モリヤ タクヤ   Takuya Moriya
  森谷 卓也
   所属   川崎医科大学  医学部
   職種   学長付特任教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Pathological Study on the Expression of Vasohibins in Peripheral Artery Disease.
掲載誌名 正式名:The Tohoku journal of experimental medicine
略  称:Tohoku J Exp Med
ISSNコード:13493329/00408727
掲載区分国外
巻・号・頁 258(2),pp.121-128
著者・共著者 Ryutaro Isoda, Ichiro Morita, Atsuhisa Ishida, Yuka Mikami, Yasumasa Monobe, Yasufumi Sato, Takuya Moriya
発行年月 2022/09
概要 Vasohibin-2 (VASH2) is a gene that promotes local angiogenesis. The tubulin carboxypeptidase activity of vasohibin causes detyrosination of alpha-tubulin and may play an important role in the regulation of various phenomena. Pathological and therapeutic angiogenesis are involved in atherosclerotic lesions. This study aimed to investigate whether the expression of VASH2 is associated with peripheral artery disease (PAD) in relation to angiogenesis, tubulin detyrosination, and severity of atherosclerotic lesions. An analysis of femoral and tibial arteries obtained from 86 patients with PAD or abdominal aortic aneurysm (AAA) was performed. The expressions of cluster of differentiation 31, VASH1, VASH2, and detyrosinated alpha-tubulin (DT-tubulin) were examined by immunohistochemistry, and their association with PAD was analyzed. The counts of VASH2 in the tunica media and adventitia in the tibial artery were significantly higher than those in the femoral artery in the PAD (P = 0.005 and P = 0.008, respectively) and AAA (P = 0.002 and P < 0.001, respectively) groups. In the tunica media and adventitia, VASH2 was significantly correlated with DT-tubulin. There was no significant difference in the expression of VASH2 and DT-tubulin in medial smooth muscle cells (McNemar test, P > 0.999). This study revealed the possible involvements of VASH2 in atherosclerosis by two methods-one maybe related to the progression of atherosclerosis by inducing angiogenesis and the second may be related to the decrease in arterial elasticity by increasing DT-tubulin in medial smooth muscle cells.
DOI 10.1620/tjem.2022.J063
PMID 35922907