Abstract:
:The Tac4 gene-derived hemokinin-1 (HK-1) is present in pain-related regions and activates the tachykinin NK1 receptor, but with binding site and signaling pathways different from Substance P (SP). NK1 receptor is involved in nociception, but our earlier data showed that it has no role in chronic neuropathic hyperalgesia, similarly to SP. Furthermore, NK1 antagonists failed in clinical trials as analgesics due to still unknown reasons. Therefore, we investigated the role of HK-1 in pain conditions of distinct mechanisms using genetically modified mice. Chronic neuropathic mechanical and cold hyperalgesia after partial sciatic nerve ligation (PSL) were determined by dynamic plantar aesthesiometry and withdrawal latency from icy water, motor coordination on the accelerating Rotarod. Peripheral nerve growth factor (NGF) production was measured by ELISA, neuronal and glia cell activation by immunohistochemistry in pain-related regions. Acute somatic and visceral chemonocifensive behaviors were assessed after intraplantar formalin or intraperitoneal acetic-acid injection, respectively. Resiniferatoxin-induced inflammatory mechanical and thermal hyperalgesia by aesthesiometry and increasing temperature hot plate. Chronic neuropathic mechanical and cold hypersensitivity were significantly decreased in HK-1 deficient mice. NGF level in the paw homogenates of intact mice were significantly lower in case of HK-1 deletion. However, it significantly increased under neuropathic condition in contrast to wildtype mice, where the higher basal concentration did not show any changes. Microglia, but not astrocyte activation was observed 14 days after PSL in the ipsilateral spinal dorsal horn of wildtype, but not HK-1-deficient mice. However, under neuropathic conditions, the number of GFAP-positive astrocytes was significantly smaller in case of HK-1 deletion. Acute visceral, but not somatic nocifensive behavior, as well as neurogenic inflammatory mechanical and thermal hypersensitivity were significantly reduced by HK-1 deficiency similarly to NK1, but not to SP deletion. We provide evidence for pro-nociceptive role of HK-1, via NK1 receptor activation in acute inflammation models, but differently from SP-mediated actions. Identification of its targets and signaling can open new directions in pain research.
journal_name
Brain Res Bulljournal_title
Brain research bulletinauthors
Hunyady Á,Hajna Z,Gubányi T,Scheich B,Kemény Á,Gaszner B,Borbély É,Helyes Zdoi
10.1016/j.brainresbull.2019.01.015subject
Has Abstractpub_date
2019-04-01 00:00:00pages
165-173eissn
0361-9230issn
1873-2747pii
S0361-9230(18)30929-8journal_volume
147pub_type
杂志文章abstract::Bone marrow stromal cells (BMSCs) are promising donor cells for transplantation therapies for a variety of diseases. However, there still lack efficient ways to induce directional differentiation of BMSCs to promote their practical use in transplantation therapy. In this study, we constructed hybrid cells by transferr...
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journal_title:Brain research bulletin
pub_type: 历史文章,杂志文章,评审
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journal_title:Brain research bulletin
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pub_type: 杂志文章
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journal_title:Brain research bulletin
pub_type: 杂志文章,评审
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journal_title:Brain research bulletin
pub_type: 评论,杂志文章
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journal_title:Brain research bulletin
pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Brain research bulletin
pub_type: 杂志文章,评审
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journal_title:Brain research bulletin
pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Brain research bulletin
pub_type: 杂志文章
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pub_type: 杂志文章
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