Nav1.7 expression is increased in painful human dental pulp.
Nav1.7 expression is increased in painful human dental pulp.
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DOI：
10.1186/1744-8069-4-16
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发表时间：
2008-04-21
期刊：
影响因子：
3.3
通讯作者：
Henry MA
中科院分区：
文献类型：
--
作者：
Luo S;Perry GM;Levinson SR;Henry MA
动物研究和一些人类研究表明，炎症损伤后钠通道(NACH)的表达发生了变化，这种变化与疼痛状态的产生有关。我们正在使用拔除的人类牙齿作为一个模型系统来研究外周疼痛的机制，并在这里检测正常和疼痛样本中Nav1.7nach亚型的表达。用抗Nav1.7、N52和PGP9.5和2)Nav1.7、CASPR(一种用于识别Ranvier结节的旁蛋白)和髓鞘碱性蛋白(MBP)的抗体标记牙髓切片，在共聚焦显微镜下获得Z系列光学切片图像。用NIH ImageJ软件对N52/PGP9.5标记的神经纤维中的Nav1.7免疫荧光进行定量，同时对CASPR识别的结节部位的有髓纤维中Nav1.7的表达进行评估，并根据CASPR关系进一步将其描述为典型或不典型。结果显示，在疼痛样本中，神经面积显著增加，Nav1.7在冠状和神经根纤维束中表达，在CASPR识别的典型和非典型结节部位表达增加。疼痛样本还显示，在缺乏MBP的局部区域，包括与CASPR确定的非典型部位相关的区域，Nav1.7的表达增强，从而确定脱髓鞘轴突内的NACH重构是可能的牙髓疼痛机制的基础。这项研究发现，在疼痛的人牙髓中，Nav1.7在完整和重塑/脱髓鞘结节的轴突表达和增强，这些变化可能有助于持续增加的诱发性和自发性疼痛反应，这是与牙痛相关的疼痛的特征。
Animal studies and a few human studies have shown a change in sodium channel (NaCh) expression after inflammatory lesions, and this change is implicated in the generation of pain states. We are using the extracted human tooth as a model system to study peripheral pain mechanisms and here examine the expression of the Nav1.7 NaCh isoform in normal and painful samples. Pulpal sections were labeled with antibodies against: 1) Nav1.7, N52 and PGP9.5, and 2) Nav1.7, caspr (a paranodal protein used to identify nodes of Ranvier), and myelin basic protein (MBP), and a z-series of optically-sectioned images were obtained with the confocal microscope. Nav1.7-immunofluorescence was quantified in N52/PGP9.5-identified nerve fibers with NIH ImageJ software, while Nav1.7 expression in myelinated fibers at caspr-identified nodal sites was evaluated and further characterized as either typical or atypical as based on caspr-relationships. Results show a significant increase in nerve area with Nav1.7 expression within coronal and radicular fiber bundles and increased expression at typical and atypical caspr-identified nodal sites in painful samples. Painful samples also showed an augmentation of Nav1.7 within localized areas that lacked MBP, including those associated with atypical caspr-identified sites, thus identifying NaCh remodeling within demyelinating axons as the basis for a possible pulpal pain mechanism. This study identifies the increased axonal expression and augmentation of Nav1.7 at intact and remodeling/demyelinating nodes within the painful human dental pulp where these changes may contribute to constant, increased evoked and spontaneous pain responses that characterize the pain associated with toothache.
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影响因子：
3
作者：
Bird, E. V.;Robinson, P. P.;Boissonade, F. M.
通讯作者：
Boissonade, F. M.
影响因子：
7.4
作者：
Henry, Michael A.;Freking, Angelique R.;Levinson, S. Rock
通讯作者：
Levinson, S. Rock
影响因子：
5.5
作者：
LAWSON, SN;WADDELL, PJ
通讯作者：
WADDELL, PJ
DOI：
10.1073/pnas.87.17.6777
发表时间：
1990-09-01
影响因子：
11.1
作者：
ENGLAND, JD;GAMBONI, F;FINGER, TE
通讯作者：
FINGER, TE
影响因子：
7.4
作者：
Hadjimichael, Olympia;Kerns, Robert D.;Vollmer, Timothy
通讯作者：
Vollmer, Timothy