The change in phospholipase C-gamma1 expression following balloon injury to the rat carotid artery.
- Author:
Seong Hoon LIM
1
;
Young Sun HEO
;
Hak Jin KIM
;
Wang Soo LEE
;
Ji Hyun AHN
;
Young Bien SONG
;
Sang Wook KIM
;
Tae Ho KIM
;
Chee Jeong KIM
;
Wang Seong RYU
;
Un Ho RYOO
Author Information
1. Department of Internal Medicine, Chung-Ang University Hospital, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Phospholipase C;
Signal Transduction;
Carotid Arteries
- MeSH:
Angiotensin II;
Animals;
Axis, Cervical Vertebra;
Blotting, Western;
Carotid Arteries*;
Carotid Artery, Common;
DNA;
Humans;
Immunohistochemistry;
Inositol;
Male;
Neointima;
Phospholipases*;
Rats*;
Rats, Wistar;
Signal Transduction;
Type C Phospholipases;
Vascular System Injuries
- From:Korean Journal of Medicine
2001;60(3):234-241
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: While inositol phospholipid-specific phospholipase C (PLC) plays a central role in signal transduction pathways, little is known about its role in the vascular response to injury. Recent studies have shown that phospholipase C-gamma1 (PLC-gamma1) is required for PDGF-induced DNA synthesis and angiotensin II signaling. This study was undertaken to determine the potential involvement of PLC-gamma1 in the in vivo response to vascular injury. METHODS: Vascular injury was achieved in the left common carotid artery of six-month-old male Wistar rats. The expression of PLC-gamma1 was evaluated at serial time points by immunohistochemistry and Western blot analysis following balloon de-endothelialization of the rat carotid artery. RESULTS: In the denuded carotid artery at 1 week, the neointima became thicker in a symmetrical manner with respect to the long axis. A strong expression of PLC-gamma1 at one week after injury was seen primarily in the thin layers of neointima. This increased immunoreactivity of PLC-gamma1 persisted at 2-3 weeks after injury, coinciding with the time when neointima gains of its mass. At 4 weeks after injury, staining intensity slightly declined but levels remained elevated. As determined by Western blot analysis, the amount of PLC-gamma1 was about 3-fold higher at 3 weeks after injury compared to uninjured vessels (p<0.01). CONCLUSION: These results suggest that the amplification of traffic within signal transduction pathways involving PLC-gamma1 occurs and may play a significant role in neointima formation following arterial injury.
