Substance P activation of rheumatoid synoviocytes: neural pathway in pathogenesis of arthritis.
Substance P activation of rheumatoid synoviocytes: neural pathway in pathogenesis of arthritis.
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DOI：
10.1097/00006254-198709000-00014
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发表时间：
1987-02
期刊：
影响因子：
56.9
通讯作者：
M. Lotz;D. Carson;J. Vaughan
中科院分区：
文献类型：
--
作者：
M. Lotz;D. Carson;J. Vaughan
一些临床特征与神经系统参与类风湿关节炎的发病机制是一致的。神经肽P物质可能是这种相互作用的媒介之一，因为它可以从初级感觉神经纤维释放到关节组织中。检测了该多肽对类风湿滑膜细胞的潜在作用。结果表明，P物质能刺激滑膜细胞释放前列腺素E_2和胶原酶。此外，在神经肽存在的情况下，滑膜细胞的增殖增加。截短形式的P物质也有类似的作用，滑膜细胞对极小剂量的神经肽(10(-9)M)敏感，其作用可被特定的拮抗剂抑制。因此，神经肽P物质对滑膜细胞的特异性刺激代表了神经系统可能直接参与类风湿关节炎发病机制的一条途径。
Several clinical features are consistent with nervous system involvement in the pathogenesis of rheumatoid arthritis. The neuropeptide substance P is one possible mediator of this interaction, since it can be released into joint tissues from primary sensory nerve fibers. The potential effects of the peptide on rheumatoid synoviocytes were examined. The results show that substance P stimulates prostaglandin E2 and collagenase release from synoviocytes. Furthermore, synoviocyte proliferation was increased in the presence of the neuropeptide. Similar effects were observed with a truncated form of substance P. Synoviocytes were sensitive to very small doses of the neuropeptide (10(-9) M), and its effects were inhibited by a specific antagonist. Thus, the specific stimulation of synoviocytes by the neuropeptide substance P represents a pathway by which the nervous system might be directly involved in the pathogenesis of rheumatoid arthritis.