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Cell Proliferation Activity (cell + proliferation_activity)
Selected AbstractsCorrelation between Musashi-1 and c-hairy-1 expression and cell proliferation activity in the developing intestine and stomach of both chicken and mouseDEVELOPMENT GROWTH & DIFFERENTIATION, Issue 8 2005Rieko Asai Musashi-1 (Msi-1) is an RNA-binding protein that plays key roles in the maintenance of neural stem cell states and in their differentiation into neural cells. Msi-1 has also been proposed as a candidate marker gene of mammalian intestinal stem cells and their immediate lineages. In this study, we examined Msi-1 expression in the small intestine and the stomach of both chicken and mouse during embryonic, fetal and postnatal development. In addition, we analyzed the expression of c-hairy-1, a chicken homologue of mouse Hes1, and assessed the proliferative activity of the cells expressing both of these factors. Significantly, during the development of these digestive organs in both species Msi-1 expression showed dynamic changes, suggesting that it is important for digestive organ development, particularly for epithelial differentiation. Based on our observations of the expression patterns of Msi-1 and c-hairy-1 in the adult small intestine, we speculate that Msi-1 is also a stem cell marker of the chicken small intestinal epithelium. [source] Induction of bovine articular chondrocyte senescence with oxidized low-density lipoprotein through lectin-like oxidized low-density lipoprotein receptor 1ARTHRITIS & RHEUMATISM, Issue 10 2009Satoshi Zushi Objective Findings of recent in vivo and in vitro studies suggest that oxidized low-density lipoprotein (ox-LDL) plays a role in the degeneration of cartilage. The purpose of this study was to determine whether ox-LDL induces chondrocyte senescence through binding to lectin-like ox-LDL receptor 1 (LOX-1). Methods The effects of ox-LDL on senescence of cultured bovine articular chondrocytes (BACs) were investigated by observing senescence-associated (SA) ,-galactosidase (,-gal) activity, cell proliferation activity, and telomerase activity. Telomerase activity was measured after adding LY294002 (a specific inhibitor of phosphatidylinositol 3-kinase [PI3K]) or after adding insulin-like growth factor 1 (IGF-1; an activator of PI3K) plus ox-LDL to the culture medium to elucidate the involvement of the PI3K/Akt pathway. Immunoblot analysis was used to investigate whether ox-LDL affects the phosphorylation of Akt. To ascertain whether these effects were attributable to ox-LDL binding to LOX-1, BACs were preincubated with TS-20, an anti-bovine LOX-1 blocking antibody. Results The activity of SA ,-gal was increased and the incorporation of bromodeoxyuridine into BACs was decreased by ox-LDL in a dose-dependent manner. The telomerase activity of BACs was suppressed by the addition of ox-LDL in a time- and dose-dependent manner. LY294002 suppressed the telomerase activity of BACs, and IGF-1 reversed the ox-LDL,induced suppression of telomerase activity. In addition, ox-LDL rapidly decreased the amount of phosphorylated Akt in BACs. Pretreatment of cultured BACs with TS-20 recovered these effects. Conclusion These data show that ox-LDL binding to LOX-1 induces stress-induced premature senescence of chondrocytes and results in suppression of telomerase activity by inactivating the PI3K/Akt pathway. Oxidized LDL may play an important role in the pathogenesis of osteoarthritis by inducing chondrocyte senescence. [source] Non-thermal cytocidal effect of infrared irradiation on cultured cancer cells using specialized deviceCANCER SCIENCE, Issue 6 2010Yohei Tanaka As infrared penetrates the skin, thermal effects of infrared irradiation on cancer cells have been investigated in the field of hyperthermia. We evaluated non-thermal effects of infrared irradiation using a specialized device (1100,18000 nm with filtering of wavelengths between 1400 and 1500 nm and contact cooling) on cancer cells. In in vitro study, five kinds of cultured cancer cell lines (MCF7 breast cancer, HeLa uterine cervical cancer, NUGC-4 gastric cancer, B16F0 melanoma, and MDA-MB435 melanoma) were irradiated using the infrared device, and then the cell proliferation activity was evaluated by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay. Proliferation of all the cancer cell lines was significantly suppressed by infrared irradiation. Total infrared output appeared to be correlated with cell survival. Increased temperature during infrared irradiation appeared not to play a role in cell survival. The maximum temperature elevation in the wells after each shot in the 20 and 40 J/cm2 culture was 3.8°C and 6.9°C, respectively. In addition, we have shown that infrared irradiation significantly inhibited the tumor growth of MCF7 breast cancer transplanted in severe combined immunodeficiency mice and MDA-MB435 melanoma transplanted in nude mice in vivo. Significant differences between control and irradiated groups were observed in tumor volume and frequencies of TUNEL-positive and Ki-67-positive cells. These results indicate that infrared, independent of thermal energy, can induce cell killing of cancer cells. As this infrared irradiation schedule reduces discomfort and side effects, reaches the deep subcutaneous tissues, and facilitates repeated irradiations, it may have potential as an application for treating various forms of cancer. (Cancer Sci 2010) [source] Decreased Expression of Bcl-x Protein during Hepatocarcinogenesis Induced Exogenously and Endogenously in RatsCANCER SCIENCE, Issue 12 2001Yutaka Hatanaka Dysregulations of apoptosis have been widely recognized as important events in multi-stage carcinogenesis. Bcl-x, a member of the Bcl-2 family, is known to act as a regulator of apoptosis. The present study was conducted to assess the role of altered Bcl-x protein expression in exogenous and endogenous hepatocarcinogenesis in rats. In the short-term exogenous models, male Fischer 344 rats, 6 weeks old, were given a single intraperitoneal injection of diethylnitrosamine (DEN) at a dose of 200 mg/kg body weight, partially hepatectomized at the end of week 3, administered phenobarbital at a concentration of 0.05% from the end of week 2 for 6 weeks, and sacrificed. In the livers, glutathione S-transferase (GST-P)-positive, putative preneoplastic lesions were induced, and Bcl-x protein expression was decreased in 24.7% of such lesions. The incidence of GST-P-positive lesions with decreased Bcl-x increased depending on the size of the lesions; 18.9%, 32.4% and 86.5% in the lesions smaller than 0.03, between 0.03 and 0.3, and larger than 0.3 mm2, respectively. In GST-P-positive lesions larger than 0.3 mm2, both apoptosis induction and cell proliferation activity were enhanced when Bcl-x protein expression was decreased. In the long-term exogenous models, rats were given 10 mg/kg of DEN, partially hepatectomized 4 h after treatment, administered 0.5 mg/kg of colchicine at the end of days 1 and 3, subjected to a selection procedure, and sacrificed at the end of week 45. Hepatocellular carcinomas were induced with the decreased Bcl-x protein expression. In the endogenous model, rats were fed a choline-deficient, l -amino acid-defined diet for 16 or 80 weeks and sacrificed. Bcl-x protein expression was decreased both in GST-P-positive lesions and hepatocellular carcinoma. These results suggest that this decrease of Bcl-x protein might serve as an indicator of the advanced form of preneoplastic lesions, and that this decrease could also be associated with a potential to progress into carcinoma in both exogenous and endogenous hepatocarcinogenesis of rats. [source] | ||||||||||