The frog trefoil factor Bm-TFF2 activates human platelets via Gq and G12/13 signaling pathway

	The frog trefoil factor Bm-TFF2 activates human platelets via Gq and G12/13 signaling pathway
	Lei WW 1,2; Huang YG 1,3; Zhang Y 1; Yu GY 1,4; Wan SG 1; Lee WH 1; Zhang Y*1; zhangy@mail.kiz.ac.cn
	2012
发表期刊	TOXICON
卷号	59 期号:1 页码:104-109
合作性质	其它
摘要	Bm-TFF2 is an amphibian trefoil factor purified from the Bombina maxima skin secretion that is highly toxic to mammals. We previously reported that Bm-TFF2 activates human platelets via protease-activated receptor 1. In this study, for a better understanding of platelet activation induced by Bm-TFF2, we used affinity chromatography and pharmacological inhibitors to investigate the downstream signaling pathway. Using Bm-TFF2-affinity chromatography, Gq was specifically eluted from the Bm-TFF2-coulped column. Pharmacological inhibitors such as U73122, Xestospongin C, BAPTA-AM and Go6976 can significantly inhibit Bm-TFF2-induced platelet aggregation. These results suggested that Gq activation and the downstream PLC beta-IP3 receptor-cytoplasmic Ca2+-PKC signaling pathway is crucial for Bm-TFF2 to stimulate platelet aggregation. Furthermore. Bm-TFF2 induced strong platelet shape change at the concentrations of 5 nM, in which the Ca2+ mobilization of the platelets stimulated was not detectable. The p160(ROCK) inhibitorY27632 totally inhibited the shape change, indicating that Bm-TFF2 may activate the G12/13 pathway which leads to the activation of RhoA-p160(ROCK). In conclusion, Bm-TFF2 induced platelet activation mainly via the Gq and G12/13 signaling pathway. This study on the signaling pathway of Bm-TFF2 stimulation may help us understand the toxicity of B. maxima skin secretion to the human platelets
关键词	Amphibian Skin Trefoil Factor Platelet Activation Signaling
资助者	This work was supported by grants from National Basic Research Program of China (973 Program, 2010CB529800), the Chinese National Natural Science Foundation (30630014, 30870304, 81101547 and 81160302), and the Chinese Academy of Sciences “Key Research Direction” (KSCX2-YW-R-088) and “Western Light Project” (Y102291081). ; This work was supported by grants from National Basic Research Program of China (973 Program, 2010CB529800), the Chinese National Natural Science Foundation (30630014, 30870304, 81101547 and 81160302), and the Chinese Academy of Sciences “Key Research Direction” (KSCX2-YW-R-088) and “Western Light Project” (Y102291081). ; This work was supported by grants from National Basic Research Program of China (973 Program, 2010CB529800), the Chinese National Natural Science Foundation (30630014, 30870304, 81101547 and 81160302), and the Chinese Academy of Sciences “Key Research Direction” (KSCX2-YW-R-088) and “Western Light Project” (Y102291081). ; This work was supported by grants from National Basic Research Program of China (973 Program, 2010CB529800), the Chinese National Natural Science Foundation (30630014, 30870304, 81101547 and 81160302), and the Chinese Academy of Sciences “Key Research Direction” (KSCX2-YW-R-088) and “Western Light Project” (Y102291081).
收录类别	SCI
语种	英语
资助者	This work was supported by grants from National Basic Research Program of China (973 Program, 2010CB529800), the Chinese National Natural Science Foundation (30630014, 30870304, 81101547 and 81160302), and the Chinese Academy of Sciences “Key Research Direction” (KSCX2-YW-R-088) and “Western Light Project” (Y102291081). ; This work was supported by grants from National Basic Research Program of China (973 Program, 2010CB529800), the Chinese National Natural Science Foundation (30630014, 30870304, 81101547 and 81160302), and the Chinese Academy of Sciences “Key Research Direction” (KSCX2-YW-R-088) and “Western Light Project” (Y102291081). ; This work was supported by grants from National Basic Research Program of China (973 Program, 2010CB529800), the Chinese National Natural Science Foundation (30630014, 30870304, 81101547 and 81160302), and the Chinese Academy of Sciences “Key Research Direction” (KSCX2-YW-R-088) and “Western Light Project” (Y102291081). ; This work was supported by grants from National Basic Research Program of China (973 Program, 2010CB529800), the Chinese National Natural Science Foundation (30630014, 30870304, 81101547 and 81160302), and the Chinese Academy of Sciences “Key Research Direction” (KSCX2-YW-R-088) and “Western Light Project” (Y102291081).
WOS记录号	WOS:000300137300013
引用统计
文献类型	期刊论文
条目标识符	http://ir.kiz.ac.cn/handle/353002/6893
专题	科研部门_生物毒素与人类疾病（张云）科研部门_动物模型与人类重大疾病机理重点实验室
通讯作者	zhangy@mail.kiz.ac.cn
作者单位	1.Key Laboratory of Animal Models and Human Disease Mechanisms, Kunming Institute of Zoology, Chinese Academy of Sciences, 32 East Jiao Chang Road, Kunming, Yunnan 650223, China 2.Laboratory of Molecular Genetics of Aging and Tumor, Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming 650224, China 3.Graduate School of Chinese Academy of Sciences, Beijing 100049, China 4.Department of Biochemistry, Kunming Medical College, Kunming, Yunnan 650032, China
推荐引用方式 GB/T 7714	Lei WW,Huang YG,Zhang Y,et al. The frog trefoil factor Bm-TFF2 activates human platelets via Gq and G12/13 signaling pathway[J]. TOXICON,2012,59(1):104-109.
APA	Lei WW.,Huang YG.,Zhang Y.,Yu GY.,Wan SG.,...&zhangy@mail.kiz.ac.cn.(2012).The frog trefoil factor Bm-TFF2 activates human platelets via Gq and G12/13 signaling pathway.TOXICON,59(1),104-109.
MLA	Lei WW,et al."The frog trefoil factor Bm-TFF2 activates human platelets via Gq and G12/13 signaling pathway".TOXICON 59.1(2012):104-109.

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