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マツウラ カツヒサ
Matsuura Katsuhisa
松浦 勝久 所属 医学部 医学科 職種 教授・基幹分野長 |
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| 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,pp.27-33 |
| 著者・共著者 | SAKAMOTO Satoru†, MATSUURA Katsuhisa*, MASUDA Shinako, HAGIWARA Nobuhisa, SHIMIZU Tatsuya |
| 担当区分 | 2nd著者,責任著者 |
| 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 |