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Mitogen-activated protein kinases regulate platelet-activating factor-induced hyperpermeability.

Peng Yu·Takuya Hatakeyama·Haruo Aramoto·Tetsuro Miyata·Hiroshi Shigematsu·Hirokazu Nagawa·Robert W Hobson·Walter N Durán
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Abstract

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(-7) M PAF increased IOI from 23.1 +/- 3.6 to 70.8 +/- 7.4 (mean +/- SEM). Inhibition of ERK-1/2 with 3 microM and 30 microM 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.

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AnimalsCapillary PermeabilityIntra-Abdominal FatMAP Kinase Signaling SystemMaleMiceMitogen-Activated Protein Kinase 3Platelet Activating Factorp38 Mitogen-Activated Protein KinasesJournal ArticleResearch Support, N.I.H., Extramural

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Peng Yu, Takuya Hatakeyama, Haruo Aramoto, Tetsuro Miyata, Hiroshi Shigematsu, Hirokazu Nagawa, Robert W Hobson, Walter N Durán. 2005. Mitogen-activated protein kinases regulate platelet-activating factor-induced hyperpermeability.. https://doi.org/10.1080/10739680500301706

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