丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPKs)是生物体内最重要的信号转导系统之一,包括细胞外信号调控蛋白激酶(extracellular signal-regulated protein kinase,ERK)、c-Jun氨基末端激酶(c-Jun N-terminal kinase,JN...丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPKs)是生物体内最重要的信号转导系统之一,包括细胞外信号调控蛋白激酶(extracellular signal-regulated protein kinase,ERK)、c-Jun氨基末端激酶(c-Jun N-terminal kinase,JNK)/应激激活蛋白激酶(stress-activated protein kinase,SAPK)、p38、ERK5/大丝裂素活化蛋白激酶1(big mitogen-activated proteinkinase,BMK1)四个家族成员,参与细胞增殖、分化、凋亡的调节,并与炎症、肿瘤等多种疾病的发生发展密切相关。牙周炎是一种慢性感染性疾病,MAPKs参与了牙周炎发生发展的过程,该文将对近年来相关研究的进展做一综述。展开更多
The mammalian target of rapamycin （mTOR） pathway is essential for maintenance of the sensitivity of certain adult sensory neurons. Here, we investigated whether the mTOR cascade is involved in scorpion envenomation-...The mammalian target of rapamycin （mTOR） pathway is essential for maintenance of the sensitivity of certain adult sensory neurons. Here, we investigated whether the mTOR cascade is involved in scorpion envenomation-induced pain hypersensitivity in rats. The results showed that intraplantar injection of a neurotoxin from Buthus martensii Karsch, BmK I （10 pg）, induced the activation of mTOR, as well as its downstream molecules p70 ribosomal S6 protein kinase （p70 S6K） and eukaryotic initiation factor 4E-binding protein 1 （4E-BP1）, in lumbar 5-6 dorsal root ganglia neurons on both sides in rats. The activation peaked at 2 h and recovered 1 day after injection. Compared with the control group, the ratios of p-mTOR/p-p70 S6K/p-4E- BP1 in three types of neurons changed significantly. The cell typology of p-mTOR/p-p70 S6K/p-4E-BP1 immuno-reactive neurons also changed. Intrathecal administration of deforolimus, a specific inhibitor of mTOR, attenuated BmK I-induced pain responses （spontaneous flinching, paroxysmal pain-like behavior, and mechanical hypersensitivity）. Together, these results imply that the mTOR signaling pathway is mobilized by and contributes to experimental scorpion sting-induced pain.展开更多
文摘丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPKs)是生物体内最重要的信号转导系统之一,包括细胞外信号调控蛋白激酶(extracellular signal-regulated protein kinase,ERK)、c-Jun氨基末端激酶(c-Jun N-terminal kinase,JNK)/应激激活蛋白激酶(stress-activated protein kinase,SAPK)、p38、ERK5/大丝裂素活化蛋白激酶1(big mitogen-activated proteinkinase,BMK1)四个家族成员,参与细胞增殖、分化、凋亡的调节,并与炎症、肿瘤等多种疾病的发生发展密切相关。牙周炎是一种慢性感染性疾病,MAPKs参与了牙周炎发生发展的过程,该文将对近年来相关研究的进展做一综述。
基金supported by grants from the National Basic Research Development Program of China(2010CB529806)the National Natural Science Foundation of China(31171064)+2 种基金the Shanghai Science and Technology CommissionChina(11JC140430010411956700 and 124119b0600)
文摘The mammalian target of rapamycin （mTOR） pathway is essential for maintenance of the sensitivity of certain adult sensory neurons. Here, we investigated whether the mTOR cascade is involved in scorpion envenomation-induced pain hypersensitivity in rats. The results showed that intraplantar injection of a neurotoxin from Buthus martensii Karsch, BmK I （10 pg）, induced the activation of mTOR, as well as its downstream molecules p70 ribosomal S6 protein kinase （p70 S6K） and eukaryotic initiation factor 4E-binding protein 1 （4E-BP1）, in lumbar 5-6 dorsal root ganglia neurons on both sides in rats. The activation peaked at 2 h and recovered 1 day after injection. Compared with the control group, the ratios of p-mTOR/p-p70 S6K/p-4E- BP1 in three types of neurons changed significantly. The cell typology of p-mTOR/p-p70 S6K/p-4E-BP1 immuno-reactive neurons also changed. Intrathecal administration of deforolimus, a specific inhibitor of mTOR, attenuated BmK I-induced pain responses （spontaneous flinching, paroxysmal pain-like behavior, and mechanical hypersensitivity）. Together, these results imply that the mTOR signaling pathway is mobilized by and contributes to experimental scorpion sting-induced pain.
