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Cell's Ability (cell + ability)
Selected AbstractsHuman articular chondrocytes suppress in vitro proliferation of anti-CD3 activated peripheral blood mononuclear cellsJOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2006Chiara Bocelli-Tyndall Objective: To investigate whether mature human articular chondrocytes (AC) exhibit an antiproliferative effect on activated peripheral blood mononuclear cells (PBMC) and to compare this effect with other cells of mesenchymal origin. Methods: AC from healthy cadaveric cartilage were grown for different passages, in the absence (control) or presence of factors enhancing cell de-differentiation (transforming growth factor (TGF),1, fibroblast growth factor (FGF)-2, and platelet derived growth factor (PDGF)bb-TFP medium). Cell ability to suppress PBMC proliferation driven by anti-CD3 antibody was measured by tritiated thymidine uptake following incubation for 48 h at different PBMC:AC ratios and expressed as percent of residual proliferation (RP). AC antiproliferative effect was compared to that of control dermal fibroblasts (DF) and bone marrow stromal cells (BMSC). Results: AC exhibited a cell number-dependent antiproliferative effect. The strongest effect (up to 2% RP) was measured using the least expanded AC cultures. The use of TFP medium for AC expansion resulted in a significantly lower antiproliferative effect, in the range of that induced by BMSC (up to 18% RP). Also DF induced a marked antiproliferative effect (up to 11% RP). Conclusion: We report for the first time that human AC have a marked antiproliferative effect on anti-CD3 stimulated PBMC, which is reduced upon culture in medium-inducing extensive cell de-differentiation. These results reflect the immunosuppressive properties observed for other different mesenchymal cell types and raise the question of a potential common physiological role in local tissue protection. J. Cell. Physiol. 209: 732,734, 2006. © 2006 Wiley-Liss, Inc. [source] Understanding cisplatin resistance using cellular modelsIUBMB LIFE, Issue 11 2007Britta Stordal Abstract Many mechanisms of cisplatin resistance have been proposed from studies of cellular models of resistance including changes in cellular drug accumulation, detoxification of the drug, inhibition of apoptosis and repair of the DNA adducts. A series of resistant models were developed from CCRF-CEM leukaemia cells with increasing doses of cisplatin from 100 ng/ml. This produced increasing resistance up to 7-fold with a treatment dose of 1.6 ,g/ml. Cisplatin resistance in these cells correlated with increases in the antioxidant glutathione, yet treatment with buthionine sulphoximine, an inhibitor of glutathione synthesis, had no effect on resistance, suggesting that the increase in glutathione was not directly involved in cisplatin resistance. Two models were developed from H69 SCLC cells, H69-CP and H69CIS200 using 100 ng/ml or 200 ng/ml cisplatin respectively. Both cell models were 2-4 fold resistant to cisplatin, and have decreased expression of p21 which may increase the cell's ability to progress through the cell cycle in the presence of DNA damage. Both the H69-CP and H69CIS200 cells showed no decrease in cellular cisplatin accumulation. However, the H69-CP cells have increased levels of cellular glutathione and are cross resistant to radiation whereas the H69CIS200 cells have neither of these changes. This suggests that increases in glutathione may contribute to cross-resistance to other drugs and radiation, but not directly to cisplatin resistance. There are multiple resistance mechanisms induced by cisplatin treatment, even in the same cell type. How then should cisplatin-resistant cancers be treated? Cisplatin-resistant cell lines are often more sensitive to another chemotherapeutic drug paclitaxel (H69CIS200), or are able to be sensitized to cisplatin with paclitaxel pre-treatment (H69-CP). The understanding of this sensitization by paclitaxel using cell models of cisplatin resistance will lead to improvements in the clinical treatment of cisplatin resistant tumours. IUBMB Life, 59: 696-699, 2007 [source] The neuropathology of frontotemporal lobar degeneration with respect to the cytological and biochemical characteristics of tau proteinNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 1 2004S. Taniguchi Pathological examinations, using a panel of tau and other antibodies, were performed on the brains from 55 consecutively acquired cases of frontotemporal lobar degeneration (FTLD). Clinically, these comprised 31 cases of frontotemporal dementia (FTD), 10 cases of motor neurone disease inclusion dementia (MNDID), seven cases of progressive aphasia (PA), four cases of semantic dementia (SD) and three cases of progressive apraxia (PAX). Tau pathology, in the form of neurofibrillary tangles (NFTs) and glial cell tangles, was present in six cases of FTD with parkinsonism linked to chromosome 17, five of these cases resulting from +16 splice-site mutation and one from +13 mutation in the tau gene. The insoluble tau proteins were comprised mostly of four-repeat (4-R) isoforms. Eight other cases of FTD, one of PA and all three cases of PAX showed tau-positive inclusions (Pick bodies) and swollen cells (Pick cells), characteristic of Pick's disease. In these cases, the insoluble tau proteins were present in most instances as three-repeat (3-R) tau isoforms, although two cases with a mixture of 3-R and 4-R isoforms were seen. One other case of FTD showed an unusual pathology characterized by massive extracellular deposition of tau protein, composed of 4-R tau isoforms, within white matter without neuronal or glial cell inclusions. However, 33 (60%) of 55 FTLD cases showed no tau pathology in the brain, except for the rare NFTs, composed of a mix of 3-R and 4-R isoforms, in some of the more elderly cases. Of these 33 cases, 13 had FTD, 10 had MNDID, six had PA and four had SD. The pathological changes present were those of a superficial cortical laminar microvacuolation with mild subpial and subcortical gliosis; the 10 MNDID cases had ubiquitin-positive inclusions in the cerebral cortex and hippocampus. These 33 nontau FTLD cases, along with five Alzheimer's disease (AD) and six Huntington's disease (HD) cases with severe pathology, showed a variable loss of soluble tau proteins, broadly comparable with the extent of neuronal loss from the cortex and loss of the intracortical perikaryal marker, NeuN, but unrelated to proteins within afferent projection fibres such as neurofilament and ,-synuclein. Levels of tau mRNA were decreased in parallel in the tau-negative FTLD cases and in the severe AD and HD cases. Hence, the loss of tau from these 33 nontau FTLD cases is just one aspect of a neurodegenerative process that destroys many components of the nerve cell machinery and does not represent a specific disordering of the cell's ability to form tau proteins or incorporate these into microtubules. [source] Engineering Propionibacterium acidipropionici for enhanced propionic acid tolerance and fermentationBIOTECHNOLOGY & BIOENGINEERING, Issue 4 2009An Zhang Abstract Propionibacterium acidipropionici, a Gram-positive, anaerobic bacterium, has been the most used species for propionic acid production from sugars. In this study, the metabolically engineered mutant ACK-Tet, which has its acetate kinase gene knocked out from the chromosome, was immobilized and adapted in a fibrous bed bioreactor (FBB) to increase its acid tolerance and ability to produce propionic acid at a high final concentration in fed-batch fermentation. After about 3 months adaptation in the FBB, the propionic acid concentration in the fermentation broth reached ,100,g/L, which was much higher than the highest concentration of ,71,g/L previously attained with the wild-type in the FBB. To understand the mechanism and factors contributing to the enhanced acid tolerance, adapted mutant cells were harvested from the FBB and characterized for their morphology, growth inhibition by propionic acid, protein expression profiles as observed in SDS,PAGE, and H+ -ATPase activity, which is related to the proton pumping and cell's ability to control its intracellular pH gradient. The adapted mutant obtained from the FBB showed significantly reduced growth sensitivity to propionic acid inhibition, increased H+ -ATPase expression and activity, and significantly elongated rod morphology. Biotechnol. Bioeng. 2009; 104: 766,773 © 2009 Wiley Periodicals, Inc. [source] 3241: Effect of glutaredoxin 2 gene knockout on lens epithelial cells against oxidative stressACTA OPHTHALMOLOGICA, Issue 2010M LOU Purpose The mitochondrial glutaredoxin 2 (Grx2) is known to possess both dethiolase and peroxidase activities, and has shown an ability to protect cells from oxidative stress-induced apoptosis in the human lens epithelial cells. In this study, we further studied the function of Grx2 by using Grx2 knockout mouse lens epithelial (MLE) cells as a model. Methods Primary culture of MLE cells was established from the lenses of wild-type (WT) and Grx2-knockout (Grx2 KO) mice. Cells were probed for ,A-crystallin and Grx2 by Western blot analysis while cell viability was examined by WST-8 assay. Glutathione (GSH) level, Grx2 and Complex I activities, and lactate dehydrogenase (LDH) release were determined by spectrophotometric assays. Reactive oxygen species was detected using DCF-DA fluorescein with a cell sorter. Apoptosis was quantified by flow cytometry. Results Both primary cell cultures were confirmed to be lens epithelial cells by the presence of ,A-crystallin. Western blotting showed normal expression of Grx2 in WT cells but absent in Grx2 KO cells. Both cell types showed similar morphology and growth rate with same level of GSH pool and complex 1 activity in the mitochondrial fraction. However, KO cells were more sensitive to oxidative stress (100 ,M H2O2 for 6 h) and exhibited lower cell viability and more LDH leakage in comparison with the WT cells. In addition, knockdown of Grx2 weakened the cell's ability to detoxify H2O2 and enhanced the H2O2-induced inactivation of complex I in the electron transport chain. Conclusion Grx2 can protect MLE cells from H2O2-induced cell injury, and the mechanism of this protection is likely associated with its ability to detoxify H2O2 and its preservation of complex I activity in the mitochondria. [source] Intracellular Ca2+ responses and cell volume regulation upon cholinergic and purinergic stimulation in an immortalized salivary cell lineEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 3 2010Marit H. Aure Aure MH, Røed A, Kanli Galtung H. Intracellular Ca2+responses and cell volume regulation upon cholinergic and purinergic stimulation in an immortalized salivary cell line. Eur J Oral Sci 2010; 118: 237,244. © 2010 The Authors. Journal compilation © 2010 Eur J Oral Sci The water channel aquaporin 5 (AQP5) seems to play a key role in salivary fluid secretion and appears to be critical in the cell volume regulation of acinar cells. Recently, the cation channel transient potential vanilloid receptor 4 (TRPV4) was shown to be functionally connected to AQP5 and also to cell volume regulation in salivary glands. We used the Simian virus 40 (SV40) immortalized cell line SMG C10 from the rat submandibular salivary gland to investigate the effect of ATP and the neurotransmitter analogue carbachol on Ca2+ signalling and cell volume regulation, as well as the involvement of TRPV4 in the responses. We used fura-2-AM imaging, cell volume measurements, and western blotting. Both carbachol and ATP increased the concentration of intracellular Ca2+, but no volume changes could be measured. Inhibition of TRPV4 with ruthenium red impaired both ATP- and carbachol-stimulated Ca2+ signals. Peak Ca2+ signalling during hyposmotic exposure was significantly decreased following inhibition of TRPV4, while the cells' ability to volume regulate appeared to be unaffected. These results show that in the SMG C10 cells, simulation of nervous stimulation did not induce cell swelling, although the cells had intact volume regulatory mechanisms. Furthermore, even though Ca2+ signals were not needed for this volume regulation, TRPV4 seems to play a role during ATP and carbachol stimulation. [source] The novel herbicide oxaziclomefone inhibits cell expansion in maize cell cultures without affecting turgor pressure or wall acidificationNEW PHYTOLOGIST, Issue 2 2005Nichola O'Looney Summary ,,Oxaziclomefone [OAC; IUPAC name 3-(1-(3,5-dichlorophenyl)-1-methylethyl)-3,4-dihydro-6-methyl-5-phenyl-2H -1,3-oxazin-4-one] is a new herbicide that inhibits cell expansion in grass roots. Its effects on cell cultures and mode of action were unknown. In principle, cell expansion could be inhibited by a decrease in either turgor pressure or wall extensibility. ,,Cell expansion was estimated as settled cell volume; cell division was estimated by cell counting. Membrane permeability to water was measured by a novel method involving simultaneous assay of the efflux of 3H2O and [14C]mannitol from a ,bed' of cultured cells. Osmotic potential was measured by depression of freezing point. ,,OAC inhibited cell expansion in cultures of maize (Zea mays), spinach (Spinacia oleracea) and rose (Rosa sp.), with an ID50 of 5, 30 and 250 nm, respectively. In maize cultures, OAC did not affect cell division for the first 40 h. It did not affect the osmotic potential of cell sap or culture medium, nor did it impede water transport across cell membranes. It did not affect cells' ability to acidify the apoplast (medium), which may be necessary for ,acid growth'. ,,As OAC did not diminish turgor pressure, its ability to inhibit cell expansion must depend on changes in wall extensibility. It could be a valuable tool for studies on cell expansion. [source] Fas Antigen Expression on the Decidual Lymphocytes of Pre-Eclamptic PatientsAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 4 2000DOROTA DARMOCHWAL-KOLARZ PROBLEM: Apoptosis has been proposed as a mechanism for maintaining the homeostasis in the immune system. Activated lymphocytes are removed by a programmed cell death process Fas/FasL-mediated called activation induced cell death. The aim of the study was to investigate Fas antigen expression on decidual cells (T CD4+ lymphocytes, T CD8+ lymphocytes and Natural Killer (NK) cells) of pre-eclamptic patients and healthy pregnant women. METHOD OF STUDY: 12 pre-eclamptic patients and 10 healthy pregnant women were studied. Lymphocytes were isolated from decidual tissues mechanically, labeled by direct staining with monoclonal antibodies, and analyzed using the flow cytometric method. RESULTS: We found Fas antigen expression on decidual NK cells and T lymphocytes. CD 95 molecule expression and fluorescence intensity on NK cells of pre-eclamptic patients were lower when compared with controls (P<0.05). CONCLUSIONS: These findings suggest that decidual NK cells and T lymphocytes are able to undergo Fas/FasL-mediated apoptosis. It seems that NK cells' ability to undergo Fas/FasL-mediated apoptosis in pre-eclamptic patients can be altered because of lower CD95 molecule expression. [source] | |||||||||||||