caa a22 4500 397556322 CHVBK 20180308164803.0 cr unu---uuuuu 161202e199609 xx s 000 0 eng 10.1093/oxfordjournals.jbchem.a021455 doi (NATIONALLICENCE)oxford-10.1093/oxfordjournals.jbchem.a021455 Expression of the Apoptosis-Mediator Fas Is Enhanced by Dysfunctional Mitochondria [Elektronische Daten] [Sadamitsu Asoh, Takashi Mori, Jun-Ichi Hayashi, Shigeo Ohta] We applied an antibody against an apoptosis mediator, Fas/APO-1/CD95, to HeLa-derived cells that completely lack mitochondrial DNA (mtDNA) or have mutant mtDNAs. The anti-Fas antibody killed the cells completely lacking mtDNA (EB8), at concentrations as low as 1 ng/ml, but not control cells harboring wild-type mtDNA (Ft2-11). TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling) and analysis of fragmented DNA indicated that the cell death of EB8 was due to apoptosis. The antibody was cytotoxic to other two cell lines harboring mutant mtDNA with a point mutation or a large-scale deletion. RT-PCR (reverse transcriptase-polymerase chain reaction) showed that the mRNA content of the Fas gene was 2 to 19-fold higher in the cells with deficient mtDNA than in the control cells. In addition, the expressed Fas protein was detected by immunohistochemical staining in the cells without mtDNA but not in the control cells. Incubating the cells containing wild-type mtDNA with the respiratory inhibitors rotenone and antimycin A enhanced the content of mRNA of the Fas gene 2 to 4-fold and sensitized cells to the antibody. Thus, defects in mitochondria caused apoptotic cell death by anti-Fas antibody and enhanced Fas gene expression. © 1996 BY THE JOURNAL OF BIOCHEMISTRY Regular Papers nationallicence apoptosis nationallicence Fas antigen nationallicence gene expression nationallicence mitochondria disease nationallicence respiratory inhibitor nationallicence Asoh Sadamitsu The Division of Biochemistry, Institute of Gerontology, Nippon Medical School Kawasaki, Kanagawa 211 aut Mori Takashi The Division of Pathology, Institute of Gerontology, Nippon Medical School Kawasaki, Kanagawa 211 aut Hayashi Jun-Ichi The Institute of Biological Sciences, University of Tsukuba Tsukuba, Ibaraki 305 aut Ohta Shigeo The Division of Biochemistry, Institute of Gerontology, Nippon Medical School Kawasaki, Kanagawa 211 aut The Journal of Biochemistry Oxford University Press 120/3(1996-09), 600-607 0021-924X 120:3<600 1996 120 jbchem https://doi.org/10.1093/oxfordjournals.jbchem.a021455 text/html Onlinezugriff via DOI 1 other jats NATIONALLICENCE 856 40 https://doi.org/10.1093/oxfordjournals.jbchem.a021455 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Asoh Sadamitsu The Division of Biochemistry, Institute of Gerontology, Nippon Medical School Kawasaki, Kanagawa 211 aut NATIONALLICENCE 700 1- Mori Takashi The Division of Pathology, Institute of Gerontology, Nippon Medical School Kawasaki, Kanagawa 211 aut NATIONALLICENCE 700 1- Hayashi Jun-Ichi The Institute of Biological Sciences, University of Tsukuba Tsukuba, Ibaraki 305 aut NATIONALLICENCE 700 1- Ohta Shigeo The Division of Biochemistry, Institute of Gerontology, Nippon Medical School Kawasaki, Kanagawa 211 aut NATIONALLICENCE 773 0- The Journal of Biochemistry Oxford University Press 120/3(1996-09), 600-607 0021-924X 120:3<600 1996 120 jbchem Metadata rights reserved CC BY-NC-4.0 http://creativecommons.org/licenses/by-nc/4.0 nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-oxford