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apoptosis


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  • Sperm apoptosis in fresh and cryopreserved bull semen detected by flow cytometry and its relationship with fertility. 11804948

    The present study was conducted to detect sperm apoptosis in fresh and frozen semen and to determine its relationship with bull fertility. Three ejaculates were collected from five breeding bulls with different fertility levels and were cryopreserved using standard methods. Two flow cytometric methods were employed to measure apoptosis: an assay for phosphatidylserine (PS) translocation across the plasma membranes using fluorescein-labeled Annexin V and propidium iodide (PI), and an assay for nicked DNA using bromodeoxyuridine (BrdU), terminal deoxynucleotidyl transferase, and fluorescein-labeled anti-BrdU monoclonal antibody. Both assays showed that fresh sperm contained 10%-20% apoptotic sperm. Significant differences in the percentage of apoptotic sperm were observed among the bulls. Cryopreservation induced translocation of PS to the outer leaflet of the plasma membrane and caused most of the necrotic cells in fresh sperm to disintegrate. Bull fertility was significantly related to the percentage of necrotic or viable sperm in fresh semen as detected by the Annexin V/PI assay, to the number of apoptotic sperm in fresh semen as detected by the TUNEL assay, and to the level of chromatin or DNA condensation as detected by PI staining. The present study suggests that the presence of apoptotic spermatozoa in fresh semen could be one of the reasons for poor fertility in breeding bulls.
    Document Type:
    Reference
    Product Catalog Number:
    APT115
    Product Catalog Name:
    Apo-BrdU™ Detection Kit

  • Bim is an apoptosis sensor that responds to loss of survival signals delivered by epidermal growth factor but not those provided by integrins. 15292207

    Anoikis is a rapid apoptosis response that is initiated within a few minutes after inhibition of integrin signaling. In mammary epithelia, anoikis is mediated by subcellular translocation of Bax from the cytosol to mitochondria where it activates the intrinsic apoptosis pathway. The Bcl-2 homology 3 domain-only protein, Bim, has been proposed to have a key role in the apoptosis response of an epithelial cell line with reduced sensitivity to loss of integrin signaling, which undergoes apoptosis over a period of several days in suspension culture. Here we tested the involvement of Bim in the rapid anoikis response of mouse mammary epithelial cells and discovered that Bim does not have a role in detecting integrin-mediated signals. Instead Bim senses the loss of survival cues mediated by epidermal growth factor. Cell lines selected over many passages in culture have lost much of their sensitivity to anoikis signals arising from an altered cellular microenvironment and may undergo apoptosis through acquired mechanisms.
    Document Type:
    Reference
    Product Catalog Number:
    36-004

  • Apoptosis Inducer Set -2510290

    Document Type:
    Certificate of Analysis
    Lot Number:
    2510290
    Product Catalog Number:
    APT800
    Product Catalog Name:
    Apoptosis Inducer Set

  • Apoptosis Inducer Set - 3895934

    Document Type:
    Certificate of Analysis
    Lot Number:
    3895934
    Product Catalog Number:
    APT800
    Product Catalog Name:
    Apoptosis Inducer Set

  • Oxidative-induced apoptosis to an immortalized ganglion cell line is caspase independent but involves the activation of poly(ADP-ribose)polymerase and apoptosis-inducing ... 18053973

    The aim of the present work was to characterize the molecular basis of oxidative-induced death, a process that has been implicated in eye diseases like glaucoma, in RGC-5 cells, an immortalized retinal ganglion cell (RGC) line. Oxidative stress was induced by treatment of RGC-5 cells with hydrogen peroxide and compared to a known effect of a light insult (1000 lx, 400-760 nm). Hydrogen peroxide causes a loss of viability of RGC-5 cells in a dose-dependent manner. Loss of cell viability was by apoptosis characterized by breakdown of DNA (TUNEL method), presence of membrane phosphatidylserine (APOPercentage method), activation of PARP-1 and AIF. Oxidative stress caused a stimulation of ROS which reached maximum levels before optimum apoptosis. Hydrogen-peroxide-induced apoptosis did not result in an activation of caspase-3 and was unaffected by the caspase inhibitor Z-VAD-fmk. However, the PARP-1 inhibitor NU-1025 counteracted the effects of hydrogen peroxide and light. Evidence is provided to show that both forms of oxidative stress caused AIF to be cleaved with the product located to the cytosolic compartment. Light-induced apoptosis was attenuated by the presence of the mitochondrial uncoupler M3778 but potentiated by the presence of cobalt. In contrast, hydrogen-peroxide-induced apoptosis was unaffected by M3778 but attenuated by cobalt. The results show that oxidative stress caused by light is dependent on functional mitochondria and that the molecular mechanisms of apoptosis caused by hydrogen peroxide or light are similar but not identical.
    Document Type:
    Reference
    Product Catalog Number:
    MAB1637
    Product Catalog Name:
    Anti-Tubulin Antibody, beta III isoform, CT, clone TU-20 (Similar to TUJ1)

  • Apoptosis Inducer Set - 4112791

    Document Type:
    Certificate of Analysis
    Lot Number:
    4112791
    Product Catalog Number:
    APT800
    Product Catalog Name:
    Apoptosis Inducer Set

  • Apoptosis in acute shigellosis is associated with increased production of Fas/Fas ligand, perforin, caspase-1, and caspase-3 but reduced production of Bcl-2 and interleuk ... 12011015

    Shigella dysenteriae type 1-induced apoptotic cell death in rectal tissues from patients infected with Shigella dysenteriae type 1 was studied by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) technique and annexin V staining. Expression of proteins and cytokines participating in the apoptotic process (caspase-1, caspase-3, Fas [CD95], Fas ligand [Fas-L], perforin, granzyme A, Bax, WAF-1, Bcl-2, interleukin-2 [IL-2], IL-18, and granulocyte-macrophage colony-stimulating factor) in tissue in the acute and convalescent stages of dysentery was quantified at the single-cell level by in situ immunostaining. Apoptotic cell death in the lamina propria was markedly up-regulated at the acute stage (P < 0.05), where an increased number of necrotic cells were also seen. Phenotypic analysis of apoptotic cells revealed that 43% of T cells (CD3), 10% of granulocytes (CD15), and 5% of macrophages (CD56) underwent apoptosis. Increased activity of caspase-1 persisted in the rectum up to 1 month after onset. More-extensive expression of Fas, Fas-L, perforin, caspase-3, and IL-18, but not IL-2, at the acute stage than at the convalescent stage was observed. Increased expression of caspase-3 and IL-18 in tissues with severe inflammation compared to expression in those with mild inflammation was evident, implying a possible role in the perpetuation of inflammation. Significantly reduced cell death during convalescence was associated with a significant up-regulation of Bcl-2, Bax, and WAF-1 expression in the rectum compared to that in the acute phase of infection. Thus, induction of apoptosis at the local site in the early phase of S. dysenteriae type 1 infection was associated with a significant up-regulation of Fas/Fas-L and perforin and granzyme A expression and a down-regulation of Bcl-2 and IL-2, which promote cell survival.
    Document Type:
    Reference
    Product Catalog Number:
    MABF334