Modification of type I collagenous gels by alveolar epithelial cells

Takeshi Umino, Hangjun Wang, Yunkui Zhu, Xiang-de Liu, Lidia S. Manouilova, John R. Spurzem, M. Patricia Leuschen, Stephen I. Rennard

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Contraction of type I collagen gels is an in vitro model of tissue remodeling. In addition to fibroblasts, some epithelial cells can mediate this process. We therefore hypothesized that alveolar epithelial cells might contract extracellular matrices and have the potential to directly participate in the remodeling of the lung after alveolar injury. A549 cells were plated on top of collagen gels, and the gels were floated in culture medium. A549 cells contracted the gels in a time- and cell density-dependent manner. A549 cells, as well as human bronchial epithelial cells (HBEC) and rat alveolar epithelial cells (RalvEC) contracted collagen gels more when they were plated on top of the gel than when they were embedded inside, in contrast to human fetal lung fibroblast (HFL1), which contracted more when cast inside. The amount of hydroxyproline in the collagen gels remained unchanged throughout the contraction. Anti-β1 integrin antibody inhibited A549 cell-mediated contraction. Transforming growth factor β augmented the contraction by A549 cells as well as that by HBEC and HFL1. Prostaglandin E2 inhibited the contraction by HFL1 but did not affect the contraction by A549 cells, HBEC, or RalvEC. Cytomix (a mixture of tumor necrosis factor-α, interleukin-1β, and interferon-γ) inhibited the contraction by HFL1 but strongly enhanced the contraction by A549 cells. Cytomix also caused a morphologic change of A549 cells from a polygonal to a spindle shape. Immunocytochemistry showed that cytomix induced α-tubulin expression in A549 cells, whereas cytokeratin, vimentin, smooth muscle actin, β1 integrin, and paxillin expressions were not changed. This study thus demonstrates that alveolar epithelial cells can cause contraction of extracellular matrices and that this process is modulated by exogenous mediators, which also modify the microtubular system. Such an activity might contribute to alveolar remodeling after injury.

Original languageEnglish (US)
Pages (from-to)702-707
Number of pages6
JournalAmerican journal of respiratory cell and molecular biology
Volume22
Issue number6
DOIs
StatePublished - Jan 1 2000

Fingerprint

Alveolar Epithelial Cells
Gels
Epithelial Cells
Collagen
Fibroblasts
Integrins
Extracellular Matrix
Rats
Paxillin
A549 Cells
Lung
Hydroxyproline
Wounds and Injuries
Transforming Growth Factors
Vimentin
Tubulin
Keratins
Collagen Type I
Interleukin-1
Dinoprostone

ASJC Scopus subject areas

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

Cite this

Modification of type I collagenous gels by alveolar epithelial cells. / Umino, Takeshi; Wang, Hangjun; Zhu, Yunkui; Liu, Xiang-de; Manouilova, Lidia S.; Spurzem, John R.; Leuschen, M. Patricia; Rennard, Stephen I.

In: American journal of respiratory cell and molecular biology, Vol. 22, No. 6, 01.01.2000, p. 702-707.

Research output: Contribution to journalArticle

Umino, T, Wang, H, Zhu, Y, Liu, X, Manouilova, LS, Spurzem, JR, Leuschen, MP & Rennard, SI 2000, 'Modification of type I collagenous gels by alveolar epithelial cells', American journal of respiratory cell and molecular biology, vol. 22, no. 6, pp. 702-707. https://doi.org/10.1165/ajrcmb.22.6.3806
Umino, Takeshi ; Wang, Hangjun ; Zhu, Yunkui ; Liu, Xiang-de ; Manouilova, Lidia S. ; Spurzem, John R. ; Leuschen, M. Patricia ; Rennard, Stephen I. / Modification of type I collagenous gels by alveolar epithelial cells. In: American journal of respiratory cell and molecular biology. 2000 ; Vol. 22, No. 6. pp. 702-707.
@article{35d79295148f4550897d3e59ae4bc4e9,
title = "Modification of type I collagenous gels by alveolar epithelial cells",
abstract = "Contraction of type I collagen gels is an in vitro model of tissue remodeling. In addition to fibroblasts, some epithelial cells can mediate this process. We therefore hypothesized that alveolar epithelial cells might contract extracellular matrices and have the potential to directly participate in the remodeling of the lung after alveolar injury. A549 cells were plated on top of collagen gels, and the gels were floated in culture medium. A549 cells contracted the gels in a time- and cell density-dependent manner. A549 cells, as well as human bronchial epithelial cells (HBEC) and rat alveolar epithelial cells (RalvEC) contracted collagen gels more when they were plated on top of the gel than when they were embedded inside, in contrast to human fetal lung fibroblast (HFL1), which contracted more when cast inside. The amount of hydroxyproline in the collagen gels remained unchanged throughout the contraction. Anti-β1 integrin antibody inhibited A549 cell-mediated contraction. Transforming growth factor β augmented the contraction by A549 cells as well as that by HBEC and HFL1. Prostaglandin E2 inhibited the contraction by HFL1 but did not affect the contraction by A549 cells, HBEC, or RalvEC. Cytomix (a mixture of tumor necrosis factor-α, interleukin-1β, and interferon-γ) inhibited the contraction by HFL1 but strongly enhanced the contraction by A549 cells. Cytomix also caused a morphologic change of A549 cells from a polygonal to a spindle shape. Immunocytochemistry showed that cytomix induced α-tubulin expression in A549 cells, whereas cytokeratin, vimentin, smooth muscle actin, β1 integrin, and paxillin expressions were not changed. This study thus demonstrates that alveolar epithelial cells can cause contraction of extracellular matrices and that this process is modulated by exogenous mediators, which also modify the microtubular system. Such an activity might contribute to alveolar remodeling after injury.",
author = "Takeshi Umino and Hangjun Wang and Yunkui Zhu and Xiang-de Liu and Manouilova, {Lidia S.} and Spurzem, {John R.} and Leuschen, {M. Patricia} and Rennard, {Stephen I.}",
year = "2000",
month = "1",
day = "1",
doi = "10.1165/ajrcmb.22.6.3806",
language = "English (US)",
volume = "22",
pages = "702--707",
journal = "American Journal of Respiratory Cell and Molecular Biology",
issn = "1044-1549",
publisher = "American Thoracic Society",
number = "6",

}

TY - JOUR

T1 - Modification of type I collagenous gels by alveolar epithelial cells

AU - Umino, Takeshi

AU - Wang, Hangjun

AU - Zhu, Yunkui

AU - Liu, Xiang-de

AU - Manouilova, Lidia S.

AU - Spurzem, John R.

AU - Leuschen, M. Patricia

AU - Rennard, Stephen I.

PY - 2000/1/1

Y1 - 2000/1/1

N2 - Contraction of type I collagen gels is an in vitro model of tissue remodeling. In addition to fibroblasts, some epithelial cells can mediate this process. We therefore hypothesized that alveolar epithelial cells might contract extracellular matrices and have the potential to directly participate in the remodeling of the lung after alveolar injury. A549 cells were plated on top of collagen gels, and the gels were floated in culture medium. A549 cells contracted the gels in a time- and cell density-dependent manner. A549 cells, as well as human bronchial epithelial cells (HBEC) and rat alveolar epithelial cells (RalvEC) contracted collagen gels more when they were plated on top of the gel than when they were embedded inside, in contrast to human fetal lung fibroblast (HFL1), which contracted more when cast inside. The amount of hydroxyproline in the collagen gels remained unchanged throughout the contraction. Anti-β1 integrin antibody inhibited A549 cell-mediated contraction. Transforming growth factor β augmented the contraction by A549 cells as well as that by HBEC and HFL1. Prostaglandin E2 inhibited the contraction by HFL1 but did not affect the contraction by A549 cells, HBEC, or RalvEC. Cytomix (a mixture of tumor necrosis factor-α, interleukin-1β, and interferon-γ) inhibited the contraction by HFL1 but strongly enhanced the contraction by A549 cells. Cytomix also caused a morphologic change of A549 cells from a polygonal to a spindle shape. Immunocytochemistry showed that cytomix induced α-tubulin expression in A549 cells, whereas cytokeratin, vimentin, smooth muscle actin, β1 integrin, and paxillin expressions were not changed. This study thus demonstrates that alveolar epithelial cells can cause contraction of extracellular matrices and that this process is modulated by exogenous mediators, which also modify the microtubular system. Such an activity might contribute to alveolar remodeling after injury.

AB - Contraction of type I collagen gels is an in vitro model of tissue remodeling. In addition to fibroblasts, some epithelial cells can mediate this process. We therefore hypothesized that alveolar epithelial cells might contract extracellular matrices and have the potential to directly participate in the remodeling of the lung after alveolar injury. A549 cells were plated on top of collagen gels, and the gels were floated in culture medium. A549 cells contracted the gels in a time- and cell density-dependent manner. A549 cells, as well as human bronchial epithelial cells (HBEC) and rat alveolar epithelial cells (RalvEC) contracted collagen gels more when they were plated on top of the gel than when they were embedded inside, in contrast to human fetal lung fibroblast (HFL1), which contracted more when cast inside. The amount of hydroxyproline in the collagen gels remained unchanged throughout the contraction. Anti-β1 integrin antibody inhibited A549 cell-mediated contraction. Transforming growth factor β augmented the contraction by A549 cells as well as that by HBEC and HFL1. Prostaglandin E2 inhibited the contraction by HFL1 but did not affect the contraction by A549 cells, HBEC, or RalvEC. Cytomix (a mixture of tumor necrosis factor-α, interleukin-1β, and interferon-γ) inhibited the contraction by HFL1 but strongly enhanced the contraction by A549 cells. Cytomix also caused a morphologic change of A549 cells from a polygonal to a spindle shape. Immunocytochemistry showed that cytomix induced α-tubulin expression in A549 cells, whereas cytokeratin, vimentin, smooth muscle actin, β1 integrin, and paxillin expressions were not changed. This study thus demonstrates that alveolar epithelial cells can cause contraction of extracellular matrices and that this process is modulated by exogenous mediators, which also modify the microtubular system. Such an activity might contribute to alveolar remodeling after injury.

UR - http://www.scopus.com/inward/record.url?scp=0034126669&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034126669&partnerID=8YFLogxK

U2 - 10.1165/ajrcmb.22.6.3806

DO - 10.1165/ajrcmb.22.6.3806

M3 - Article

C2 - 10837367

AN - SCOPUS:0034126669

VL - 22

SP - 702

EP - 707

JO - American Journal of Respiratory Cell and Molecular Biology

JF - American Journal of Respiratory Cell and Molecular Biology

SN - 1044-1549

IS - 6

ER -