Impaired pain sensation in mice lacking prokineticin 2.
Impaired pain sensation in mice lacking prokineticin 2.
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DOI：
10.1186/1744-8069-2-35
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发表时间：
2006-11-15
期刊：
影响因子：
3.3
通讯作者：
Zhou QY
中科院分区：
文献类型：
--
作者：
Hu WP;Zhang C;Li JD;Luo ZD;Amadesi S;Bunnett N;Zhou QY
原激动素(Prokineticins，PKs)是一对新发现的调节肽，由PK1和PK2组成。两个密切相关的G蛋白偶联受体PKR1和PKR2介导PKs的信号转导。PKS/PKRs参与调节从发育到成人生理的各种生物过程。许多研究表明PKS/PKRs参与了伤害性感受。这里我们证明了PK2是伤害性感受的敏感剂。足底注射重组PK2后，大鼠对伤害性刺激产生强烈的局部痛敏，痛觉阈值降低。PK2在分离的背根神经节(DRG)神经元上激活钙离子。缺乏PK2基因的小鼠在热刺激和化学刺激(包括辣椒素)诱导的伤害感受方面表现出强烈的减少。然而，PK2突变小鼠对辣椒素的炎症反应没有差异。由于大多数PK2反应的DRG神经元也表达瞬时受体电位香草素(TRPV1)，并且对辣椒素敏感，TRPV1可能是PK2信号的重要下游分子。综上所述，这些结果表明PK2在不影响炎症的情况下敏化伤害性感受。
Prokineticins (PKs), consisting of PK1 and PK2, are a pair of newly identified regulatory peptides. Two closely related G-protein coupled receptors, PKR1 and PKR2, mediate the signaling of PKs. PKs/PKRs participate in the regulation of diverse biological processes, ranging from development to adult physiology. A number of studies have indicated the involvement of PKs/PKRs in nociception. Here we show that PK2 is a sensitizer for nociception. Intraplantar injection of recombinant PK2 resulted in a strong and localized hyperalgesia with reduced thresholds to nociceptive stimuli. PK2 mobilizes calcium in dissociated dorsal root ganglion (DRG) neurons. Mice lacking the PK2 gene displayed strong reduction in nociception induced by thermal and chemical stimuli, including capsaicin. However, PK2 mutant mice showed no difference in inflammatory response to capsaicin. As the majority of PK2-responsive DRG neurons also expressed transient receptor potential vanilloid (TRPV1) and exhibited sensitivity to capsaicin, TRPV1 is likely a significant downstream molecule of PK2 signaling. Taken together, these results reveal that PK2 sensitize nociception without affecting inflammation.
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影响因子：
64.8
作者：
Cheng, MY;Bullock, CM;Zhou, QY
通讯作者：
Zhou, QY
影响因子：
7.4
作者：
Abbadie, C;Taylor, BK;Basbaum, AI
通讯作者：
Basbaum, AI
DOI：
10.1016/s0167-4781(02)00546-8
发表时间：
2002-12-12
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA-GENE STRUCTURE AND EXPRESSION
影响因子：
--
作者：
Soga, T;Matsumoto, SI;Furuichi, K
通讯作者：
Furuichi, K
影响因子：
7.3
作者：
Martucci, C;Franchi, S;Sacerdote, P
通讯作者：
Sacerdote, P
影响因子：
7.3
作者：
Negri, L;Lattanzi, R;Melchiorri, P
通讯作者：
Melchiorri, P