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Updated: Jun 27, 2026

Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery
Published on: December 23, 2014
Role of Rho-associated kinase in neointima formation after vascular injury
1Internal Medicine III and Cardiovascular Research Institute, Kurume University School of Medicine, Kurume, Japan.
Background:
The Rho/Rho-associated kinase (Rho-kinase) system is implicated in various cellular functions, including migration, proliferation, and apoptosis. Because a possible role of the system is suggested in neointima formation after vascular injury, we sought to examine whether a new specific Rho-kinase inhibitor, Y27632, prevents neointima formation of the balloon-injured rat carotid artery, and if so, to investigate the effects of Y27632 on migration, proliferation, and apoptosis of smooth muscle cells (SMCs) in the injured artery.
Methods And Results:
Y27632 was administered intraperitoneally from 1 day before to 14 days after vascular injury. Treatment with Y27632 inhibited phenylephrine-induced Rho-kinase activation in the carotid artery on the basis of immunoblotting against the phosphorylated myosin-binding subunit of myosin phosphatase. Y27632 markedly prevented neointima formation at days 7 and 14. In controls, BrdU(+) proliferating and TUNEL(+) apoptotic SMCs were transiently and coincidentally increased in the neointima, with a peak at day 7. Y27632 significantly increased the neointimal TUNEL(+) SMCs at days 7 and 14, but not BrdU(+) SMCs. Y27642 significantly decreased the number of intimal SMCs at day 4, while not affecting the number of BrdU(+) or TUNEL(+) SMCs. Reendothelialization after balloon injury was not significantly affected by Y27632 at days 7 and 14.
Conclusions:
Y27632 inhibited neointima formation by enhancing SMC apoptosis and probably by suppressing early SMC migration. Therefore, a role of Rho-kinase is suggested in neointima formation after vascular injury.
Insights
The Rho-kinase inhibitor Y27632 effectively prevents neointima formation after vascular injury in rats. It works by increasing smooth muscle cell apoptosis and potentially reducing migration, highlighting Rho-kinase
Area of Science:
- Vascular Biology
- Cell Signaling
- Pharmacology
Background:
- The Rho/Rho-associated kinase (Rho-kinase) system regulates cellular functions like migration, proliferation, and apoptosis.
- This system is potentially involved in neointima formation following vascular injury.
Purpose of the Study:
- To investigate if the Rho-kinase inhibitor Y27632 prevents neointima formation in balloon-injured rat carotid arteries.
- To determine the effects of Y27632 on smooth muscle cell (SMC) migration, proliferation, and apoptosis in injured arteries.
Main Methods:
- Rats received Y27632 intraperitoneally before and after balloon injury.
- Rho-kinase activation was assessed via immunoblotting.
- Neointima formation, SMC proliferation (BrdU+), apoptosis (TUNEL+), and reendothelialization were evaluated at various time points.
Main Results:
- Y27632 treatment significantly inhibited neointima formation at 7 and 14 days post-injury.
- The inhibitor increased SMC apoptosis (TUNEL+) but did not affect proliferation (BrdU+).
- Y27632 also appeared to suppress early SMC migration and did not impact reendothelialization.
Conclusions:
- Y27632 inhibits neointima formation by promoting SMC apoptosis and suppressing migration.
- These findings suggest a significant role for Rho-kinase in the development of neointima after vascular injury.
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