Intimal hyperplasia in loop-injured carotid arteries is attenuated in transglutaminase 2-null mice.
Intimal hyperplasia in loop-injured carotid arteries is attenuated in transglutaminase 2-null mice.
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DOI：
10.3346/jkms.2014.29.3.363
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发表时间：
2014-03
影响因子：
4.5
通讯作者：
Kim IG
中科院分区：
文献类型：
--
作者：
Min SK;Min SI;Jeong EM;Cho SY;Ha J;Kim SJ;Kim IG
开放性或血管内手术后由于内膜增生经常发生动脉再狭窄。由于已知组织转氨酶（TG 2）参与纤维化、伤口愈合和细胞外基质重塑，我们使用TG 2缺失小鼠研究了TG 2在内膜增生过程中的作用。通过两种不同的损伤模型：颈动脉结扎和颈动脉环损伤，比较TG 2-null和野生型（C57 BL/6）小鼠之间的新生内膜形成。结扎模型中，两组内膜厚度无差异。在袢损伤模型中，两组均出现内膜增生，TG 2基因敲除小鼠的内膜/中膜面积比显著降低（P = 0.007）。2周时新生内膜细胞TG 2强染色。与未损伤的动脉相比，损伤动脉中TG 2的原位活性稳步增加，直到4周。总之，在TG 2基因敲除小鼠中内膜增生显著减少，表明TG 2在内膜增生的发展中具有重要作用。提示TG 2可能成为预防血管术后再狭窄的新靶点。
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.