Regulation of α7-integrin expression in vascular smooth muscle by injury-induced atherosclerosis

Jun Tzu Chao, Gerald A. Meininger, Jan L. Patterson, Sarah A L Jones, Charles R. Partridge, Jessemy D. Neiger, E. Spencer Williams, Stephen J. Kaufman, Kenneth Ramos, Emily Wilson

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Injury of vascular smooth muscle cells (VSMCs) by allylamine (AAM) leads to phenotypic changes associated with atherogenic progression including increased proliferation, migration, and alterations in cell adhesion. In the present study, the relationship between AAM-induced vascular injury and expression of the α7-integrin subunit was investigated. The α7-mRNA and protein expression were examined using real-time RT-PCR, fluorescence-activated cell sorting analysis (FACS), immunohistochemistry, and immunoblotting. In cultured VSMCs from aortas of AAM-treated rats (70 mg/kg for 20 days), α7-mRNA levels were increased more than twofold compared with control cells. No change was seen in β1-integrin expression. FACS analysis revealed increased cell surface expression of α7-protein (25 ± 9%; *P < 0.05). AAM treatment of naive VSMCs enhanced α7-mRNA expression (2.4 ± 0.7-fold, mean ± SE; *P < 0.05). The increased α7-mRNA expression was attenuated by the amine oxidase inhibitor semicarbazide and the antioxidant pyrrolidine dithiocarbamate, which confirms a role for oxidative stress in modulating α7- expression. In vivo α7-mRNA and protein expression were enhanced in the aortas of AAM-treated rats. In addition, increased α7-integrin expression facilitated AAM VSMC adhesion to laminin more efficiently compared with control (51 ± 2%; *P < 0.05). Chemical injury induced by AAM significantly enhances α7- integrin expression in VSMCs. These findings implicate for the first time the expression of α7-integrin during the response of VSMCs to vascular injury.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume287
Issue number1 56-1
DOIs
StatePublished - Jul 2004
Externally publishedYes

Fingerprint

Allylamine
Vascular Smooth Muscle
Integrins
Atherosclerosis
Smooth Muscle Myocytes
Wounds and Injuries
Messenger RNA
Vascular System Injuries
Cell Adhesion
Aorta
Flow Cytometry
Proteins
Laminin
Immunoblotting
Amines
Real-Time Polymerase Chain Reaction
Oxidoreductases
Oxidative Stress
Antioxidants
Immunohistochemistry

Keywords

  • Aorta
  • Cell adhesion
  • Laminin
  • Vascular injury

ASJC Scopus subject areas

  • Physiology

Cite this

Chao, J. T., Meininger, G. A., Patterson, J. L., Jones, S. A. L., Partridge, C. R., Neiger, J. D., ... Wilson, E. (2004). Regulation of α7-integrin expression in vascular smooth muscle by injury-induced atherosclerosis. American Journal of Physiology - Heart and Circulatory Physiology, 287(1 56-1). https://doi.org/10.1152/ajpheart.00939.2003

Regulation of α7-integrin expression in vascular smooth muscle by injury-induced atherosclerosis. / Chao, Jun Tzu; Meininger, Gerald A.; Patterson, Jan L.; Jones, Sarah A L; Partridge, Charles R.; Neiger, Jessemy D.; Williams, E. Spencer; Kaufman, Stephen J.; Ramos, Kenneth; Wilson, Emily.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 287, No. 1 56-1, 07.2004.

Research output: Contribution to journalArticle

Chao, JT, Meininger, GA, Patterson, JL, Jones, SAL, Partridge, CR, Neiger, JD, Williams, ES, Kaufman, SJ, Ramos, K & Wilson, E 2004, 'Regulation of α7-integrin expression in vascular smooth muscle by injury-induced atherosclerosis', American Journal of Physiology - Heart and Circulatory Physiology, vol. 287, no. 1 56-1. https://doi.org/10.1152/ajpheart.00939.2003
Chao, Jun Tzu ; Meininger, Gerald A. ; Patterson, Jan L. ; Jones, Sarah A L ; Partridge, Charles R. ; Neiger, Jessemy D. ; Williams, E. Spencer ; Kaufman, Stephen J. ; Ramos, Kenneth ; Wilson, Emily. / Regulation of α7-integrin expression in vascular smooth muscle by injury-induced atherosclerosis. In: American Journal of Physiology - Heart and Circulatory Physiology. 2004 ; Vol. 287, No. 1 56-1.
@article{ccfb0e06b44a4cc19a9324c482dd15ba,
title = "Regulation of α7-integrin expression in vascular smooth muscle by injury-induced atherosclerosis",
abstract = "Injury of vascular smooth muscle cells (VSMCs) by allylamine (AAM) leads to phenotypic changes associated with atherogenic progression including increased proliferation, migration, and alterations in cell adhesion. In the present study, the relationship between AAM-induced vascular injury and expression of the α7-integrin subunit was investigated. The α7-mRNA and protein expression were examined using real-time RT-PCR, fluorescence-activated cell sorting analysis (FACS), immunohistochemistry, and immunoblotting. In cultured VSMCs from aortas of AAM-treated rats (70 mg/kg for 20 days), α7-mRNA levels were increased more than twofold compared with control cells. No change was seen in β1-integrin expression. FACS analysis revealed increased cell surface expression of α7-protein (25 ± 9{\%}; *P < 0.05). AAM treatment of naive VSMCs enhanced α7-mRNA expression (2.4 ± 0.7-fold, mean ± SE; *P < 0.05). The increased α7-mRNA expression was attenuated by the amine oxidase inhibitor semicarbazide and the antioxidant pyrrolidine dithiocarbamate, which confirms a role for oxidative stress in modulating α7- expression. In vivo α7-mRNA and protein expression were enhanced in the aortas of AAM-treated rats. In addition, increased α7-integrin expression facilitated AAM VSMC adhesion to laminin more efficiently compared with control (51 ± 2{\%}; *P < 0.05). Chemical injury induced by AAM significantly enhances α7- integrin expression in VSMCs. These findings implicate for the first time the expression of α7-integrin during the response of VSMCs to vascular injury.",
keywords = "Aorta, Cell adhesion, Laminin, Vascular injury",
author = "Chao, {Jun Tzu} and Meininger, {Gerald A.} and Patterson, {Jan L.} and Jones, {Sarah A L} and Partridge, {Charles R.} and Neiger, {Jessemy D.} and Williams, {E. Spencer} and Kaufman, {Stephen J.} and Kenneth Ramos and Emily Wilson",
year = "2004",
month = "7",
doi = "10.1152/ajpheart.00939.2003",
language = "English (US)",
volume = "287",
journal = "American Journal of Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "1 56-1",

}

TY - JOUR

T1 - Regulation of α7-integrin expression in vascular smooth muscle by injury-induced atherosclerosis

AU - Chao, Jun Tzu

AU - Meininger, Gerald A.

AU - Patterson, Jan L.

AU - Jones, Sarah A L

AU - Partridge, Charles R.

AU - Neiger, Jessemy D.

AU - Williams, E. Spencer

AU - Kaufman, Stephen J.

AU - Ramos, Kenneth

AU - Wilson, Emily

PY - 2004/7

Y1 - 2004/7

N2 - Injury of vascular smooth muscle cells (VSMCs) by allylamine (AAM) leads to phenotypic changes associated with atherogenic progression including increased proliferation, migration, and alterations in cell adhesion. In the present study, the relationship between AAM-induced vascular injury and expression of the α7-integrin subunit was investigated. The α7-mRNA and protein expression were examined using real-time RT-PCR, fluorescence-activated cell sorting analysis (FACS), immunohistochemistry, and immunoblotting. In cultured VSMCs from aortas of AAM-treated rats (70 mg/kg for 20 days), α7-mRNA levels were increased more than twofold compared with control cells. No change was seen in β1-integrin expression. FACS analysis revealed increased cell surface expression of α7-protein (25 ± 9%; *P < 0.05). AAM treatment of naive VSMCs enhanced α7-mRNA expression (2.4 ± 0.7-fold, mean ± SE; *P < 0.05). The increased α7-mRNA expression was attenuated by the amine oxidase inhibitor semicarbazide and the antioxidant pyrrolidine dithiocarbamate, which confirms a role for oxidative stress in modulating α7- expression. In vivo α7-mRNA and protein expression were enhanced in the aortas of AAM-treated rats. In addition, increased α7-integrin expression facilitated AAM VSMC adhesion to laminin more efficiently compared with control (51 ± 2%; *P < 0.05). Chemical injury induced by AAM significantly enhances α7- integrin expression in VSMCs. These findings implicate for the first time the expression of α7-integrin during the response of VSMCs to vascular injury.

AB - Injury of vascular smooth muscle cells (VSMCs) by allylamine (AAM) leads to phenotypic changes associated with atherogenic progression including increased proliferation, migration, and alterations in cell adhesion. In the present study, the relationship between AAM-induced vascular injury and expression of the α7-integrin subunit was investigated. The α7-mRNA and protein expression were examined using real-time RT-PCR, fluorescence-activated cell sorting analysis (FACS), immunohistochemistry, and immunoblotting. In cultured VSMCs from aortas of AAM-treated rats (70 mg/kg for 20 days), α7-mRNA levels were increased more than twofold compared with control cells. No change was seen in β1-integrin expression. FACS analysis revealed increased cell surface expression of α7-protein (25 ± 9%; *P < 0.05). AAM treatment of naive VSMCs enhanced α7-mRNA expression (2.4 ± 0.7-fold, mean ± SE; *P < 0.05). The increased α7-mRNA expression was attenuated by the amine oxidase inhibitor semicarbazide and the antioxidant pyrrolidine dithiocarbamate, which confirms a role for oxidative stress in modulating α7- expression. In vivo α7-mRNA and protein expression were enhanced in the aortas of AAM-treated rats. In addition, increased α7-integrin expression facilitated AAM VSMC adhesion to laminin more efficiently compared with control (51 ± 2%; *P < 0.05). Chemical injury induced by AAM significantly enhances α7- integrin expression in VSMCs. These findings implicate for the first time the expression of α7-integrin during the response of VSMCs to vascular injury.

KW - Aorta

KW - Cell adhesion

KW - Laminin

KW - Vascular injury

UR - http://www.scopus.com/inward/record.url?scp=3042523734&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=3042523734&partnerID=8YFLogxK

U2 - 10.1152/ajpheart.00939.2003

DO - 10.1152/ajpheart.00939.2003

M3 - Article

C2 - 14988073

AN - SCOPUS:3042523734

VL - 287

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6143

IS - 1 56-1

ER -