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 Israel Rennard, Hajime Takizawa

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

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
Volume35
Issue number1
DOIs
StatePublished - Feb 1 2009

Fingerprint

Fibroblasts
C-Reactive Protein
Plasma (human)
Lung
Fibronectins
p38 Mitogen-Activated Protein Kinases
Mitogen-Activated Protein Kinases
Protein Kinase Inhibitors
Wound Healing
Cell Movement
Fibrosis
Western Blotting
Inflammation

Keywords

  • C-reactive protein MAPK
  • Lung fibroblast
  • Migration

ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry

Cite this

Kikuchi, K., Kohyama, T., Yamauchi, Y., Kato, J., Takami, K., Okazaki, H., ... Takizawa, H. (2009). C-reactive protein modulates human lung fibroblast migration. Experimental Lung Research, 35(1), 48-58. https://doi.org/10.1080/01902140802404138

C-reactive protein modulates human lung fibroblast migration. / Kikuchi, Kazuhiko; Kohyama, Tadashi; Yamauchi, Yasuhiro; Kato, Jun; Takami, Kazutaka; Okazaki, Hitoshi; Desaki, Masashi; Nagase, Takahide; Rennard, Stephen Israel; Takizawa, Hajime.

In: Experimental Lung Research, Vol. 35, No. 1, 01.02.2009, p. 48-58.

Research output: Contribution to journalArticle

Kikuchi, K, Kohyama, T, Yamauchi, Y, Kato, J, Takami, K, Okazaki, H, Desaki, M, Nagase, T, Rennard, SI & Takizawa, H 2009, 'C-reactive protein modulates human lung fibroblast migration', Experimental Lung Research, vol. 35, no. 1, pp. 48-58. https://doi.org/10.1080/01902140802404138
Kikuchi K, Kohyama T, Yamauchi Y, Kato J, Takami K, Okazaki H et al. C-reactive protein modulates human lung fibroblast migration. Experimental Lung Research. 2009 Feb 1;35(1):48-58. https://doi.org/10.1080/01902140802404138
Kikuchi, Kazuhiko ; Kohyama, Tadashi ; Yamauchi, Yasuhiro ; Kato, Jun ; Takami, Kazutaka ; Okazaki, Hitoshi ; Desaki, Masashi ; Nagase, Takahide ; Rennard, Stephen Israel ; Takizawa, Hajime. / C-reactive protein modulates human lung fibroblast migration. In: Experimental Lung Research. 2009 ; Vol. 35, No. 1. pp. 48-58.
@article{8780a209895644cb9751bdadfce99666,
title = "C-reactive protein modulates human lung fibroblast migration",
abstract = "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.",
keywords = "C-reactive protein MAPK, Lung fibroblast, Migration",
author = "Kazuhiko Kikuchi and Tadashi Kohyama and Yasuhiro Yamauchi and Jun Kato and Kazutaka Takami and Hitoshi Okazaki and Masashi Desaki and Takahide Nagase and Rennard, {Stephen Israel} and Hajime Takizawa",
year = "2009",
month = "2",
day = "1",
doi = "10.1080/01902140802404138",
language = "English (US)",
volume = "35",
pages = "48--58",
journal = "Experimental Lung Research",
issn = "0190-2148",
publisher = "Informa Healthcare",
number = "1",

}

TY - JOUR

T1 - C-reactive protein modulates human lung fibroblast migration

AU - Kikuchi, Kazuhiko

AU - Kohyama, Tadashi

AU - Yamauchi, Yasuhiro

AU - Kato, Jun

AU - Takami, Kazutaka

AU - Okazaki, Hitoshi

AU - Desaki, Masashi

AU - Nagase, Takahide

AU - Rennard, Stephen Israel

AU - Takizawa, Hajime

PY - 2009/2/1

Y1 - 2009/2/1

N2 - 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.

AB - 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.

KW - C-reactive protein MAPK

KW - Lung fibroblast

KW - Migration

UR - http://www.scopus.com/inward/record.url?scp=60749099456&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=60749099456&partnerID=8YFLogxK

U2 - 10.1080/01902140802404138

DO - 10.1080/01902140802404138

M3 - Article

VL - 35

SP - 48

EP - 58

JO - Experimental Lung Research

JF - Experimental Lung Research

SN - 0190-2148

IS - 1

ER -