Key role of mitochondria in apoptosis of lymphocytes

被引:7
作者
Boichuk, SV
Minnebaev, MM
Mustafin, IG
机构
[1] Kazan State Med Univ, Dept Pathophysiol, Kazan, Russia
[2] Tartar Minist Hlth, Republican Ctr AIDS Control, Kazan, Russia
关键词
apoptosis; lymphocyte; mitochondrial potential; phosphatidylserine; DNA fragmentation;
D O I
10.1023/A:1014555130494
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Changes in the mitochondrial potential, expression of phosphatidylserine, parameters of direct and lateral light scattering, and DNA fragmentation during spontaneous and induced apoptosis in peripheral blood lymphocytes were studied by flow cytofluorometry. Dexamethasone and Ca2+ ionophore A23187 served as inductors of apoptosis. A decrease in the mitochondrial potential is an early sip of spontaneous and induced apoptosis. Phosphatidylserine expression on the outer plasma membrane occurred later and inversely depended on the mitochondrial potential. Our results indicate that the involvement of mitochondria in spontaneous and induced apoptosis accompanied by a decrease in the mitochondrial potential is an early and key event of programmed lymphocyte death. The decrease in the mitochondrial potential of lymphocytes induced degradation of their nuclei (DNA fragmentation) and promoted elimination of apoptotic cells (phosphatidylserine expression).
引用
收藏
页码:1166 / 1168
页数:3
相关论文
共 15 条
[1]  
Banki K, 1999, J IMMUNOL, V162, P1466
[2]   Caspase independent/dependent regulation of K+, cell shrinkage, and mitochondrial membrane potential during lymphocyte apoptosis [J].
Bortner, CD ;
Cidlowski, JA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (31) :21953-21962
[3]   BCL-2 INHIBITS GLUCOCORTICOID-INDUCED APOPTOSIS BUT ONLY PARTIALLY BLOCKS CALCIUM IONOPHORE OR CYCLOHEXIMIDE-REGULATED APOPTOSIS IN S49 CELLS [J].
CARONLESLIE, LAM ;
EVANS, RB ;
CIDLOWSKI, JA .
FASEB JOURNAL, 1994, 8 (09) :639-645
[4]  
Castedo M, 1996, J IMMUNOL, V157, P512
[5]   MITOCHONDRIAL MODIFICATIONS DURING RAT THYMOCYTE APOPTOSIS - A STUDY AT THE SINGLE-CELL LEVEL [J].
COSSARIZZA, A ;
KALASHNIKOVA, G ;
GRASSILLI, E ;
CHIAPPELLI, F ;
SALVIOLI, S ;
CAPRI, M ;
BARBIERI, D ;
TROIANO, L ;
MONTI, D ;
FRANCESCHI, C .
EXPERIMENTAL CELL RESEARCH, 1994, 214 (01) :323-330
[6]   BCL-2 BLOCKS APOPTOSIS IN CELLS LACKING MITOCHONDRIAL-DNA [J].
JACOBSON, MD ;
BURNE, JF ;
KING, MP ;
MIYASHITA, T ;
REED, JC ;
RAFF, MC .
NATURE, 1993, 361 (6410) :365-369
[7]   INTRACELLULAR CA2+ SIGNALS ACTIVATE APOPTOSIS IN THYMOCYTES - STUDIES USING THE CA2+-ATPASE INHIBITOR THAPSIGARGIN [J].
JIANG, S ;
CHOW, SC ;
NICOTERA, P ;
ORRENIUS, S .
EXPERIMENTAL CELL RESEARCH, 1994, 212 (01) :84-92
[8]   Mitochondrial control of apoptosis [J].
Kroemer, G ;
Zamzami, N ;
Susin, SA .
IMMUNOLOGY TODAY, 1997, 18 (01) :44-51
[9]   Mitochondria-dependent and -independent regulation of granzyme B-induced apoptosis [J].
MacDonald, G ;
Shi, LF ;
Velde, CV ;
Lieberman, J ;
Greenberg, AH .
JOURNAL OF EXPERIMENTAL MEDICINE, 1999, 189 (01) :131-143
[10]   PROTEOLYSIS OF FODRIN (NONERYTHROID SPECTRIN) DURING APOPTOSIS [J].
MARTIN, SJ ;
OBRIEN, GA ;
NISHIOKA, WK ;
MCGAHON, AJ ;
MAHBOUBI, A ;
SAIDO, TC ;
GREEN, DR .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (12) :6425-6428