Immunohistochemical Detection of Leukemia Inhibitory Factor After Focal Cerebral Ischemia in Rats

Immunohistochemical Detection of Leukemia Inhibitory Factor After Focal Cerebral Ischemia in Rats
复制标题

大鼠局灶性脑缺血后白血病抑制因子的免疫组织化学检测

DOI:
--
复制
发表时间:
2000
影响因子:
6.3
通讯作者:
Y. Fukuuchi
Y. Fukuuchi
中科院分区:
医学1区
文献类型:
--
作者:
Shigeaki Suzuki;Kortaro Tanaka;S. Nogawa;D. Ito;T. Dembo;A. Kosakai;Y. Fukuuchi

文献摘要

参考文献

被引文献

相似文献

细胞因子白血病抑制因子(LIF)在发育过程中调节神经元功能,并促进周围神经损伤后神经元的存活,但对脑缺血后LIF的表达知之甚少。在本研究中,LIF蛋白的定位进行了免疫组织化学检查后3.5,12,24,48,和96小时的大鼠大脑中动脉闭塞(MCAO)1.5小时的线栓法诱导的再灌注。还进行了微管相关蛋白2(MAP 2)、胶质细胞酸性蛋白(GFAP)、凝集素组织化学和白细胞介素(IL)6的免疫组织化学双染色。假手术组和免疫吸附试验未显示任何明确的LIF免疫反应性。明确的LIF免疫反应性首先检测到12小时后,再灌注在每个大脑区域检查:缺血核心,梗死周围区域,对侧皮质。然而,LIF的表达是最突出的在梗死周围区域在每个时间点,在24小时达到高峰,然后逐渐下降,直到96小时的再灌注。梗死周围区部分LIF阳性神经元表达IL-6。再灌注96小时,梗死核心周围的GFAP标记的星形胶质细胞也表达LIF蛋白。逆转录聚合酶链反应和蛋白质印迹分析也证实了LIF mRNA和蛋白的诱导。这些结果表明,LIF表达缺血威胁神经元可能反映了对缺血损伤的修复或防御机制。
The cytokine leukemia inhibitory factor (LIF) modulates neuronal function during development and promotes neuronal survival after peripheral nerve injury, but little is known about LIF expression after cerebral ischemia. In the present study, the localization of LIF protein was immunohistochemically examined in rats after 3.5, 12, 24, 48, and 96 hours of reperfusion following 1.5 hours of middle cerebral artery occlusion (MCAO) induced by the intraluminal suture method. Double-staining immunohistochemistry with microtubule-associated protein-2 (MAP2), glial fibrillary acidic protein (GFAP), lectin histochemistry, and interleukin (IL) 6 was also performed. The sham group and immunosorption test did not show any clear LIF immunoreactivity. Definite LIF immunoreactivity was first detected after 12 hours of reperfusion in each of the brain regions examined: ischemic core, periinfarct region, and contralateral cortex. However, expression of LIF was most prominent in the periinfarct region at each time point, peaked at 24 hours, and then gradually declined until 96 hours of reperfusion. Some LIF-positive neurons in the periinfarct region expressed IL-6. At 96 hours of reperfusion, GFAP-labeled astrocytes around the infarct core also expressed LIF protein. Induction of LIF mRNA and protein was also confirmed by reverse transcription polymerase chain reaction and western blot analysis, respectively. These findings suggest that LIF expression in ischemically threatened neurons may reflect a repair or defense mechanism against the ischemic insult.
DOI: 10.1161/01.str.26.11.2135
发表时间: 1995-11-01
期刊: STROKE
影响因子: 8.3
作者:
STROEMER, RP;KENT, TA;HULSEBOSCH, CE
通讯作者: HULSEBOSCH, CE
DOI: 10.1161/01.str.29.9.1972
发表时间: 1998-09-01
期刊: STROKE
影响因子: 8.3
作者:
Li, Y;Jiang, N;Chopp, M
通讯作者: Chopp, M
白血病抑制因子诱导细胞因子表达。
DOI: 10.1172/jci116363
发表时间: 1993
期刊: The Journal of clinical investigation
影响因子: --
作者:
Villiger,PM;Geng,Y;Lotz,M
通讯作者: Lotz,M