Lipoteichoic acid-stimulated p42/p44 MAPK activation via Toll-like receptor 2 in tracheal smooth muscle cells

Chiang Wen Lee, Chin Sung Chien, Chuen Mao Yang*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

45 Scopus citations

Abstract

Lipoteichoic acid (LTA), the principal component of the cell wall of gram-positive bacteria, triggers several inflammatory responses. However, the mechanisms underlying its action on human tracheal smooth muscle cells (HTSMCs) were largely unknown. This study was to investigate the mechanisms underlying LTA-stimulated p42/p44 mitogen-activated protein kinase (MAPK) using Western blotting assay. LTA stimulated phosphorylation of p42/p44 MAPK via a Toll-like receptor 2 (TLR2). Pretreatment with pertussis toxin attenuated the LTA-induced responses. LTA-stimulated phosphorylation of p42/p44 MAPK was attenuated by inhibitors of tyrosine kinase (genistein), phosphatidylcholine-phospholipase C (PLC; D609), phosphatidylinositol (PI)-PLC (U-73122), PKC (staurosporine, Gö-6976, rottlerin, or Ro-318220), MEK1/2 (U-0126), PI 3-kinase (LY-294002 and wortmannin), and an intracellular Ca2+ chelator (BAPTA-AM). LTA directly evoked initial transient peak of [Ca2+]i, supporting the involvement of Ca2+ mobilization in LTA-induced responses. These results suggest that in HTSMCs, LTA-stimulated p42/p44 MAPK phosphorylation is mediated through a TLR2 receptor and involves tyrosine kinase, PLC, PKC, Ca2+, MEK, and PI 3-kinase.

Original languageEnglish
Pages (from-to)L921-L930
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume286
Issue number5 30-5
DOIs
StatePublished - 05 2004

Keywords

  • Calcium
  • Human
  • Phospholipase C
  • Protein kinase C

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