration of cell-surface coat negative charge. Electrophoretic mobility after treatment of cell surface with degradative enzymes showed that the cell-surface negative charges were attributable to sialic acid, chondroitin sulphates, hyaluronic acid, and heparan sulphate. Two-dimensional electrophoresis of 3H-glucosamine incorporated glycosaminoglycans (GAGs) revealed that heparan sulphate was the main component of GAGs on the fibroblast cell surface and that the relative amount of heparan sulphate among GAGs on the cell surface increased in vitro with the number of passages. Growth kinetics of fibroblasts on sheets of fixed cells treated with a fixative (glutaraldehyde) and degradative enzymes were examined to elucidate the role of cell-surface GAGs in the regulation of cell proliferation. Cell growth was inhibited 40% when the fibroblasts were cultured on the fixed sheets of late passage cells. Treatment of the fixed cell sheets with heparitinase or nitrous acid resulted in complete recovery from the growth inhibition. Cell growth on sheets of fixed cells derived from young, middle, and senescent fibroblasts showed that the surface of the senescent cells had the greatest inhibitory effect. These inhibitory effects of fixed cell sheets correlated well with both the amount of heparan sulphate relative to the total GAGs on the surface and to the saturation density of cell growth at each passage. These findings strongly suggest that heparan sulphate, or its complex, on the cell surface is involved in the regulation of cell proliferation.(ABSTRACT TRUNCATED AT 400 WORDS)
Adolescent↗
Reproductive status influences cell proliferation and cell survival in the dentate gyrus of adult female meadow voles: a possible regulatory role for estradiol.
Galea and McEwen [Galea and McEwan (1999) Neuroscience 89, 955-964] found that cell proliferation was suppressed in female meadow voles trapped during the breeding season relative to females trapped during the non-breeding season. We investigated the effect of reproductive status and estradiol level on cell proliferation and cell survival in adult laboratory-reared female meadow voles to control for the variables of age, experience and pregnancy that could confound the results derived from a wild sample. Voles were housed in either a long- or short-photoperiod to simulate season and a male or female cage partner was introduced to influence reproductive status. Because females are reflex ovulators, exposure to a male rapidly induces behavioural estrous and high levels of estradiol. Forty-eight hours after introducing a cage partner, we injected either bromodeoxyuridine or [3H]thymidine to mark cell synthesis and then examined labelled cells 2h (cell proliferation) or five weeks (cell survival) later, respectively. To determine whether estradiol mimicked the effect of reproductive status, groups of reproductively inactive females were given a single injection of estradiol benzoate (10 microg) either four or 48h prior to bromodeoxyuridine labelling. The density of proliferating cells in the granule cell layer and the hilus was elevated in reproductively inactive females compared to reproductively active females and was correlated negatively with serum estradiol level. Exposure to estradiol benzoate initially increased cell proliferation (within 4h) but subsequently suppressed cell proliferation (within 48h). In addition, the density of surviving cells was greater in reproductively inactive females relative to reproductively active females but reproductively active females had a greater rate of cell survival than did reproductively inactive females. Reproductive status did not influence the number of pyknotic cells in the dentate gyrus (at either 2h or five weeks).We conclude that reproductive status regulates cell proliferation in adult female meadow voles, possibly via an estradiol-regulated mechanism. The results from the present study showed that reproductively active female meadow voles have suppressed rates of cell proliferation in the dentate gyrus relative compared with reproductively inactive female meadow voles. Administering estradiol initially (within 4h) elevates the cell proliferation within the dentate gyrus of adult females but subsequently (within 48h) suppresses cell proliferation. However, more new cells survived in females with high endogenous levels of estradiol (reproductively active females). In conclusion, reproductive status regulates the level of cell proliferation and survival through a complex estradiol regulated mechanism(s).
Adrenal Glands↗
Patterns of cell proliferation and cell death in the developing retina and optic tectum of the brown trout.
We have analyzed the patterns of cell proliferation and cell death in the retina and optic tectum of the brown trout (Salmo trutta fario) throughout embryonic and postembryonic stages. Cell proliferation was detected by immunohistochemistry with an antibody against the proliferating cell nuclear antigen (PCNA), and apoptosis by means of the TUNEL method. Haematoxylin and DAPI staining were also used to demonstrate apoptotic cells. Photoreceptor cell differentiation was assessed by immunohistochemistry with antibodies against opsins. Throughout embryonic development, PCNA-immunoreactive (PCNA-ir) cells become progressively restricted to the peripheral growth zone of the retina, which appears to be the principal source of new retinal cells from late embryos to adults. However, some PCNA-ir cells are observed secondarily in the differentiated retina, first in the inner nuclear layer of 15-mm alevins and later in the outer nuclear layer of 16-mm alevins, after differentiation of the first rods in the central retina, as demonstrated with opsin immunocytochemistry. Our observations also support the view that the PCNA-ir cells observed secondarily in the INL of the central retina of alevins are photoreceptor precursors. The number and distribution of apoptotic cells in the retina and optic tectum of the trout change throughout development, allowing distinction of several waves of apoptosis. Cell death is detected in proliferating areas at early stages, then in postmitotic or differentiating areas, and later concurring temporal and spatially with the establishment of visual circuits, thus indicating a relationship between apoptosis and proliferation, differentiation and synaptogenesis.
Animals↗
Effects of tomato paste extracts on cell proliferation, cell-cycle arrest and apoptosis in LNCaP human prostate cancer cells.
Since tomato consumption is associated with decreased risk of prostate cancer, cell proliferation, cell cycle progression and apoptosis by LNCaP human prostate cancer cells might elucidate action of tomatoes. To discover possible bioactive fractions of tomatoes, whole tomato paste and its water and hexane extract were used and biomarkers of carcinogenesis were measured. After 6, 24 and 48 hr of incubation, cells were harvested and determined cell growth. Tomato paste hexane extract inhibited cell proliferation by 33% compared to the control after 48 hr incubation. Whole tomato paste and its water extract showed only modest growth inhibition. Tomato paste hexane extract at 5 microM lycopene increased G2/M-phase of the cell cycle from 13 to 28% and decreased S-phase cells from 45 to 29%. Apoptosis was observed at the 5 microM hexane extract at the late stages during 24 and 48 hr treatment. Tomato, therefore, deserves study as a potential chemopreventive/chemotherapeutic agent.
Annexin A5↗
Negative regulation of p21 by beta-catenin/TCF signaling: a novel mechanism by which cell adhesion molecules regulate cell proliferation.
Cell proliferation is regulated in part by cell-cell interactions mediated by cadherin and connexin. Here we present evidence that these two molecules act synergistically to suppress HEK293 cell proliferation by prolonging the G2/M phase. This event was accompanied by expression of p21, a potent Cdc2 kinase inhibitor. Not surprisingly, there was a concomitant decline in Cdc2 kinase activity. beta-Catenin/TCF signaling, which was downregulated by overexpression of N-cadherin, was found to inhibit transactivation of p21 gene expression. The effect of N-cadherin on cell proliferation and p21 expression was augmented by co-expression of connexin-43. Moreover, the magnitude of the connexin's effect was dependent on its ability to mediate intercellular communication. We conclude, therefore, that two major components of cell-cell interaction synergistically regulate cell cycle progression in HEK293 cells by regulating p21 expression in a beta-catenin/TCF-dependent manner.
Cadherins↗
Cell proliferation by cell cycle analysis in young and old dietary restricted mice.
The effect of dietary restriction (DR) on cell proliferation determined by cell cycle analysis in tissues of young and old mice was investigated. Using the percentage of S-phase cells as an index of cell proliferation, we found that DR inhibited cell proliferation in spleen and thymus in young mice. No significant changes were found in bone marrow and kidney in the ad libitum (AL) or DR mice regardless of age. In old mice, the DR effect was observed in spleen only. When age increased, a parallel decline in cell proliferation was evidenced by a reduced % of S-phase cells. DR produces a greater cell cycle effect in the young mice than in the old mice. The present data suggests that inhibition of cell proliferation by DR may be affected by type of tissue, age, length of DR, and capacity or rate of cell proliferation.
Aging↗
Dynamics of cell proliferation and cell death during the emergence of primitive neuroectodermal tumors of the immature central nervous system in transgenic mice.
Cell proliferation and cell death play critical roles in embryonic development, postnatal tissue maintenance, and tumor formation. To understand the interplay between cell proliferation and death in tumor formation, we studied these two processes in nascent primitive neuroectodermal tumors that arose postnatally from neuroepithelial cells ventral to the median eminence of transgenic mice (designated rTH-Tag mice) carrying a Simian virus 40 large T antigen transgene driven by a rat tyrosine hydroxylase promoter. Cell proliferation continued in the neuroepithelium of the ventral median eminence in wild-type and transgenic animals for the first 2 weeks of postnatal life but subsided completely in the wild-type mice after 2 weeks of age. In contrast, mitotic activity persisted in these progenitor cells of the rTH-Tag mice, and there was a dramatic increase in mitotic activity after 10 weeks leading to the formation of primitive neuroectodermal tumors despite sustained cell death activity. We conclude that primitive neuroectodermal tumors originate from progenitor cells in the ventral median eminence of rTH-Tag mice in early postnatal life when progenitors fail to respond to signals to exit the cell cycle. Thus, the disruption of mechanisms that regulate cell proliferation and cell death in the developing brain may underlie the emergence of primitive neuroectodermal tumors in the rTH-Tag mice.
Animals↗