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Am J Physiol Lung Cell Mol Physiol 279: L1075-L1082, 2000;
1040-0605/00 $5.00
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Vol. 279, Issue 6, L1075-L1082, December 2000

Role of microtubules in LPS-induced macrophage inflammatory protein-2 production from rat pneumocytes

Noritaka Isowa, Shaf H. Keshavjee, and Mingyao Liu

Thoracic Surgery Research Laboratory, Toronto General Hospital, University Health Network, and Department of Surgery, University of Toronto, Toronto, Ontario, Canada M5G 2C4

We have recently demonstrated that primary cultured rat pneumocytes produce macrophage inflammatory protein-2 (MIP-2) in response to lipopolysaccharide (LPS) stimulation. In this study, we found that brefeldin A, by blocking anterograde transport from the endoplasmic reticulum (ER) to the Golgi apparatus, decreased LPS-induced MIP-2 in the culture medium and increased its storage in cells. This suggests that MIP-2 is secreted via a pathway from the ER to the Golgi apparatus, a process commonly regulated by microtubules. We further found that LPS induced depolymerization of microtubules as early as 1 min after LPS stimulation, and it lasted at least for 4 h. Preventing depolymerization of microtubules with paclitaxel (Taxol; 10 nM to 10 µM) partially inhibited LPS-induced MIP-2 production, whereas the microtubule-depolymerizing agents colchicine (1-10 µM) and nocodazole (1-100 µM) increased LPS-induced MIP-2 protein production without affecting MIP-2 mRNA expression. These results suggest that in pneumocytes, LPS-induced microtubule depolymerization is involved in LPS-induced MIP-2 production and that secretion of MIP-2 from pneumocytes is via the ER-Golgi pathway.

cytoskeleton; cytokine; chemokine; alveolar epithelial cells


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