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

doi:10.1080/01902140802404138

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

Pulmonary, Critical Care, & Sleep Medicine

Research output: Contribution to journal › Article › peer-review

10 Scopus citations

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 language	English (US)
Pages (from-to)	48-58
Number of pages	11
Journal	Experimental Lung Research
Volume	35
Issue number	1
DOIs	https://doi.org/10.1080/01902140802404138
State	Published - Feb 2009

Keywords

C-reactive protein MAPK
Lung fibroblast
Migration

ASJC Scopus subject areas

Molecular Biology
Pulmonary and Respiratory Medicine
Clinical Biochemistry

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10.1080/01902140802404138

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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 I.} and Hajime Takizawa",

note = "Funding Information: Declaration of interest: This work was supported in part by grants-in-aid for Scientific Research from the Ministry of Education, Science, Sports, Culture and Technology of Japan, a grant to the Respiratory Failure Research Group from the Ministry of Health, Labour and Welfare, Japan, and grants-in-aid for Comprehensive Research on Aging and Health from the Ministry of Health, Labour and Welfare, Japan. The authors thank Makiko Kase for her excellent technical assistance.",

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doi = "10.1080/01902140802404138",

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volume = "35",

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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 I.

AU - Takizawa, Hajime

N1 - Funding Information: Declaration of interest: This work was supported in part by grants-in-aid for Scientific Research from the Ministry of Education, Science, Sports, Culture and Technology of Japan, a grant to the Respiratory Failure Research Group from the Ministry of Health, Labour and Welfare, Japan, and grants-in-aid for Comprehensive Research on Aging and Health from the Ministry of Health, Labour and Welfare, Japan. The authors thank Makiko Kase for her excellent technical assistance.

PY - 2009/2

Y1 - 2009/2

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.

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C-reactive protein modulates human lung fibroblast migration

Abstract

Keywords

ASJC Scopus subject areas

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