Expression of transforming growth factor-β1 and interleukin-1β mRNA in rat brain following transient forebrain ischemia

Expression of transforming growth factor-β1 and interleukin-1β mRNA in rat brain following transient forebrain ischemia
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DOI:
10.1007/bf00228578
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发表时间:
2004
影响因子:
12.7
通讯作者:
C. Wiessner;J. Gehrmann;D. Lindholm;R. Töpper;G. Kreutzberg;K. Hossmann
C. Wiessner;J. Gehrmann;D. Lindholm;R. Töpper;G. Kreutzberg;K. Hossmann
中科院分区:
医学1区
文献类型:
--
作者:
C. Wiessner;J. Gehrmann;D. Lindholm;R. Töpper;G. Kreutzberg;K. Hossmann

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采用原位杂交技术研究了大鼠全脑缺血30 min后脑内转化生长因子-β1(TGF-β1)和白细胞介素-1 β mRNA的表达。缺血产生的四血管闭塞,然后通过不同的再循环时间范围在15分钟和7天之间。缺血后3d,海马、皮质II/III层、纹状体和腹侧丘脑部分区域均可检测到TGF-β1 mRNA表达。再灌流后7 d,海马CA 1区TGF-β1 mRNA表达显著增加。然而,白细胞介素1β mRNA的诱导不太明显,仅限于缺血后3和7天的头侧纹状体。缺血后7天TGF-β1的表达与神经元变性和随后的星形胶质细胞和小胶质细胞活化发生的区域的组织学定位密切相关。在邻近脑切片中,7天后TGF-β1 mRNA的分布与活化小胶质细胞的免疫染色模式非常相似,表明此时TGF-β1 mRNA主要由小胶质细胞产生。缺血后TGF-β1 mRNA的晚期诱导表明参与了持续的胶质反应而不是最初的胶质活化。白细胞介素-1 β mRNA诱导的差异模式表明缺血性脑损伤后细胞因子产生的区域差异。
Transforming growth factor-β1 (TGF-β1) and interleukin-1β mRNA expression were studied in rat brains after 30 min of global ischemia by in situ hybridization. Ischemia was produced by four-vessel occlusion followed by different recirculation times ranging between 15 min and 7 days. TGF-β1 mRNA could first be detected 3 days after ischemia in the hippocampus, in layers II/III of cortex, in the striatum and in parts of the ventral thalamus. At 7 days after recirculation a prominent increase in TGF-β1 mRNA was observed in the CA1 sector of the hippocampus. Induction of interleukin-1β mRNA, however, was less marked and limited to the rostral striatum 3 and 7 days after ischemia. TGF-β1 expression 7 days after ischemia correlated well with the histological localization of regions where neuronal degeneration and subsequent astrocytic and microglial activation had occurred. In adjacent brain sections, the distribution of TGF-β1 mRNA after 7 days closely resembled that of the immunostaining pattern of activated microglia, indicating that at this time point TGF-β1 mRNA was mainly produced by microglial cells. The late induction of TGF-β1 mRNA after ischemia points to an involvement in the persistent glial response rather than the initial glial activation. The differential pattern of interleukin-1β mRNA induction indicates regional variations of cytokine production after ischemic brain lesions.