Increase of galectin-3 expression in microglia by hyperthermia in delayed neuronal death of hippocampal CA1 following transient forebrain ischemia

被引:31
作者
Satoh, Kunio [2 ]
Niwa, Masayuki [1 ,3 ]
Nguyen Huy Binh [2 ]
Nakashima, Masaya [3 ]
Kobayashi, Kazuhiro [2 ]
Takamatsu, Manabu [2 ]
Hara, Akira [2 ]
机构
[1] Gifu Univ, United Grad Sch Drug Discovery & Med Informat Sci, Div Med Sci, Gifu 5011194, Japan
[2] Gifu Univ, Grad Sch Med, Dept Tumor Pathol, Gifu 5011194, Japan
[3] Gifu Univ, Sch Med, Med Educ Dev Ctr, Gifu 5011194, Japan
关键词
Galectin-3; Microglia; Hyperthermia; Delayed neuronal death; Hippocampus; Gerbil; NUCLEAR-DNA FRAGMENTATION; GERBIL HIPPOCAMPUS; BRAIN TEMPERATURE; CEREBRAL-ISCHEMIA; TEMPORAL PROFILE; GLOBAL-ISCHEMIA; IN-SITU; DAMAGE; HYPOTHERMIA; INJURY;
D O I
10.1016/j.neulet.2011.09.015
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The ischemic damage in the hippocampal CM region following transient forebrain ischemia, delayed neuronal death, is a typical apoptotic response, but the underlying mechanisms are not fully understood. We have reported that mild hyperthermia (38 degrees C) accelerates DNA fragmentation of the gerbil CA1 pyramidal neurons following transient forebrain ischemia. Recently, we reported that galectin-3, a beta-galactosidase-binding lectin, is spatio-temporally expressed only by activated microglial cells located within CM region following transient forebrain ischemia in gerbils. Furthermore, expression of galectin-3 and Iba-1 (a specific microglial cell marker) are strongly reduced by hypothermia during ischemic insult. To further elucidate the effect of hyperthermia on the expression of galectin-3 by micloglia in delayed neuronal death, we examined immunohistochemical expression of galectin-3 and Iba-1, in situ terminal dUTP-biotin nick end labeling of DNA fragmentation (for determination of cell death) and hematoxylin and eosin staining (for morphological observation). We observed that between 37 degrees C and 39 degrees C, there was a temperature-dependent enhancement of galectin-3 expression in microglial cells in the CA1 region following transient ischemia. Apoptotic DNA fragmentation, detected by TUNEL staining, was observed in CA1 region in normothermia. This TUNEL staining was enhanced by hyperthermia at 37.5 degrees C and 38 degrees C, but not at 39 degrees C. Ischemia-induced neuronal degeneration in CM region in gerbil hippocampus subjected to hyperthermia (37.5 degrees C, 38 degrees C and 39 degrees C) observed by HE staining is similar to that in normothermic gerbils. These findings imply that galectin-3 expression in microglia may influence the survival of CA1 pyramidal neurons in cases such as hyperthermia-related neuronal injury. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:199 / 203
页数:5
相关论文
共 26 条
[2]   EFFECTS OF NORMOTHERMIC VERSUS MILD HYPERTHERMIC FOREBRAIN ISCHEMIA IN RATS [J].
DIETRICH, WD ;
BUSTO, R ;
VALDES, I ;
LOOR, Y .
STROKE, 1990, 21 (09) :1318-1325
[3]   INTERRELATIONSHIPS BETWEEN INCREASED VASCULAR-PERMEABILITY AND ACUTE NEURONAL DAMAGE FOLLOWING TEMPERATURE-CONTROLLED BRAIN ISCHEMIA IN RATS [J].
DIETRICH, WD ;
HALLEY, M ;
VALDES, I ;
BUSTO, R .
ACTA NEUROPATHOLOGICA, 1991, 81 (06) :615-625
[4]   IDENTIFICATION OF PROGRAMMED CELL-DEATH INSITU VIA SPECIFIC LABELING OF NUCLEAR-DNA FRAGMENTATION [J].
GAVRIELI, Y ;
SHERMAN, Y ;
BENSASSON, SA .
JOURNAL OF CELL BIOLOGY, 1992, 119 (03) :493-501
[5]  
GLOBUS MYT, 1995, J NEUROCHEM, V65, P1250
[6]   Failure of preventive effects of 2-deoxy-D-glucose on ischemia-induced gerbil hippocampal neuronal damage by induced hyperthermia [J].
Hara, A ;
Niwa, M ;
Iwai, T ;
Yano, H ;
Nakashima, M ;
Bunai, Y ;
Uematsu, T ;
Yoshimi, N ;
Mori, H .
BRAIN RESEARCH, 1999, 840 (1-2) :167-170
[7]   Increase of fragmented DNA transport in apical dendrites of gerbil CA1 pyramidal neurons following transient forebrain ischemia by mild hypothermia [J].
Hara, A ;
Niwa, M ;
Iwai, T ;
Yano, H ;
Bunai, Y ;
Uematsu, T ;
Yoshimi, N ;
Mori, H .
NEUROSCIENCE LETTERS, 2000, 280 (01) :73-77
[8]   Protective effect of apoptosis-inhibitory agent, N-tosyl-L-phenylalanyl chloromethyl ketone against ischemia-induced hippocampal neuronal damage [J].
Hara, A ;
Niwa, M ;
Nakashima, M ;
Iwai, T ;
Uematsu, T ;
Yoshimi, N ;
Mori, H .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1998, 18 (08) :819-823
[9]   REGIONAL VARIABILITY IN DNA FRAGMENTATION AFTER GLOBAL-ISCHEMIA EVIDENCED BY COMBINED HISTOLOGICAL AND GEL-ELECTROPHORESIS OBSERVATIONS IN THE RAT-BRAIN [J].
HERON, A ;
POLLARD, H ;
DESSI, F ;
MOREAU, J ;
LASBENNES, F ;
BENARI, Y ;
CHARRIAUTMARLANGUE, C .
JOURNAL OF NEUROCHEMISTRY, 1993, 61 (05) :1973-1976
[10]   TEMPORAL PROFILE OF NUCLEAR-DNA FRAGMENTATION IN-SITU IN GERBIL HIPPOCAMPUS FOLLOWING TRANSIENT FOREBRAIN ISCHEMIA [J].
IWAI, T ;
HARA, A ;
NIWA, M ;
NOZAKI, M ;
UEMATSU, T ;
SAKAI, N ;
YAMADA, H .
BRAIN RESEARCH, 1995, 671 (02) :305-308