Mitogen-activated protein kinases regulate platelet-activating factor-induced hyperpermeability.
Mitogen-activated protein kinases regulate platelet-activating factor-induced hyperpermeability.
复制标题
丝裂原激活蛋白激酶调节血小板激活因子诱导的通透性过高。
DOI：
10.1080/10739680500301706
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发表时间：
2005
期刊：
影响因子：
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通讯作者：
Duran,WalterN
中科院分区：
文献类型：
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作者：
Yu,Peng;Hatakeyama,Takuya;Aramoto,Haruo;Miyata,Tetsuro;Shigematsu,Hiroshi;Nagawa,Hirokazu;Hobson,RobertW;Duran,WalterN
目的：验证p42/44-(ERK-1/2)和/或p38-丝裂原激活蛋白激酶(MAPK)是血小板活化因子(PAF)激活的刺激微血管高通透性的信号通路中的体内调节元件的假说。结果：应用10−7M PAF后，IOI由2 3.1±3.6增至70.8±7.4(平均扫描电子显微镜)。用3μM和30μM AG126抑制ERK-1/2使IOI值降至32.3±2.5。同样，用6 nM、60 nM和600 nM的SB203580抑制p38-MAPK后，IOI降至29.1±2.4。结论：ERK-1/2和p38MAPK参与了体内PAF诱导的微血管高通透性的信号转导。
Objective:The authors tested the hypothesis that p42/44- (ERK-1/2) and/or p38-mitogen-activated protein kinases (MAPK) are in vivo regulatory elements in the platelet-activating factor (PAF) activated signaling cascade that stimulates microvascular hyperpermeability.Methods:FITC-dextran 70 was used as the macromolecular tracer for microvascular permeability in the mouse mesenteric fat tissue. Interstitial integrated optical intensity (IOI) was used as an index of permeability.Results:An application of 10−7M PAF increased IOI from 23.1 ± 3.6 to 70.8 ± 7.4 (mean ± SEM). Inhibition of ERK-1/2 with 3 μM and 30 μM AG126 reduced IOI to 32.3 ± 2.5. Similarly, inhibition of p38-MAPK with 6 nM, 60 nM and 600 nM SB203580 lowered IOI to 29.1 ± 2.4.Conclusions:The results demonstrate that ERK-1/2 and p38MAPK participate in the signaling cascade that regulates PAF-induced microvascular hyperpermeability in vivo.