Inhibition of 15‐lipoxygenase leads to delayed organelle degradation in the reticulocyte

FEBS Letters

Grüllich, Carsten¹  van Leyen, Klaus²  Wiedmann, Martin³  Duvoisin, Robert M.⁴ 

[1] Molecular Pharmacology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA;Cellular Biochemistry and Biophysics Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA;Graduate School of Medical Sciences, Cornell University, 1300 York Avenue, New York, NY 10021, USA;Dyson Vision Research Institute, Weill Medical College, New York, NY 10021, USA

关键词: Lipoxygenase;    Reticulocyte;    Mitochondrion;    Eicosatetraynoic acid;    Organelle degradation;    Red blood cell;    Terminal differentiation;    15-LOX;    15-lipoxygenase;    ETYA;    eicosatetraynoic acid;    DMSO;    dimethyl sulfoxide;    PBS;    phosphate-buffered saline;    ER;    endoplasmic reticulum;    SDS–PAGE;    sodium dodecyl sulfate–polyacrylamide gel electrophoresis;    EDTA;    ethylenediaminetetraacetate;    PDI;    protein disulfide isomerase;    MMCoAMutase;    methylmalonyl coenzyme A mutase;   

DOI  :  10.1016/S0014-5793(01)02080-4

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Mammalian cells are characterized by an endomembrane system. Nevertheless, some cells lose these membranes during their terminal differentiation, e.g. red blood cells and lens fiber cells of the eye. 15-Lipoxygenase is believed to be critical for this membrane degradation. Here we use cultivated rabbit reticulocytes in the presence or absence of a lipoxygenase inhibitor to provide further evidence for the importance of 15-lipoxygenase for the in vivo degradation of mitochondria. We find that inhibitor treatment retarded mitochondrial degradation, as shown by persistence of marker proteins and by direct visualization of mitochondria by electron microscopy.

【 授权许可】

Unknown