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Essential roles of C-type lectin Mincle in induction of neuropathic pain in mice

発表形態:
原著論文
主要業績:
主要業績
単著・共著:
共著
発表年月:
2019年01月
DOI:
10.1038/s41598-018-37318-8
会議属性:
指定なし
査読:
有り
リンク情報:

日本語フィールド

著者:
Ishikawa A, Miyake Y, Kobayashi K, Murata Y, Iizasa S, Iizasa E, Yamasaki S, Hirakawa N, Hara H Yoshida H, Yasaka T
題名:
Essential roles of C-type lectin Mincle in induction of neuropathic pain in mice
発表情報:
Sci Rep. 巻: 9 号: 1 ページ: 872
キーワード:
概要:
Increasing evidence indicates that pattern recognition receptors (PRRs) are involved in neuropathic pain after peripheral nerve injury (PNI). While a significant number of studies support an association between neuropathic pain and the innate immune response mediated through Toll-like receptors, a family of PRRs, the roles of other types of PRRs are largely unknown. In this study, we have focused on the macrophage-inducible C-type lectin (Mincle), a PRR allocated to the C-type lectin receptor family. Here, we show that Mincle is involved in neuropathic pain after PNI. Mincle-deficient mice showed impaired PNI-induced mechanical allodynia. After PNI, expression of Mincle mRNA was rapidly increased in the injured spinal nerve. Most Mincle-expressing cells were identified as infiltrating leucocytes, although the migration of leucocytes was also observed in Mincle-deficient mice. Furthermore, Mincle-deficiency affected the induction of genes, which are reported to contribute to neuropathic pain after PNI in the dorsal root ganglia and spinal dorsal horn. These results suggest that Mincle is involved in triggering sequential processes that lead to the pathogenesis of neuropathic pain.
抄録:

英語フィールド

Author:
Ishikawa A, Miyake Y, Kobayashi K, Murata Y, Iizasa S, Iizasa E, Yamasaki S, Hirakawa N, Hara H Yoshida H, Yasaka T
Title:
Essential roles of C-type lectin Mincle in induction of neuropathic pain in mice
Announcement information:
Sci Rep. Vol: 9 Issue: 1 Page: 872
An abstract:
Increasing evidence indicates that pattern recognition receptors (PRRs) are involved in neuropathic pain after peripheral nerve injury (PNI). While a significant number of studies support an association between neuropathic pain and the innate immune response mediated through Toll-like receptors, a family of PRRs, the roles of other types of PRRs are largely unknown. In this study, we have focused on the macrophage-inducible C-type lectin (Mincle), a PRR allocated to the C-type lectin receptor family. Here, we show that Mincle is involved in neuropathic pain after PNI. Mincle-deficient mice showed impaired PNI-induced mechanical allodynia. After PNI, expression of Mincle mRNA was rapidly increased in the injured spinal nerve. Most Mincle-expressing cells were identified as infiltrating leucocytes, although the migration of leucocytes was also observed in Mincle-deficient mice. Furthermore, Mincle-deficiency affected the induction of genes, which are reported to contribute to neuropathic pain after PNI in the dorsal root ganglia and spinal dorsal horn. These results suggest that Mincle is involved in triggering sequential processes that lead to the pathogenesis of neuropathic pain.


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