Apoptosis and white matter injury in preterm infants

被引:42
作者
Chamnanvanakij, S
Margraf, LR
Burns, D
Perlman, JM
机构
[1] Univ Texas, SW Med Ctr, Dept Pediat, Dallas, TX 75390 USA
[2] Univ Texas, SW Med Ctr, Dept Pathol, Dallas, TX 75390 USA
关键词
premature infants; intraventricular hemorrhage; white matter injury; apoptosis; terminal deoxytransferase-mediated dUTD nick-end labeling assay;
D O I
10.1007/s10024-001-0205-0
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
White matter injury in premature infants with or without intraventricular hemorrhage (IVH) remains an important cause of neonatal mortality and neurologic morbidity. The contribution of apoptosis to the cellular death in white matter injury in the preterm infant is unclear, The objective of this study was to determine whether apoptosis contributes to the cellular death in premature infants with cranial ultrasound (US) evidence of IVH and asymmetric periventricular echogenicity (PVE). Brain tissue incorporating frontoparietal white matter was obtained from 21 infants: 6 infants with severe IVH and asymmetric PVE (grade 1V IVH) on US (group I); 9 infants with minimal IVH or normal US who died within 21 days (group II); and 6 infants with minimal IVH or normal US who died later (group III). The presence of DNA fragmentation, typical of apoptosis, was determined using a terminal deoxytransferase-mediated dUTD nick-end labeling (TUNEL) assay. The TUNEL index for group I infants was significantly greater, i.e., 2.75 +/- 1.94% versus 0.84 +/- 0.70%, for group II and 0.42 +/- 0.22 for group III infants (P = 0.004). Most cells showing reactivity had morphologic characteristics consistent with astrocytes and oligodendroglia. The number of white matter cells showing morphologic changes consistent with apoptosis, such as nuclear blebs and karyorrhexis, was also quantitated and was significantly more numerous in group I than in group II infants, i.e., 0.51 +/- 0.64% versus 0.02 +/- 0.05% (P = 0.0005), and group III infants, i.e., 0.10 +/- 0.18% (P = 0.03). These findings implicate apoptosis as a contributing mechanism for the cellular death in infants with IVH and asymmetric PVE. Strategies aimed at preventing the white matter injury will need to incorporate methods of inhibiting the ongoing process of apoptosis.
引用
收藏
页码:184 / 189
页数:6
相关论文
共 26 条
[1]  
ALLEN WC, 1997, ARCH PEDIAT ADOLESC, V151, P581
[2]   GLUTAMATE-INDUCED NEURONAL DEATH - A SUCCESSION OF NECROSIS OR APOPTOSIS DEPENDING ON MITOCHONDRIAL-FUNCTION [J].
ANKARCRONA, M ;
DYPBUKT, JM ;
BONFOCO, E ;
ZHIVOTOVSKY, B ;
ORRENIUS, S ;
LIPTON, SA ;
NICOTERA, P .
NEURON, 1995, 15 (04) :961-973
[3]  
Back SA, 1997, MENT RETARD DEV D R, V3, P96, DOI 10.1002/(SICI)1098-2779(1997)3:1<96::AID-MRDD12>3.0.CO
[4]  
2-M
[5]  
BEILHARTZ E, 1995, MOL BRAIN RES, V29, P174
[6]  
Bittigau D, 1999, ANN NEUROL, V45, P724, DOI 10.1002/1531-8249(199906)45:6<724::AID-ANA6>3.0.CO
[7]  
2-P
[8]  
Blaschke AJ, 1996, DEVELOPMENT, V122, P1165
[9]   APOPTOSIS AND NECROSIS - 2 DISTINCT EVENTS INDUCED, RESPECTIVELY, BY MILD AND INTENSE INSULTS WITH N-METHYL-D-ASPARTATE OR NITRIC-OXIDE SUPEROXIDE IN CORTICAL CELL-CULTURES [J].
BONFOCO, E ;
KRAINC, D ;
ANKARCRONA, M ;
NICOTERA, P ;
LIPTON, SA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (16) :7162-7166
[10]   Apoptosis in the brains of infants suffering intrauterine cerebral injury [J].
Edwards, AD ;
Cox, P ;
Hope, PL ;
Azzopardi, DV ;
Squier, MV ;
Mehmet, H .
PEDIATRIC RESEARCH, 1997, 42 (05) :684-689