Trilodothyronine is a survival factor for developing oligodendrocytes

被引:61
作者
Jones, SA
Jolson, DM
Cuta, KK
Mariash, CN
Anderson, GW
机构
[1] Univ Minnesota, Dept Med, Div Endocrinol & Diabet, Minneapolis, MN 55455 USA
[2] Hennepin Cty Med Ctr, Dept Med, Minneapolis, MN 55415 USA
关键词
thyroid hormone; development; rat brain; oligodendrocyte;
D O I
10.1016/S0303-7207(02)00296-4
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Thyroid hormone plays an important role in oligodendrocyte development. The studies presented here suggest that thyroid hormone is required for oligodendrocyte survival during development. Oligodendrocyte precursor cells, astrocytes and microglia were cultured in a defined media. Oligodendrocyte precursor cell differentiation was induced by growth factor removal. Time course studies revealed that oligodendrocytes cultured in the presence or absence of triiodothyronine (T3) develop similarly during the first 3 days of development. Oligodendrocytes cultured in the absence of T3, however, die after developmental day 3. TdT-Mediated dUDP Nick End Labeling assay and Hoechst staining indicate that T3 rescues developing oligodendrocytes from death by apoptosis. Apoptosis is likely induced by the presence of the cytokines TNFalpha and IL-1beta. However, expression of these cytokines is not altered by thyroid hormone administration. Thus, thyroid hormone has been demonstrated to effect proliferation, myelin gene expression and now the survival of developing oligodendrocytes. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:49 / 60
页数:12
相关论文
共 66 条
[1]   Effects of thyroid hormone on embryonic oligodendrocyte precursor call development in vivo and in vitro [J].
Ahlgren, SC ;
Wallace, H ;
Bishop, J ;
Neophytou, C ;
Raff, MC .
MOLECULAR AND CELLULAR NEUROSCIENCE, 1997, 9 (5-6) :420-432
[2]   Oligodendrocyte apoptosis and primary demyelination induced by local TNF/p55TNF receptor signaling in the central nervous system of transgenic mice - Models for multiple sclerosis with primary oligodendrogliopathy [J].
Akassoglou, K ;
Bauer, J ;
Kassiotis, G ;
Pasparakis, M ;
Lassmann, H ;
Kollias, G ;
Probert, L .
AMERICAN JOURNAL OF PATHOLOGY, 1998, 153 (03) :801-813
[3]   Morphological and biochemical characterization and analysis of apoptosis [J].
Allen, RT ;
Hunter, WJ ;
Agrawal, DK .
JOURNAL OF PHARMACOLOGICAL AND TOXICOLOGICAL METHODS, 1997, 37 (04) :215-228
[4]   EXPRESSION OF NEUROTROPHINS AND THE TRK FAMILY OF NEUROTROPHIN RECEPTORS IN NORMAL AND HYPOTHYROID FAT BRAIN [J].
ALVAREZDOLADO, M ;
IGLESIAS, T ;
RODRIGUEZPENA, A ;
BERNAL, J ;
MUNOZ, A .
MOLECULAR BRAIN RESEARCH, 1994, 27 (02) :249-257
[5]   Thyroid hormones and the brain - Commentary [J].
Anderson, GW .
FRONTIERS IN NEUROENDOCRINOLOGY, 2001, 22 (01) :1-17
[6]  
Andrews T, 1998, J NEUROSCI RES, V54, P574, DOI 10.1002/(SICI)1097-4547(19981201)54:5<574::AID-JNR2>3.0.CO
[7]  
2-0
[8]  
Baas D, 1997, GLIA, V19, P324, DOI 10.1002/(SICI)1098-1136(199704)19:4<324::AID-GLIA5>3.0.CO
[9]  
2-X
[10]   EFFECT OF NEONATAL THYROIDECTOMY ON MYELINATION IN RAT BRAIN [J].
BALAZS, R ;
BROOKSBANK, BW ;
DAVISON, AN ;
EAYRS, JT ;
WILSON, DA .
BRAIN RESEARCH, 1969, 15 (01) :219-+