Hypoxia prolongs neutrophil survival in vitro

[1]  T. Behrens,et al.  Bcl-xL rescues WEHI 231 B lymphocytes from oxidant-mediated death following diverse apoptotic stimuli. , 1995, Journal of immunology.

[2]  M. Raff,et al.  Programmed cell death and Bcl-2 protection in very low oxygen , 1995, Nature.

[3]  Y. Tsujimoto,et al.  Prevention of hypoxia-induced cell death by Bcl-2 and Bcl-xL , 1995, Nature.

[4]  R. Muschel,et al.  Induction of apoptosis at different oxygen tensions: evidence that oxygen radicals do not mediate apoptotic signaling. , 1995, Cancer research.

[5]  G. Cox,et al.  Macrophage engulfment of apoptotic neutrophils contributes to the resolution of acute pulmonary inflammation in vivo. , 1995, American journal of respiratory cell and molecular biology.

[6]  P. O'dwyer,et al.  Apoptosis in human adenocarcinoma HT29 cells induced by exposure to hypoxia. , 1995, Journal of the National Cancer Institute.

[7]  C. Stevens,et al.  The joint, a redox sensitive microenvironment?--an hypothesis. , 1995, Scandinavian journal of rheumatology. Supplement.

[8]  D. Rosenbaum,et al.  Evidence for hypoxia‐induced, programmed cell death of cultured neurons , 1994, Annals of neurology.

[9]  H. Namiki,et al.  Apoptotic cell death induced by serum and its prevention by thiols , 1994, Journal of cellular physiology.

[10]  H. Horvitz,et al.  C. elegans cell survival gene ced-9 encodes a functional homolog of the mammalian proto-oncogene bcl-2 , 1994, Cell.

[11]  D. Bredesen,et al.  Bcl-2 inhibition of neural death: decreased generation of reactive oxygen species. , 1993, Science.

[12]  Z. Oltvai,et al.  Bcl-2 functions in an antioxidant pathway to prevent apoptosis , 1993, Cell.

[13]  C. Haslett,et al.  Inhibition of apoptosis and prolongation of neutrophil functional longevity by inflammatory mediators , 1993, Journal of leukocyte biology.

[14]  C. Haslett,et al.  Impairment of function in aging neutrophils is associated with apoptosis. , 1993, Journal of immunology.

[15]  D. Das,et al.  Molecular adaptation of cellular defences following preconditioning of the heart by repeated ischaemia. , 1993, Cardiovascular research.

[16]  J. Cidlowski,et al.  Apoptosis: the biochemistry and molecular biology of programmed cell death. , 1993, Endocrine reviews.

[17]  C. Rice-Evans,et al.  A novel method for measuring antioxidant capacity and its application to monitoring the antioxidant status in premature neonates. , 1993, Clinical science.

[18]  J. E. Mejía,et al.  Apoptosis induced by oxysterols in murine lymphoma cells and in normal thymocytes. , 1993, Immunology.

[19]  C. Haslett,et al.  Phagocyte recognition of cells undergoing apoptosis. , 1993, Immunology today.

[20]  F. Herrmann,et al.  Prolongation of survival of human polymorphonuclear neutrophils by granulocyte-macrophage colony-stimulating factor is caused by inhibition of programmed cell death. , 1992, Blood.

[21]  C. Haslett.  Resolution of acute inflammation and the role of apoptosis in the tissue fate of granulocytes. , 1992, Clinical science.

[22]  A. Mantovani,et al.  Modulation of granulocyte survival and programmed cell death by cytokines and bacterial products. , 1992, Blood.

[23]  C. Haslett,et al.  Phagocytosis of apoptotic neutrophils does not induce macrophage release of thromboxane B2 , 1992, Journal of leukocyte biology.

[24]  M. Hengartner,et al.  Caenorhabditis elegans gene ced-9 protects cells from programmed cell death , 1992, Nature.

[25]  K. Albermann,et al.  Nuclear Factor Kb: An Oxidative Stress-Responsive Transcription Factor of Eukaryotic Cells (A Review) , 1992 .

[26]  C. Haslett,et al.  Neutrophil apoptosis and clearance from neonatal lungs , 1991, The Lancet.

[27]  S. Korsmeyer,et al.  Deregulated Bcl-2 gene expression selectively prolongs survival of growth factor-deprived hemopoietic cell lines. , 1990, Journal of immunology.

[28]  M. Walport,et al.  Macrophage phagocytosis of aging neutrophils in inflammation. Programmed cell death in the neutrophil leads to its recognition by macrophages. , 1989, The Journal of clinical investigation.

[29]  S. Weiss.  Tissue destruction by neutrophils. , 1989, The New England journal of medicine.

[30]  J I Gallin,et al.  Current concepts: immunology. Neutrophils in human diseases. , 1987, The New England journal of medicine.

[31]  P. Nowell,et al.  Regulation of bcl-2 proto-oncogene expression during normal human lymphocyte proliferation. , 1987, Science.

[32]  C. Haslett,et al.  Modulation of multiple neutrophil functions by preparative methods or trace concentrations of bacterial lipopolysaccharide. , 1985, The American journal of pathology.

[33]  A. Janoff.  Elastase in tissue injury. , 1985, Annual review of medicine.

[34]  W. Maltzman,et al.  UV irradiation stimulates levels of p53 cellular tumor antigen in nontransformed mouse cells , 1984, Molecular and cellular biology.

[35]  Chemotactic peptide modulation of actin assembly and locomotion in neutrophils , 1984, The Journal of cell biology.

[36]  G. Salvesen,et al.  Human plasma proteinase inhibitors. , 1983, Annual review of biochemistry.

[37]  J. McCord,et al.  Free radicals and inflammation. Protection of phagocytosine leukocytes by superoxide dismutase. , 1975, The Journal of clinical investigation.

[38]  I. Fridovich,et al.  Superoxide dismutase. An enzymic function for erythrocuprein (hemocuprein). , 1969, The Journal of biological chemistry.

[39]  I W SIZER,et al.  A spectrophotometric method for measuring the breakdown of hydrogen peroxide by catalase. , 1952, The Journal of biological chemistry.