Vasoconstrictive effect of tenascin-C on cerebral arteries in rats.

Vasoconstrictive effect of tenascin-C on cerebral arteries in rats.
复制标题

DOI:
10.1007/978-3-319-04981-6_17
复制
发表时间:
2015-01-01
期刊:
Acta neurochirurgica. Supplement
影响因子:
--
通讯作者:
Suzuki, Hidenori
Suzuki, Hidenori
中科院分区:
其他
文献类型:
--
作者:
Fujimoto, Masashi;Shiba, Masato;Suzuki, Hidenori

文献摘要

被引文献

相似文献

背景与目的:作者报道了一种基质细胞蛋白tenascin-C (TNC)在蛛网膜下腔出血(SAH)后被诱导,与脑血管痉挛相关。在这项研究中,我们研究了TNC是否单独引起大鼠颅内颈内动脉(ICAs)的脑血管痉挛样收缩,重点研究了p38丝裂原活化蛋白激酶(MAPK)介导的机制。方法:首先在健康大鼠大池内注射TNC 10杯,观察TNC给药后24 ~ 72 h是否引起左ICA收缩。其次,我们检测了SB203580 (p38 MAPK抑制剂)在24 h时对健康大鼠左ICA血管直径的影响。第三,我们评估了SB203580在24 h时对tnc诱导的健康大鼠左ICA收缩的影响。TNC显著诱导左侧ICA脑血管痉挛样血管造影收缩,这种收缩至少持续72小时。SB203580本身对正常ICA直径没有影响,但消除了TNC诱导的左侧ICA血管收缩作用。结论:这些发现表明TNC通过激活p38 MAPK导致左ICA收缩,类似于sah后血管痉挛,提示TNC可能参与了脑血管痉挛的发病机制。
BACKGROUND AND PURPOSE: The authors have reported that tenascin-C (TNC), a matricellular protein, is induced after subarachnoid hemorrhage (SAH), associated with cerebral vasospasm. In this study, we examined whether TNC alone causes cerebral vasospasm-like constriction of the intracranial internal carotid arteries (ICAs) in rats, focusing on the p38 mitogen-activated protein kinase (MAPK)-mediated mechanisms.METHODS: First, we injected 10 mug of TNC into the cisterna magna of healthy rats and studied morphologically whether TNC caused constriction of the left ICA at 24-72 h after administration. Second, we examined the effect of SB203580 (a p38 MAPK inhibitor) on the vessel diameter of the left ICA in healthy rats at 24 h. Third, we evaluated the effect of SB203580 on TNC-induced constriction of the left ICA in healthy rats at 24 h.RESULTS: TNC significantly induced cerebral vasospasm-like angiographic constriction of the left ICAs, which continued at least for 72 h. SB203580 itself had no effect on the diameter of normal ICAs, but abolished the TNC-induced vasoconstrictive effect on the left ICA.CONCLUSION: These findings show that TNC causes left ICA constriction via activation of p38 MAPK, resembling post-SAH vasospasm, and suggest the possible involvement of TNC in the pathogenesis of cerebral vasospasm.