Certain Cells (certain + cell)

Distribution by Scientific Domains

Terms modified by Certain Cells

  • certain cell type

  • Selected Abstracts


    Matrigel: A complex protein mixture required for optimal growth of cell culture

    PROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 9 2010
    Chris S. Hughes
    Abstract Numerous cell types require a surface for attachment to grow and proliferate. Certain cells, particularly primary and stem cells, necessitate the use of specialized growth matrices along with specific culture media conditions to maintain the cells in an undifferentiated state. A gelatinous protein mixture derived from mouse tumor cells and commercialized as Matrigel is commonly used as a basement membrane matrix for stem cells because it retains the stem cells in an undifferentiated state. However, Matrigel is not a well-defined matrix, and therefore can produce a source of variability in experimental results. In this study, we present an in-depth proteomic analysis of Matrigel using a dynamic iterative exclusion method coupled with fractionation protocols that involve ammonium sulfate precipitation, size exclusion chromatography, and one-dimensional SDS-PAGE. The ability to identify the low mass and abundance components of Matrigel illustrates the utility of this method for the analysis of the extracellular matrix, as well as the complexity of the matrix itself. [source]


    p38, MAP kinase protects rat mesangial cells from TNF-,-induced apoptosis

    JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 4 2001
    Yan-Lin Guo
    Abstract p38 MAP kinases (p38) and c-Jun N-terminal protein kinases (JNK) have been associated with TNF-,-induced apoptosis. However, recent studies indicate that an early but brief activation of JNK and/or p38 may actually protect some cells from TNF-,-induced apoptosis. Whether the activation of JNK and p38 provides a pro- or anti-apoptotic signal for TNF-, has been controversial. In this study, we investigated the role of p38 in the regulation of TNF-, cytotoxicity in rat mesangial cells. Treatment of the cells with TNF-, alone had little effect on their viability, but they became very sensitive to apoptosis when treated with TNF-, in the presence of the p38 inhibitor SB 203580. These results suggested that the p38 pathway is critical for mesangial cells to survive the toxic effect of TNF-,. Using adenovirus-mediated gene transfer technique, we further demonstrated that p38,, but not p38,, is essential to protect the cells from TNF-, toxicity. It has been speculated that there is a synergetic interaction between the p38 and the nuclear factor-,B (NF-,B) pathways in protecting certain cells from apoptosis. However, expression of neither p38, nor its dominant negative mutant in mesangial cells interfered with TNF-,-induced translocation of NF-,B, the initial step of NF-,B activation. While it is unclear whether p38, regulates NF-,B transcription activity at other steps, it is apparent that p38, does not affect TNF-,-induced NF-,B activation at the stage of nuclear translocation. J. Cell. Biochem. 82: 556,565, 2001. © 2001 Wiley-Liss, Inc. [source]


    The highly specialized secretory epithelium in the buccal cavity of the alkalinity adapted Lake Magadi cichlid, Oreochromis alcalicus grahami (Teleostei: Cichlidae): a scanning and transmission electron microscope study

    JOURNAL OF ZOOLOGY, Issue 4 2000
    J. N. Maina
    Abstract Oreochromis alcalicus grahami is a small cichlid fish that lives in the hot, highly alkaline, highly saline peripheral lagoons of Lake Magadi, Kenya. The fish faces profound diurnal oscillations of oxygen concentration. During the day, from photosynthetic activity of cyanobacteria (blue-green algae), the water is supersaturated with oxygen but after sunset when photosynthetic activity stops the water is virtually anoxic as a result of bacterial respiration. During the night and after explosive exercise, O. a. grahami characteristically skims the surface of the water with the mouth agape, suggesting that the buccal cavity is used as a gas-exchange organ. Contrary to expectation, however, the buccal cavity was found to be conspicuously non-vascularized: the surface epithelial lining was fundamentally of a mucus secretory type. In addition, certain cells in the deeper layers showed extensive lateral labyrinths similar to the epithelium of the renal tubules. These morphological features respectively indicated roles of secreting a protective film and regulation of ions taken across the epithelial lining of the buccal cavity. The allocation of gas-exchange to the gills and the air-bladder, osmoregulation essentially to the gills, and mucus secretion/protection to the buccal cavity displays an adaptive trade-off process in an elite animal. Effective use of the buccal cavity as a gas-exchanger would entail air-gulping followed by brief retention of it in the cavity to allow oxygen uptake. During such interval, both the gills and the air-bladder would of necessity be rendered temporarily non-functional. Skimming the top layer of water with the mouth open ensures that the gills are passively ventilated with well aerated water and the air-bladder is simultaneously used for gas-exchange, a strategy that should enhance oxygen acquisition, especially at higher ambient temperatures. [source]


    v-Ha- ras mitogenic signaling through superoxide and derived reactive oxygen species

    MOLECULAR CARCINOGENESIS, Issue 4 2002
    Ji-Qin Yang
    Abstract The ras proto-oncogene is frequently mutated in human tumors and functions to constitutively stimulate signal transduction cascades, resulting in unchecked proliferation and malignant transformation. In certain cells, superoxide functions as a signal-transduction messenger, mediating the downstream effects of ras and rac. We demonstrated previously that v-Ha -ras,transfected rat kidney epithelial cells (RECs) overproduced superoxide anion and that this superoxide production was mediated by ras. In the present study, we further demonstrated that v-Ha -ras overexpression transformed immortal nonmalignant RECs into malignant cancer cells; v-Ha -ras,transfected cells formed clones in soft agar, had high plating efficiency, and formed tumors in nude mice. Our data suggest that superoxide radical plays a role in ras-induced transformation; modulation of intracellular superoxide level by overexpression of manganese-containing superoxide dismutase or copper- and zinc-containing superoxide dismutase inhibited ras-induced transformation, as evidenced by in vitro studies of plating efficiency and by in vivo studies of tumor formation in nude mice. Overexpression of catalase (CAT) alone was found to have little effect on tumor cell growth, but overexpression of glutathione peroxidase 1 (GPx1) completely suppressed tumor cell growth in nude mice. This finding suggests that peroxides removed by GPx1, but not by CAT, are also involved in ras-induced transformation. © 2002 Wiley-Liss, Inc. [source]


    Expression of HSP72 after ELF-EMF exposure in three cell lines,

    BIOELECTROMAGNETICS, Issue 7 2007
    Eric Gottwald
    Abstract It has been reported that magnetic fields with flux densities ranging from µT to mT are able to induce heat shock factor, HSP72 mRNA or heat shock proteins in various cells. In this study we investigated changes in the HSP72 mRNA transcription level in three cell lines (HL-60, H9c2, and Girardi heart cells) and in the intracellular HSP72 protein content in two cell lines (HL-60 and Girardi heart cells) after treatment schemes using electromagnetic fields with a flux density of 2 µT to 4 mT, a frequency of 50 Hz and exposure times from 15 to 30 min. None of the treatments or modalities showed any significant effect on the HSP72 protein level, although HSP72 mRNA could be induced, at least to some extent, with one of the parameter combinations in all cell lines tested. Obviously, HSP72 mRNA transcription and translation are not necessarily coupled in certain cells. This leads to the conclusion that electromagnetic field effects on HSP72 mRNA levels are not indicative for downstream effects unless increased mRNA levels can be correlated with increased HSP72 protein levels as well. Bioelectromagnetics 28:509,518, 2007. © 2007 Wiley-Liss, Inc. [source]


    Cyclophosphamide, methotrexate, and cytarabine embropathy: Is apoptosis the common pathway?,

    BIRTH DEFECTS RESEARCH, Issue 6 2003
    Keith K. Vaux
    BACKGROUND Cyclophosphamide (CP) is an alkylating agent primarily used for the treatment of autoimmune disease and cancer. The purpose of this article is two-fold: first, to indicate that CP is a recognized human teratogen based on the features seen in a child prenatally exposed to this agent, as well as features seen in the previously reported cases; second, to suggest a common pathway to explain the similarity in the pattern of malformation seen in infants prenatally exposed to CP, in infants prenatally exposed to methotrexate (MTX), and in infants prenatally exposed to cytosine arabinoside (CA). METHODS Case report and review of the literature of an infant prenatally exposed to CP during the first trimester with a specific pattern of malformation. Features are compared to seven previous reports. RESULTS A common pattern of malformation is delineated including growth deficiency, hypoplasia of the calvarial and facial bones, and oligodactyly. CONCLUSIONS The finding of a similar pattern of malformation among eight infants prenatally exposed to CP suggests that CP is a human teratogen. MTX and CA produce similar patterns of malformation in prenatally exposed infants despite very different pharmocologic profiles and metabolism. We speculate that the phenotype is a consequence of apoptosis in certain cells which are susceptible to the effects of the teratogen at specific stages of development. Birth Defects Research (Part A) 67403,408, 2003. Published 2003 Wiley-Liss, Inc. [source]


    Tumor blood flow interruption after radiotherapy strongly inhibits tumor regrowth

    CANCER SCIENCE, Issue 7 2008
    Katsuyoshi Hori
    To clarify the therapeutic significance of interrupting tumor blood flow after irradiation, we investigated X-irradiation-induced changes in hemodynamic parameters (blood flow, extravasation and washout of fluorescein isothiocyanate-dextran, and interstitial fluid pressure) in a variant of Yoshida sarcoma, LY80. Tumors in anesthetized male Donryu rats received local irradiation (10 Gy). At 48 h after irradiation, tumor blood flow increased significantly; at 72,96 h after irradiation, a 2,2.5-fold increase was observed. All parameters then consistently showed improved tumor microcirculation, which probably contributed to regrowth of cancer because certain cells survived irradiation. Rats received an intravenous dose (10 mg/kg) of a combretastatin derivative, AC7700 (AVE8062), which interrupts tumor blood flow and disrupts tumor vessels. At all times evaluated after irradiation, AC7700 completely stopped tumor blood flow. Radiotherapy efficacy was significantly enhanced when combined with AC7700: AC7700 given 48 h after irradiation, when tumor blood flow increased significantly, remarkably suppressed tumor regrowth compared with AC7700 given 48 h before irradiation. Also, postirradiation AC7700 completely inhibited not only primary tumor regrowth but also regional lymph node metastases in half of tumor-bearing rats and led to a significant improvement in survival. These results strongly suggest that the combination effect was enhanced via interruption of increased tumor blood flow after irradiation. This therapeutic combination and timing may have important benefits, even in tumors with low sensitivity to either treatment alone, because the effect was considerably greater than additive. Our data thus show that destruction of tumor microcirculation after irradiation is quite effective for preventing cancer recurrence. (Cancer Sci 2008; 99: 1485,1491) [source]