Botulinum toxin complex increases paracellular permeability in intestinal epithelial cells via activation of p38 mitogen-activated protein kinase.

Botulinum toxin complex increases paracellular permeability in intestinal epithelial cells via activation of p38 mitogen-activated protein kinase.
复制标题

DOI:
10.1292/jvms.13-0164
复制
发表时间:
2013-12-30
期刊:
The Journal of veterinary medical science
影响因子:
--
通讯作者:
Niwa K
Niwa K
中科院分区:
其他
文献类型:
--
作者:
Miyashita S;Sagane Y;Inui K;Hayashi S;Miyata K;Suzuki T;Ohyama T;Watanabe T;Niwa K

文献摘要

参考文献

被引文献

相似文献

肉毒梭菌产生一种大的毒素复合体(L-TC),通过一种尚不清楚的机制增加肠道上皮细胞的细胞旁通透性。在这里,我们表明,丝裂原激活的蛋白激酶(MAPK)参与了这种通透性的增加。FITC-葡聚糖通透法测定大鼠肠上皮细胞IEC-6单层通透性,免疫印迹法检测MAPK活性。D型肉毒弧菌的L-TC能增加IEC-6细胞的胞外葡聚糖流量,激活细胞外信号调节激酶p38,但不能激活c-jun氨基末端激酶。P38抑制剂SB203580可阻断L-TC引起的通透性增加。这些结果表明,L-TC通过激活p38而不是通过激活JNK和ERK来增加细胞旁通透性。
Clostridium botulinum produces a large toxin complex (L-TC) that increases paracellular permeability in intestinal epithelial cells by a mechanism that remains unclear. Here, we show that mitogen-activated protein kinases (MAPKs) are involved in this permeability increase. Paracellular permeability was measured by FITC-dextran flux through a monolayer of rat intestinal epithelial IEC-6 cells, and MAPK activation was estimated from western blots. L-TC of C. botulinum serotype D strain 4947 increased paracellular dextran flux and activated extracellular signal-regulated kinase (ERK), p38, but not c-Jun N-terminal kinase (JNK) in IEC-6 cells. The permeability increase induced by L-TC was abrogated by the p38 inhibitor SB203580. These results indicate that L-TC increases paracellular permeability by activating p38, but not JNK and ERK.
DOI: 10.1074/jbc.m703446200
发表时间: 2007-08-24
影响因子: 4.8
作者:
Hasegawa, Kimiko;Watanabe, Toshihiro;Ohyama, Tohru
通讯作者: Ohyama, Tohru
DOI: 10.1073/pnas.251194298
发表时间: 2001-11-20
影响因子: 11.1
作者:
Bennett, BL;Sasaki, DT;Anderson, DW
通讯作者: Anderson, DW
灌注梭状芽胞杆菌肠毒素片段从紧密连接链中去除特定的克劳丁:直接参与Claudins在紧密连接屏障中的证据。
DOI: 10.1083/jcb.147.1.195
发表时间: 1999-10-04
期刊: The Journal of cell biology
影响因子: --
作者:
Sonoda N;Furuse M;Sasaki H;Yonemura S;Katahira J;Horiguchi Y;Tsukita S
通讯作者: Tsukita S
DOI: 10.1016/j.bbrc.2009.04.095
发表时间: 2009-06-19
影响因子: 3.1
作者:
Miyata, Keita;Yoneyama, Tohru;Ohyama, Tohru
通讯作者: Ohyama, Tohru
DOI: 10.1128/iai.17.3.491-496.1977
发表时间: 1977-01-01
影响因子: 3.1
作者:
SUGII, S;OHISHI, I;SAKAGUCHI, G
通讯作者: SAKAGUCHI, G