C-reactive protein modulates human lung fibroblast migration

Kazuhiko Kikuchi, Tadashi Kohyama, Yasuhiro Yamauchi, Jun Kato, Kazutaka Takami, Hitoshi Okazaki, Masashi Desaki, Takahide Nagase, Stephen I. Rennard, Hajime Takizawa

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


C-reactive protein (CRP) has been classically used as a marker of inflammation. The aim of this study was to investigate the effect of CRP on migration of human fetal lung fibroblasts (HFL-1) to human plasma fibronectin (HFn). Using the blindwell chamber technique, CRP inhibited HFL-1 migration in a dose-dependent fashion (at 1 μg/mL, inhibition: 32.5% ± 7.1%; P <.05). Western blot analysis showed that CRP inhibited the p38 mitogen-activated protein kinase (MAPK) activity in the presence of HFn. Moreover, the MAPK inhibitors SB202190 (25 μM) and SB203580 (25 μM) inhibited HFn-induced cell migration, suggesting an important role of p38 MAPK in HFn-induced migration. Taken together, these results suggest that the inhibitory effect of CRP is mediated by blocking MAPK. In summary, this study demonstrates that CRP directly modulates human lung fibroblasts migration. Thus, CRP may contribute to regulation of wound healing and may be endogenous antifibrotic factor acting on lung fibrosis.

Original languageEnglish (US)
Pages (from-to)48-58
Number of pages11
JournalExperimental Lung Research
Issue number1
StatePublished - Feb 2009


  • C-reactive protein MAPK
  • Lung fibroblast
  • Migration

ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry


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