Ultrafine carbon black particles inhibit human lung fibroblast-mediated collagen gel contraction

Huijung Kim, Xiang-de Liu, Tetsu Kobayashi, Tadashi Kohyama, Fu Qiang Wen, Debra Romberger, Heather Conner, Peter S. Gilmour, Kenneth Donaldson, William MacNee, Stephen I. Rennard

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

Both acute and chronic exposure to particulates have been associated with increased mortality and morbidity from a number of causes, including chronic obstructive pulmonary disease and other chronic lung diseases. The current study evaluated the hypothesis that ultrafine carbon particles, a component of ambient particulates, could affect tissue repair. To assess this, the three-dimensional collagen gel contraction model was used. Ultrafine carbon black particles, but not fine carbon black, inhibited fibroblast-mediated collagen gel contraction. Although previous research has indicated that inflammatory effects of ultrafine carbon black particles are mediated by oxidant mechanisms, the current study suggests that ultrafine carbon black's inhibition of fibroblast gel contraction is mediated by the binding of both fibronectin and transforming growth factor (TGF)-β to the ultrafine particles. Binding of TGF-β was associated with a reduction in nuclear localization of Smads, indicative of inhibition of TGF-β signal transduction. There was also a decrease in fibronectin mRNA, consistent with a decrease in TGF-β-mediated response. Taken together, these results demonstrate the ability of ultrafine particles to contribute to altered tissue repair and extend the known mechanisms by which these biologically active particles exert their effects.

Original languageEnglish (US)
Pages (from-to)111-121
Number of pages11
JournalAmerican journal of respiratory cell and molecular biology
Volume28
Issue number1
DOIs
StatePublished - Jan 1 2003

Fingerprint

Soot
Fibroblasts
Collagen
Gels
Transforming Growth Factors
Lung
Pulmonary diseases
Fibronectins
Repair
Tissue
Signal transduction
Oxidants
Chronic Obstructive Pulmonary Disease
Lung Diseases
Ultrafine
Signal Transduction
Chronic Disease
Carbon
Morbidity
Messenger RNA

ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry
  • Cell Biology

Cite this

Ultrafine carbon black particles inhibit human lung fibroblast-mediated collagen gel contraction. / Kim, Huijung; Liu, Xiang-de; Kobayashi, Tetsu; Kohyama, Tadashi; Wen, Fu Qiang; Romberger, Debra; Conner, Heather; Gilmour, Peter S.; Donaldson, Kenneth; MacNee, William; Rennard, Stephen I.

In: American journal of respiratory cell and molecular biology, Vol. 28, No. 1, 01.01.2003, p. 111-121.

Research output: Contribution to journalArticle

Kim, H, Liu, X, Kobayashi, T, Kohyama, T, Wen, FQ, Romberger, D, Conner, H, Gilmour, PS, Donaldson, K, MacNee, W & Rennard, SI 2003, 'Ultrafine carbon black particles inhibit human lung fibroblast-mediated collagen gel contraction', American journal of respiratory cell and molecular biology, vol. 28, no. 1, pp. 111-121. https://doi.org/10.1165/rcmb.4796
Kim, Huijung ; Liu, Xiang-de ; Kobayashi, Tetsu ; Kohyama, Tadashi ; Wen, Fu Qiang ; Romberger, Debra ; Conner, Heather ; Gilmour, Peter S. ; Donaldson, Kenneth ; MacNee, William ; Rennard, Stephen I. / Ultrafine carbon black particles inhibit human lung fibroblast-mediated collagen gel contraction. In: American journal of respiratory cell and molecular biology. 2003 ; Vol. 28, No. 1. pp. 111-121.
@article{390ccd91b30544c49c2ebba30cfbc153,
title = "Ultrafine carbon black particles inhibit human lung fibroblast-mediated collagen gel contraction",
abstract = "Both acute and chronic exposure to particulates have been associated with increased mortality and morbidity from a number of causes, including chronic obstructive pulmonary disease and other chronic lung diseases. The current study evaluated the hypothesis that ultrafine carbon particles, a component of ambient particulates, could affect tissue repair. To assess this, the three-dimensional collagen gel contraction model was used. Ultrafine carbon black particles, but not fine carbon black, inhibited fibroblast-mediated collagen gel contraction. Although previous research has indicated that inflammatory effects of ultrafine carbon black particles are mediated by oxidant mechanisms, the current study suggests that ultrafine carbon black's inhibition of fibroblast gel contraction is mediated by the binding of both fibronectin and transforming growth factor (TGF)-β to the ultrafine particles. Binding of TGF-β was associated with a reduction in nuclear localization of Smads, indicative of inhibition of TGF-β signal transduction. There was also a decrease in fibronectin mRNA, consistent with a decrease in TGF-β-mediated response. Taken together, these results demonstrate the ability of ultrafine particles to contribute to altered tissue repair and extend the known mechanisms by which these biologically active particles exert their effects.",
author = "Huijung Kim and Xiang-de Liu and Tetsu Kobayashi and Tadashi Kohyama and Wen, {Fu Qiang} and Debra Romberger and Heather Conner and Gilmour, {Peter S.} and Kenneth Donaldson and William MacNee and Rennard, {Stephen I.}",
year = "2003",
month = "1",
day = "1",
doi = "10.1165/rcmb.4796",
language = "English (US)",
volume = "28",
pages = "111--121",
journal = "American Journal of Respiratory Cell and Molecular Biology",
issn = "1044-1549",
publisher = "American Thoracic Society",
number = "1",

}

TY - JOUR

T1 - Ultrafine carbon black particles inhibit human lung fibroblast-mediated collagen gel contraction

AU - Kim, Huijung

AU - Liu, Xiang-de

AU - Kobayashi, Tetsu

AU - Kohyama, Tadashi

AU - Wen, Fu Qiang

AU - Romberger, Debra

AU - Conner, Heather

AU - Gilmour, Peter S.

AU - Donaldson, Kenneth

AU - MacNee, William

AU - Rennard, Stephen I.

PY - 2003/1/1

Y1 - 2003/1/1

N2 - Both acute and chronic exposure to particulates have been associated with increased mortality and morbidity from a number of causes, including chronic obstructive pulmonary disease and other chronic lung diseases. The current study evaluated the hypothesis that ultrafine carbon particles, a component of ambient particulates, could affect tissue repair. To assess this, the three-dimensional collagen gel contraction model was used. Ultrafine carbon black particles, but not fine carbon black, inhibited fibroblast-mediated collagen gel contraction. Although previous research has indicated that inflammatory effects of ultrafine carbon black particles are mediated by oxidant mechanisms, the current study suggests that ultrafine carbon black's inhibition of fibroblast gel contraction is mediated by the binding of both fibronectin and transforming growth factor (TGF)-β to the ultrafine particles. Binding of TGF-β was associated with a reduction in nuclear localization of Smads, indicative of inhibition of TGF-β signal transduction. There was also a decrease in fibronectin mRNA, consistent with a decrease in TGF-β-mediated response. Taken together, these results demonstrate the ability of ultrafine particles to contribute to altered tissue repair and extend the known mechanisms by which these biologically active particles exert their effects.

AB - Both acute and chronic exposure to particulates have been associated with increased mortality and morbidity from a number of causes, including chronic obstructive pulmonary disease and other chronic lung diseases. The current study evaluated the hypothesis that ultrafine carbon particles, a component of ambient particulates, could affect tissue repair. To assess this, the three-dimensional collagen gel contraction model was used. Ultrafine carbon black particles, but not fine carbon black, inhibited fibroblast-mediated collagen gel contraction. Although previous research has indicated that inflammatory effects of ultrafine carbon black particles are mediated by oxidant mechanisms, the current study suggests that ultrafine carbon black's inhibition of fibroblast gel contraction is mediated by the binding of both fibronectin and transforming growth factor (TGF)-β to the ultrafine particles. Binding of TGF-β was associated with a reduction in nuclear localization of Smads, indicative of inhibition of TGF-β signal transduction. There was also a decrease in fibronectin mRNA, consistent with a decrease in TGF-β-mediated response. Taken together, these results demonstrate the ability of ultrafine particles to contribute to altered tissue repair and extend the known mechanisms by which these biologically active particles exert their effects.

UR - http://www.scopus.com/inward/record.url?scp=0037215649&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037215649&partnerID=8YFLogxK

U2 - 10.1165/rcmb.4796

DO - 10.1165/rcmb.4796

M3 - Article

C2 - 12495939

AN - SCOPUS:0037215649

VL - 28

SP - 111

EP - 121

JO - American Journal of Respiratory Cell and Molecular Biology

JF - American Journal of Respiratory Cell and Molecular Biology

SN - 1044-1549

IS - 1

ER -