Search results for "programme"
showing 10 items of 874 documents
Glutamine potentiates TNF-α-induced tumor cytotoxicity
2001
L-glutamine (Gln) sensitizes tumor cells to tumor necrosis factor (TNF)-alpha-induced cytotoxicity. The type and mechanism of cell death induced by TNF-alpha was studied in Ehrlich ascites tumor (EAT)-bearing mice fed a Gln-enriched diet (GED; where 30% of the total dietary nitrogen was from Gln). A high rate of Gln oxidation promotes a selective depletion of mitochondrial glutathione (mtGSH) content to approximately 58% of the level found in tumor mitochondria of mice fed a nutritionally complete elemental diet (standard diet, SD). The mechanism of mtGSH depletion involves a glutamate-induced inhibition of GSH transport from the cytosol into mitochondria. The increase in reactive oxygen in…
Catchup: a mouse model for imaging-based tracking and modulation of neutrophil granulocytes
2015
Neutrophil granulocyte biology is a central issue of immunological research, but the lack of animal models that allow for neutrophil-selective genetic manipulation has delayed progress. By modulating the neutrophil-specific locus Ly6G with a knock-in allele expressing Cre recombinase and the fluorescent protein tdTomato, we generated a mouse model termed Catchup that exhibits strong neutrophil specificity. Transgene activity was found only in very few eosinophils and basophils and was undetectable in bone marrow precursors, including granulomonocytic progenitors (GMPs). Cre-mediated reporter-gene activation allowed for intravital two-photon microscopy of neutrophils without adoptive transfe…
Cell death and oxidative stress in gliomas.
1999
In gliomas, apoptosis and necrosis are determined by a number of promoting and inhibiting factors including oxidative cell stress mediated by nitric oxide synthases (NOS) and reduced by superoxide dismutases. Therefore, in 46 gliomas (including astrocytomas, oligodendrogliomas, oligo-astrocytomas, and glioblastomas), the relationship of apoptosis and necrosis and the expression of apoptosis-promoting (p53, bax, Fas, Fas-L) and inhibiting (bcl-2) factors as well as of different isoforms of NOS (NOSb, NOSe, NOSi) and manganese superoxide dismutase (MnSOD) were studied. Apoptosis was measured in situ by the TUNEL method while expression profiles of apoptosis-related and oxidative stress-associ…
Intrinsically determined cell death of developing cortical interneurons.
2009
The cell death of inhibitory neurons, which originate far from the cortical areas to which they migrate during embryonic development, is determined autonomously rather than by competition for trophic signals from other cell types. It has long been known that apoptosis, a form of programmed cell death, eliminates young cells from developing tissues. In the field of neurobiology, it is widely believed that developmental neuronal-cell death results from cellular competition for environmentally derived survival signals that selects for an optimally sized and properly wired population of neurons. This study of developmental cell death in the mouse cortex in vivo, in vitro and after transplantati…
Regulation of X-Chromosome-Linked Inhibitor of Apoptosis Protein in Kainic Acid-Induced Neuronal Death in the Rat Hippocampus
2001
XIAP (X-chromosome-linked inhibitor of apoptosis protein) is an antiapoptotic protein which inhibits the activity of caspases and suppresses cell death. However, little is known about the presence and function of XIAP in the nervous system. Here we report that XIAP mRNA is expressed in developing and adult rat brain. Using a specific antibody, we observed XIAP-immunoreactive cells in different brain regions, among others, in the hippocampus and cerebral cortex. Kainic acid, which induces delayed cell death of specific neurons, increased the levels of XIAP in the CA3 region of hippocampus. XIAP was, however, largely absent in cells undergoing cell death, as shown by TUNEL labeling and staini…
PINK1 displays tissue-specific subcellular location and regulates apoptosis and cell growth in breast cancer cells.
2010
The PINK1 gene is mutated in the germ line of patients with hereditary early-onset Parkinson disease, and PINK1 prosurvival function at neuronal mitochondria has been related with the etiology of this disease. However, the expression and function of PINK1 protein in nonneuronal tissues has not been determined yet. Here, we have analyzed PINK1 protein expression and subcellular distribution in normal and neoplastic human tissues and investigated the function of PINK1 in breast carcinoma cells. PINK1 protein, as stained by a specific anti-PINK1 monoclonal antibody, was widely expressed in human tissues, displaying high expression in epithelial tissues and in the central nervous system and low…
PED is overexpressed and mediates TRAIL resistance in human non-small cell lung cancer
2008
PED (phosphoprotein enriched in diabetes) is a death-effector domain (DED) family member with a broad anti-apoptotic action. PED inhibits the assembly of the death-inducing signalling complex (DISC) of death receptors following stimulation. Recently, we reported that the expression of PED is increased in breast cancer cells and determines the refractoriness of these cells to anticancer therapy. In the present study, we focused on the role of PED in non-small cell lung cancer (NSCLC), a tumour frequently characterized by evasion of apoptosis and drug resistance. Immunohistochemical analysis of a tissue microarray, containing 160 lung cancer samples, indicated that PED was strongly expressed …
CEP63 deficiency promotes p53-dependent microcephaly and reveals a role for the centrosome in meiotic recombination
2015
Artículo escrito por un elevado número de autores, solo se referencian el que aparece en primer lugar, el nombre del grupo de colaboración, si le hubiere, y los autores pertenecientes a la UAM
Mitochondrial alterations and tendency to apoptosis in peripheral blood cells from children with Down syndrome
2006
Different types of cells from subjects with Down syndrome (DS) have an increased susceptibility to cell death. We have studied apoptosis and mitochondrial (mt) membrane potential (DeltaPsi(m)) in peripheral blood mononuclear cells (PBMC) from DS children and age-matched healthy donors after in vitro treatment with apoptogenic molecules, along with mtDNA content. We found that PBMC from DS and healthy controls had a similar tendency to undergo apoptosis and a similar amount of mtDNA. However, in cells from DS subjects, mitochondria showed a higher loss of DeltaPsi(m), underlying the presence of an increasing susceptibility of these organelles to damaging agents.
Cerebrospinal fluid tau protein is not a biological marker in amyotrophic lateral sclerosis.
2009
Background: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder leading to progressive motor neuron cell death. Etiopathogenesis is still imperfectly known and much effort have been undertaken to find a biological marker that could help in the early diagnosis and in the monitoring of disease progression. Cerebrospinal fluid (CSF) concentrations of tau, an axonal microtubule-associated protein, have been measured in ALS with levels found increased in some studies and unchanged in others. Methods: Total CSF tau level was assayed in a population of ALS patients (n = 57) and controls (n = 110) using a specific ELISA method. Results: No significant differences in the median CS…