Intimal Hyperplasia in Loop-Injured Carotid Arteries Is Attenuated in Transglutaminase 2-Null Mice.
10.3346/jkms.2014.29.3.363
- Author:
Seung Kee MIN
1
;
Sang Il MIN
;
Eui Man JEONG
;
Sung Yup CHO
;
Jongwon HA
;
Sang Joon KIM
;
In Gyu KIM
Author Information
1. Department of Surgery, Seoul National University College of Medicine, Seoul, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Tissue Transglutaminase;
Intimal Hyperplasia;
Carotid Artery Injury
- MeSH:
Animals;
Carotid Arteries/pathology/*surgery;
Disease Models, Animal;
GTP-Binding Proteins/deficiency/genetics/*metabolism;
Hyperplasia;
Mice;
Mice, Inbred C57BL;
Transglutaminases/deficiency/genetics/*metabolism;
Tunica Intima/*pathology
- From:Journal of Korean Medical Science
2014;29(3):363-369
- CountryRepublic of Korea
- Language:English
-
Abstract:
Arterial restenosis frequently develops after open or endovascular surgery due to intimal hyperplasia. Since tissue transglutaminase (TG2) is known to involve in fibrosis, wound healing, and extracellular matrix remodeling, we examined the role of TG2 in the process of intimal hyperplasia using TG2-null mice. The neointimal formation was compared between TG2-null and wild-type (C57BL/6) mice by two different injury models; carotid ligation and carotid loop injury. In ligation model, there was no difference in intimal thickness between two groups. In loop injury model, intimal hyperplasia developed in both groups and the intimal/medial area ratio was significantly reduced in TG2-null mice (P = 0.007). TG2 was intensely stained in neointimal cells in 2 weeks. In situ activity of TG2 in the injured arteries steadily increased until 4 weeks compared to uninjured arteries. Taken together, intimal hyperplasia was significantly reduced in TG2-null mice, indicating that TG2 has an important role in the development of intimal hyperplasia. This suggests that TG2 may be a novel target to prevent the arterial restenosis after vascular surgery.
