マツウラ カツヒサ   MATSUURA Katsuhisa
  松浦 勝久
   所属   研究施設 研究施設
   職種   准教授
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Heart-derived fibroblasts express LYPD-1 and negatively regulate angiogenesis in rat
掲載誌名 正式名:Regenerative Therapy
略  称:Regen Ther
ISSNコード:23523204
掲載区分国外
出版社 Science Direct
巻・号・頁 15,27-33頁
著者・共著者 SAKAMOTO Satoru†, MATSUURA Katsuhisa*, MASUDA Shinako, HAGIWARA Nobuhisa, SHIMIZU Tatsuya
発行年月 2020/12
概要 Abstract
Angiogenesis is regulated by a balance between promoting and inhibitory mechanisms. Although angiogenesis-promoting mechanisms have been well studied in ischemic heart diseases, angiogenesis-inhibitory mechanisms have not. Recently, we identified LYPD-1 as a novel anti-angiogenic factor derived from human heart-derived fibroblasts, which suppresses endothelial cell network formation in co-culture. However, it remains unclear whether the low angiogenicity of heart-derived fibroblasts with high expression of LYPD-1 is also observed in other mammalian species, and the properties of LYPD-1 under normal and pathological conditions remain elusive. Fibroblasts isolated from neonatal and adult rat heart also express LYPD-1 and inhibit endothelial network formation in co-culture. Moreover, immunohistochemical analysis revealed that LYPD-1 was predominantly observed in the interstitial tissues of rat heart and LYPD1 expression levels were identical from late developmental period to adult. Conversely, LYPD-1 mRNA expression was significantly downregulated temporally in myocardial infarction model rats, suggesting that angiogenesis-inhibitory mechanisms might not be sufficiently suppressed to promote angiogenesis in ischemic heart diseases. These findings suggest that heart has relatively low angiogenicity compared with other organs via the high expression of LYPD-1 by fibroblasts. Moreover, understanding the regulatory mechanisms of LYPD-1-mediated inhibition of angiogenesis might lead a novel angiogenic therapy for ischemic heart diseases and contribute to development of bioengineered cardiac tissue.
DOI 10.1016/j.reth.2020.03.010
PMID 32514414