Cell-matrix and cell-cell interactions modulate apoptosis of bronchial epithelial cells

Kazutetsu Aoshiba, Stephen I. Rennard, John R. Spurzem

Research output: Contribution to journalArticle

83 Citations (Scopus)

Abstract

Apoptosis is an important process maintaining cell number and tissue structure. To determine whether cell-extracellular matrix (ECM) and cell- cell interactions modulate apoptosis in bronchial epithelium, we cultured human bronchial epithelial cells in different conditions and evaluated the cells for apoptosis. We found that plating cells in conditions that prevent cell-ECM adhesion induced apoptosis. Plating cells on type I collagen, fibronectin, and biosynthesized matrix prevented apoptosis, due at least in part to integrin-mediated adhesion. When cells were cultured at high density but under conditions preventing cell-substratum adhesion, aggregation occurred. Apoptosis was inversely correlated with aggregation. Cell-cell adhesion in these conditions was mediated at least partly by integrins containing α(y). Cell aggregation was not associated with activation of a signaling pathway that is usually activated by cell-ECM adhesion, phosphorylation of focal adhesion kinase, but was associated with Bcl-2 protein expression, consistent with the concept that Bcl-2 protects against apoptosis. We conclude that both cell-ECM and cell-cell interactions, likely mediated in part by integrins, modulate apoptosis in bronchial epithelium.

Original languageEnglish (US)
Pages (from-to)L28-L37
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume272
Issue number1 16-1
StatePublished - Jan 1 1997

Fingerprint

Cell Communication
Epithelial Cells
Apoptosis
Extracellular Matrix
Integrins
Cell-Matrix Junctions
Cell Adhesion
Epithelium
Focal Adhesion Protein-Tyrosine Kinases
Cell Aggregation
Collagen Type I
Fibronectins
Cultured Cells
Cell Count
Phosphorylation
Proteins

Keywords

  • cell-cell adhesion
  • extracellular matrix
  • integrins
  • lung

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

Cite this

Cell-matrix and cell-cell interactions modulate apoptosis of bronchial epithelial cells. / Aoshiba, Kazutetsu; Rennard, Stephen I.; Spurzem, John R.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 272, No. 1 16-1, 01.01.1997, p. L28-L37.

Research output: Contribution to journalArticle

Aoshiba, Kazutetsu ; Rennard, Stephen I. ; Spurzem, John R. / Cell-matrix and cell-cell interactions modulate apoptosis of bronchial epithelial cells. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 1997 ; Vol. 272, No. 1 16-1. pp. L28-L37.
@article{5af5155c02c24b2480dead386598fc72,
title = "Cell-matrix and cell-cell interactions modulate apoptosis of bronchial epithelial cells",
abstract = "Apoptosis is an important process maintaining cell number and tissue structure. To determine whether cell-extracellular matrix (ECM) and cell- cell interactions modulate apoptosis in bronchial epithelium, we cultured human bronchial epithelial cells in different conditions and evaluated the cells for apoptosis. We found that plating cells in conditions that prevent cell-ECM adhesion induced apoptosis. Plating cells on type I collagen, fibronectin, and biosynthesized matrix prevented apoptosis, due at least in part to integrin-mediated adhesion. When cells were cultured at high density but under conditions preventing cell-substratum adhesion, aggregation occurred. Apoptosis was inversely correlated with aggregation. Cell-cell adhesion in these conditions was mediated at least partly by integrins containing α(y). Cell aggregation was not associated with activation of a signaling pathway that is usually activated by cell-ECM adhesion, phosphorylation of focal adhesion kinase, but was associated with Bcl-2 protein expression, consistent with the concept that Bcl-2 protects against apoptosis. We conclude that both cell-ECM and cell-cell interactions, likely mediated in part by integrins, modulate apoptosis in bronchial epithelium.",
keywords = "cell-cell adhesion, extracellular matrix, integrins, lung",
author = "Kazutetsu Aoshiba and Rennard, {Stephen I.} and Spurzem, {John R.}",
year = "1997",
month = "1",
day = "1",
language = "English (US)",
volume = "272",
pages = "L28--L37",
journal = "American Journal of Physiology - Renal Physiology",
issn = "0363-6127",
publisher = "American Physiological Society",
number = "1 16-1",

}

TY - JOUR

T1 - Cell-matrix and cell-cell interactions modulate apoptosis of bronchial epithelial cells

AU - Aoshiba, Kazutetsu

AU - Rennard, Stephen I.

AU - Spurzem, John R.

PY - 1997/1/1

Y1 - 1997/1/1

N2 - Apoptosis is an important process maintaining cell number and tissue structure. To determine whether cell-extracellular matrix (ECM) and cell- cell interactions modulate apoptosis in bronchial epithelium, we cultured human bronchial epithelial cells in different conditions and evaluated the cells for apoptosis. We found that plating cells in conditions that prevent cell-ECM adhesion induced apoptosis. Plating cells on type I collagen, fibronectin, and biosynthesized matrix prevented apoptosis, due at least in part to integrin-mediated adhesion. When cells were cultured at high density but under conditions preventing cell-substratum adhesion, aggregation occurred. Apoptosis was inversely correlated with aggregation. Cell-cell adhesion in these conditions was mediated at least partly by integrins containing α(y). Cell aggregation was not associated with activation of a signaling pathway that is usually activated by cell-ECM adhesion, phosphorylation of focal adhesion kinase, but was associated with Bcl-2 protein expression, consistent with the concept that Bcl-2 protects against apoptosis. We conclude that both cell-ECM and cell-cell interactions, likely mediated in part by integrins, modulate apoptosis in bronchial epithelium.

AB - Apoptosis is an important process maintaining cell number and tissue structure. To determine whether cell-extracellular matrix (ECM) and cell- cell interactions modulate apoptosis in bronchial epithelium, we cultured human bronchial epithelial cells in different conditions and evaluated the cells for apoptosis. We found that plating cells in conditions that prevent cell-ECM adhesion induced apoptosis. Plating cells on type I collagen, fibronectin, and biosynthesized matrix prevented apoptosis, due at least in part to integrin-mediated adhesion. When cells were cultured at high density but under conditions preventing cell-substratum adhesion, aggregation occurred. Apoptosis was inversely correlated with aggregation. Cell-cell adhesion in these conditions was mediated at least partly by integrins containing α(y). Cell aggregation was not associated with activation of a signaling pathway that is usually activated by cell-ECM adhesion, phosphorylation of focal adhesion kinase, but was associated with Bcl-2 protein expression, consistent with the concept that Bcl-2 protects against apoptosis. We conclude that both cell-ECM and cell-cell interactions, likely mediated in part by integrins, modulate apoptosis in bronchial epithelium.

KW - cell-cell adhesion

KW - extracellular matrix

KW - integrins

KW - lung

UR - http://www.scopus.com/inward/record.url?scp=0031034304&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031034304&partnerID=8YFLogxK

M3 - Article

C2 - 9038899

AN - SCOPUS:0031034304

VL - 272

SP - L28-L37

JO - American Journal of Physiology - Renal Physiology

JF - American Journal of Physiology - Renal Physiology

SN - 0363-6127

IS - 1 16-1

ER -