Injury induces increase of von Willebrand factor in rat endothelial cells

M. A. Reidy, M. Chopek, S. Chao, T. McDonald, S. M. Schwartz

Research output: Contribution to journalArticle

58 Citations (Scopus)

Abstract

This study examined the effects of injury on the content of von Willebrand factor (vWF) in rat aortic endothelium. Endothelial cells from normal, endotoxin-treated, and balloon-injured rats were stained with vWF antibodies and visualized using a biotinylated secondary antibody and avidin-tagged peroxidase. Endotoxin treatment and balloon injury caused a threefold increase in intracellular vWF, and immunoelectron microscopy showed the endoplasmic reticulum to stain heavily by the vWF antibody. Weibel-Palade bodies were not observed in all the cell profiles examined. The basement membrane of the endothelialized vessels showed no vWF staining; however, after endothelial denudation this matrix was clearly stained by the antibody. These results suggest that endothelial injury leads to an increased intracellular content of vWF that is localized primarily in the endoplasmic reticulum.

Original languageEnglish (US)
Pages (from-to)857-864
Number of pages8
JournalAmerican Journal of Pathology
Volume134
Issue number4
StatePublished - Jan 1 1989

Fingerprint

von Willebrand Factor
Endothelial Cells
Wounds and Injuries
Antibodies
Endotoxins
Endoplasmic Reticulum
Weibel-Palade Bodies
Immunoelectron Microscopy
Avidin
Basement Membrane
Peroxidase
Endothelium
Coloring Agents
Staining and Labeling

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Reidy, M. A., Chopek, M., Chao, S., McDonald, T., & Schwartz, S. M. (1989). Injury induces increase of von Willebrand factor in rat endothelial cells. American Journal of Pathology, 134(4), 857-864.

Injury induces increase of von Willebrand factor in rat endothelial cells. / Reidy, M. A.; Chopek, M.; Chao, S.; McDonald, T.; Schwartz, S. M.

In: American Journal of Pathology, Vol. 134, No. 4, 01.01.1989, p. 857-864.

Research output: Contribution to journalArticle

Reidy, MA, Chopek, M, Chao, S, McDonald, T & Schwartz, SM 1989, 'Injury induces increase of von Willebrand factor in rat endothelial cells', American Journal of Pathology, vol. 134, no. 4, pp. 857-864.
Reidy, M. A. ; Chopek, M. ; Chao, S. ; McDonald, T. ; Schwartz, S. M. / Injury induces increase of von Willebrand factor in rat endothelial cells. In: American Journal of Pathology. 1989 ; Vol. 134, No. 4. pp. 857-864.
@article{7185f9251aee43db8e0d977480725981,
title = "Injury induces increase of von Willebrand factor in rat endothelial cells",
abstract = "This study examined the effects of injury on the content of von Willebrand factor (vWF) in rat aortic endothelium. Endothelial cells from normal, endotoxin-treated, and balloon-injured rats were stained with vWF antibodies and visualized using a biotinylated secondary antibody and avidin-tagged peroxidase. Endotoxin treatment and balloon injury caused a threefold increase in intracellular vWF, and immunoelectron microscopy showed the endoplasmic reticulum to stain heavily by the vWF antibody. Weibel-Palade bodies were not observed in all the cell profiles examined. The basement membrane of the endothelialized vessels showed no vWF staining; however, after endothelial denudation this matrix was clearly stained by the antibody. These results suggest that endothelial injury leads to an increased intracellular content of vWF that is localized primarily in the endoplasmic reticulum.",
author = "Reidy, {M. A.} and M. Chopek and S. Chao and T. McDonald and Schwartz, {S. M.}",
year = "1989",
month = "1",
day = "1",
language = "English (US)",
volume = "134",
pages = "857--864",
journal = "American Journal of Pathology",
issn = "0002-9440",
publisher = "Elsevier Inc.",
number = "4",

}

TY - JOUR

T1 - Injury induces increase of von Willebrand factor in rat endothelial cells

AU - Reidy, M. A.

AU - Chopek, M.

AU - Chao, S.

AU - McDonald, T.

AU - Schwartz, S. M.

PY - 1989/1/1

Y1 - 1989/1/1

N2 - This study examined the effects of injury on the content of von Willebrand factor (vWF) in rat aortic endothelium. Endothelial cells from normal, endotoxin-treated, and balloon-injured rats were stained with vWF antibodies and visualized using a biotinylated secondary antibody and avidin-tagged peroxidase. Endotoxin treatment and balloon injury caused a threefold increase in intracellular vWF, and immunoelectron microscopy showed the endoplasmic reticulum to stain heavily by the vWF antibody. Weibel-Palade bodies were not observed in all the cell profiles examined. The basement membrane of the endothelialized vessels showed no vWF staining; however, after endothelial denudation this matrix was clearly stained by the antibody. These results suggest that endothelial injury leads to an increased intracellular content of vWF that is localized primarily in the endoplasmic reticulum.

AB - This study examined the effects of injury on the content of von Willebrand factor (vWF) in rat aortic endothelium. Endothelial cells from normal, endotoxin-treated, and balloon-injured rats were stained with vWF antibodies and visualized using a biotinylated secondary antibody and avidin-tagged peroxidase. Endotoxin treatment and balloon injury caused a threefold increase in intracellular vWF, and immunoelectron microscopy showed the endoplasmic reticulum to stain heavily by the vWF antibody. Weibel-Palade bodies were not observed in all the cell profiles examined. The basement membrane of the endothelialized vessels showed no vWF staining; however, after endothelial denudation this matrix was clearly stained by the antibody. These results suggest that endothelial injury leads to an increased intracellular content of vWF that is localized primarily in the endoplasmic reticulum.

UR - http://www.scopus.com/inward/record.url?scp=0024566301&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024566301&partnerID=8YFLogxK

M3 - Article

C2 - 2650559

AN - SCOPUS:0024566301

VL - 134

SP - 857

EP - 864

JO - American Journal of Pathology

JF - American Journal of Pathology

SN - 0002-9440

IS - 4

ER -