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Apoptotic Genes (apoptotic + gene)

Distribution by Scientific Domains

Medical Sciences	80%

Selected Abstracts

Expression Pattern of Apoptotic Genes in Vitrified-Thawed Bovine Oocytes

REPRODUCTION IN DOMESTIC ANIMALS, Issue 5 2010
VM Anchamparuthy
Contents This study describes a method for quantification of transcripts from low numbers of bovine oocytes using real time RT-PCR. The objective was to evaluate the expression pattern of apoptotic genes (Fas, FasL, Bax and Bcl-2) in vitrified-thawed oocytes. Oocytes were evaluated at germinal vesicle stage; at 15 h of maturation; after vitrification and warming at 15 h of maturation and at 9 h of additional maturation. All transcripts showed an increase in at least 1.2-fold change post-vitrification warming, but the levels tended to decrease at 9 h of maturation post-vitrification warming. Transcript abundance for Fas mRNA was 1.4-fold for oocytes after vitrification and warming. The level of Fas mRNA upon maturation was 0.8-fold. The increase in the abundance of FasL mRNA was 2.1, while it was 0.5-fold relative to control. Vitrification resulted in 1.5-fold change in Bax mRNA expression in oocytes. After 9 h of maturation post-vitrification warming, the level for Bax mRNA was 0.6-fold. The mRNA for Bcl-2 was nearly the same after vitrification and warming. The abundance of mRNA for Bcl-2 was 1.2-fold in vitrified oocytes and fell (p = 0.05) to 0.5 at 9 h of maturation post-vitrification and warming. The up-regulation of apoptotic genes in vitrified oocytes may be an early indicator of reduced developmental competence following vitrification. Yet, results from terminal deoxynucleotidyl transferase dUTP nick end labelling and caspase assays did not support the evidence of apoptosis in embryos derived from large numbers of vitrified oocytes. [source]

Analysis of genomic dose-response information on arsenic to inform key events in a mode of action for carcinogenicity

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 1 2010
P. Robinan Gentry
Abstract A comprehensive literature search was conducted to identify information on gene expression changes following exposures to inorganic arsenic compounds. This information was organized by compound, exposure, dose/concentration, species, tissue, and cell type. A concentration-related hierarchy of responses was observed, beginning with changes in gene/protein expression associated with adaptive responses (e.g., preinflammatory responses, delay of apoptosis). Between 0.1 and 10 ,M, additional gene/protein expression changes related to oxidative stress, proteotoxicity, inflammation, and proliferative signaling occur along with those related to DNA repair, cell cycle G2/M checkpoint control, and induction of apoptosis. At higher concentrations (10,100 ,M), changes in apoptotic genes dominate. Comparisons of primary cell results with those obtained from immortalized or tumor-derived cell lines were also evaluated to determine the extent to which similar responses are observed across cell lines. Although immortalized cells appear to respond similarly to primary cells, caution must be exercised in using gene expression data from tumor-derived cell lines, where inactivation or overexpression of key genes (e.g., p53, Bcl-2) may lead to altered genomic responses. Data from acute in vivo exposures are of limited value for evaluating the dose-response for gene expression, because of the transient, variable, and uncertain nature of tissue exposure in these studies. The available in vitro gene expression data, together with information on the metabolism and protein binding of arsenic compounds, provide evidence of a mode of action for inorganic arsenic carcinogenicity involving interactions with critical proteins, such as those involved in DNA repair, overlaid against a background of chemical stress, including proteotoxicity and depletion of nonprotein sulfhydryls. The inhibition of DNA repair under conditions of toxicity and proliferative pressure may compromise the ability of cells to maintain the integrity of their DNA. Environ. Mol. Mutagen., 2010. © 2009 Wiley-Liss, Inc. [source]

Expression of Apoptosis Regulatory Genes and Incidence of Apoptosis in Different Morphological Quality Groups of In Vitro-produced Bovine Pre-implantation Embryos

REPRODUCTION IN DOMESTIC ANIMALS, Issue 5 2010
MG Melka
Contents Apoptosis occurs during early development in both in vivo - and in vitro -produced embryos, and is considered as one of the causes of embryonic loss. The objectives of this study were, therefore, investigating stage-specific expression profiles of apoptosis regulatory genes in three quality groups of in vitro -produced bovine pre-implantation embryos; and analysing the relationship between cell number and DNA fragmentation with expressions of those genes. The relative abundance of mRNA of 9 pro- (Bax, caspase-9, Bcl-xs, P53, Caspase-3 and Fas) and anti- (Bcl-w and Mcl-1) apoptotic genes was analysed. Differential cell staining and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labelling were performed to analyse the variation in cell numbers and detect apoptotic nuclei respectively. Expression of Bax and Caspase-3 genes was significantly (p < 0.05) higher in poor quality pre-implantation embryos as compared with that of morphologically good quality embryos of the same developmental stages. Moreover, Mcl-1 expression was significantly higher in good quality immature oocytes than that in the poor quality group. Moreover, higher DNA fragmentation was evidenced in morphologically poor quality blastocysts. In conclusion, our study demonstrates that Bax, caspase-3 and Mcl-1 can be used as potential markers of embryo quality to evaluate in vitro -produced bovine embryos. Further studies are required to investigate specific molecular signatures that can be used in evaluating in vivo -derived embryos. [source]

Expression Pattern of Apoptotic Genes in Vitrified-Thawed Bovine Oocytes

Prolactin alters the mechanisms of B cell tolerance induction

ARTHRITIS & RHEUMATISM, Issue 6 2009
Subhrajit Saha
Objective Autoimmune diseases predominantly affect women, suggesting that female sex hormones may play a role in the pathogenesis of such diseases. We have previously shown that persistent mild-to-moderate elevations in serum prolactin levels induce a break in self tolerance in mice with a BALB/c genetic background. The aim of this study was to evaluate the effects of hyperprolactinemia on the mechanisms of B cell tolerance induction. Methods Effects of prolactin on splenic B cell subsets were studied in female BALB/c mice. B cell receptor (BCR),mediated apoptosis and proliferation of transitional B cells were analyzed by flow cytometry. Expression of apoptotic genes was examined by microarrays and real-time polymerase chain reaction analysis. B cells coexpressing ,/, light chains were assessed by flow cytometry and immunohistochemistry. Activation status of transitional type 3 (T3) B cells was evaluated by BCR-induced calcium influx studies. Results BCR-mediated apoptosis of the T1 B cell subset, a major checkpoint for negative selection of autoreactive specificities, was decreased in prolactin-treated mice. Microarray studies indicated that this event may be mediated by the prolactin-induced up-regulation of the antiapoptotic gene interferon-, receptor type II and down-regulation of the proapoptotic gene Trp63. Prolactin treatment also altered the amount of receptor editing, as indicated by the increased number of transitional B cells coexpressing ,/, light chains. Additionally, hyperprolactinemia modified the level of B cell anergy by increasing the degree of BCR-induced calcium influx in the T3 B cells. Conclusion Persistently elevated serum prolactin levels interfere with B cell tolerance induction by impairing BCR-mediated clonal deletion, deregulating receptor editing, and decreasing the threshold for activation of anergic B cells, thereby promoting autoreactivity. [source]