RNA interference for discoidin domain receptor 2 attenuates neointimal formation in balloon injured rat carotid artery

Kou-Gi Shyu, Bao Wei Wang, Peiliang Kuan, Hang Chang

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Objectives - Discoidin domain receptor 2 (DDR2) plays potential roles in the regulation of collagen turnover mediated by smooth muscle cells (SMCs) in atherosclerosis. Little is known about the function of DDR2 in vascular system. We investigated whether inhibition of DDR2 by small interfering RNA (siRNA) can reduce neointimal formation after arterial injury. Methods and Results - SMCs from thoracic aorta of adult Wistar rats were cultured. The carotid artery from adult Wistar rats was injured by balloon catheter. DDR2 significantly increased migration and proliferation of SMCs. DDR2 siRNA inhibited 86% of DDR2 protein expression in cultured SMCs. DDR2 protein and mRNA expression significantly increased at 14 days after carotid injury. DDR2 siRNA significantly reduced DDR2 protein and mRNA expression induced by balloon injury. The immunohistochemical stain demonstrated that DDR2 siRNA decreased MMP2 protein labeling induced by balloon injury, a pattern similar to that of DDR2 protein labeling. Neointimal area was significantly increased after carotid injury and was significantly reduced by DDR2 siRNA. Conclusions - DDR2 increases migration and proliferation of SMCs, and expression of DDR2 in carotid artery significantly increases after injury. DDR2 siRNA attenuates neointimal formation after carotid injury. DDR2 may play a pivotal role in the pathogenesis of neointimal thickening after mechanical injury.

Original languageEnglish
Pages (from-to)1447-1453
Number of pages7
JournalArteriosclerosis, Thrombosis, and Vascular Biology
Volume28
Issue number8
DOIs
Publication statusPublished - Aug 2008

Fingerprint

RNA Interference
Carotid Arteries
Small Interfering RNA
Smooth Muscle Myocytes
Wounds and Injuries
Discoidin Domain Receptor 2
Proteins
Wistar Rats
Messenger RNA
Thoracic Aorta
Blood Vessels
Atherosclerosis

Keywords

  • Discoidin domain receptor 2
  • RNA interference
  • Smooth muscle cell
  • Vascular injury

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

RNA interference for discoidin domain receptor 2 attenuates neointimal formation in balloon injured rat carotid artery. / Shyu, Kou-Gi; Wang, Bao Wei; Kuan, Peiliang; Chang, Hang.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 28, No. 8, 08.2008, p. 1447-1453.

Research output: Contribution to journalArticle

@article{fcb7ea8e96594badaeb164c05dbf9948,
title = "RNA interference for discoidin domain receptor 2 attenuates neointimal formation in balloon injured rat carotid artery",
abstract = "Objectives - Discoidin domain receptor 2 (DDR2) plays potential roles in the regulation of collagen turnover mediated by smooth muscle cells (SMCs) in atherosclerosis. Little is known about the function of DDR2 in vascular system. We investigated whether inhibition of DDR2 by small interfering RNA (siRNA) can reduce neointimal formation after arterial injury. Methods and Results - SMCs from thoracic aorta of adult Wistar rats were cultured. The carotid artery from adult Wistar rats was injured by balloon catheter. DDR2 significantly increased migration and proliferation of SMCs. DDR2 siRNA inhibited 86{\%} of DDR2 protein expression in cultured SMCs. DDR2 protein and mRNA expression significantly increased at 14 days after carotid injury. DDR2 siRNA significantly reduced DDR2 protein and mRNA expression induced by balloon injury. The immunohistochemical stain demonstrated that DDR2 siRNA decreased MMP2 protein labeling induced by balloon injury, a pattern similar to that of DDR2 protein labeling. Neointimal area was significantly increased after carotid injury and was significantly reduced by DDR2 siRNA. Conclusions - DDR2 increases migration and proliferation of SMCs, and expression of DDR2 in carotid artery significantly increases after injury. DDR2 siRNA attenuates neointimal formation after carotid injury. DDR2 may play a pivotal role in the pathogenesis of neointimal thickening after mechanical injury.",
keywords = "Discoidin domain receptor 2, RNA interference, Smooth muscle cell, Vascular injury",
author = "Kou-Gi Shyu and Wang, {Bao Wei} and Peiliang Kuan and Hang Chang",
year = "2008",
month = "8",
doi = "10.1161/ATVBAHA.108.165993",
language = "English",
volume = "28",
pages = "1447--1453",
journal = "Arteriosclerosis, Thrombosis, and Vascular Biology",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",
number = "8",

}

TY - JOUR

T1 - RNA interference for discoidin domain receptor 2 attenuates neointimal formation in balloon injured rat carotid artery

AU - Shyu, Kou-Gi

AU - Wang, Bao Wei

AU - Kuan, Peiliang

AU - Chang, Hang

PY - 2008/8

Y1 - 2008/8

N2 - Objectives - Discoidin domain receptor 2 (DDR2) plays potential roles in the regulation of collagen turnover mediated by smooth muscle cells (SMCs) in atherosclerosis. Little is known about the function of DDR2 in vascular system. We investigated whether inhibition of DDR2 by small interfering RNA (siRNA) can reduce neointimal formation after arterial injury. Methods and Results - SMCs from thoracic aorta of adult Wistar rats were cultured. The carotid artery from adult Wistar rats was injured by balloon catheter. DDR2 significantly increased migration and proliferation of SMCs. DDR2 siRNA inhibited 86% of DDR2 protein expression in cultured SMCs. DDR2 protein and mRNA expression significantly increased at 14 days after carotid injury. DDR2 siRNA significantly reduced DDR2 protein and mRNA expression induced by balloon injury. The immunohistochemical stain demonstrated that DDR2 siRNA decreased MMP2 protein labeling induced by balloon injury, a pattern similar to that of DDR2 protein labeling. Neointimal area was significantly increased after carotid injury and was significantly reduced by DDR2 siRNA. Conclusions - DDR2 increases migration and proliferation of SMCs, and expression of DDR2 in carotid artery significantly increases after injury. DDR2 siRNA attenuates neointimal formation after carotid injury. DDR2 may play a pivotal role in the pathogenesis of neointimal thickening after mechanical injury.

AB - Objectives - Discoidin domain receptor 2 (DDR2) plays potential roles in the regulation of collagen turnover mediated by smooth muscle cells (SMCs) in atherosclerosis. Little is known about the function of DDR2 in vascular system. We investigated whether inhibition of DDR2 by small interfering RNA (siRNA) can reduce neointimal formation after arterial injury. Methods and Results - SMCs from thoracic aorta of adult Wistar rats were cultured. The carotid artery from adult Wistar rats was injured by balloon catheter. DDR2 significantly increased migration and proliferation of SMCs. DDR2 siRNA inhibited 86% of DDR2 protein expression in cultured SMCs. DDR2 protein and mRNA expression significantly increased at 14 days after carotid injury. DDR2 siRNA significantly reduced DDR2 protein and mRNA expression induced by balloon injury. The immunohistochemical stain demonstrated that DDR2 siRNA decreased MMP2 protein labeling induced by balloon injury, a pattern similar to that of DDR2 protein labeling. Neointimal area was significantly increased after carotid injury and was significantly reduced by DDR2 siRNA. Conclusions - DDR2 increases migration and proliferation of SMCs, and expression of DDR2 in carotid artery significantly increases after injury. DDR2 siRNA attenuates neointimal formation after carotid injury. DDR2 may play a pivotal role in the pathogenesis of neointimal thickening after mechanical injury.

KW - Discoidin domain receptor 2

KW - RNA interference

KW - Smooth muscle cell

KW - Vascular injury

UR - http://www.scopus.com/inward/record.url?scp=49449110219&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=49449110219&partnerID=8YFLogxK

U2 - 10.1161/ATVBAHA.108.165993

DO - 10.1161/ATVBAHA.108.165993

M3 - Article

VL - 28

SP - 1447

EP - 1453

JO - Arteriosclerosis, Thrombosis, and Vascular Biology

JF - Arteriosclerosis, Thrombosis, and Vascular Biology

SN - 1079-5642

IS - 8

ER -