| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2019-04-10 |
| タイトル |
|
|
タイトル |
Involvement of β-arrestin in Endothelin Receptor Signaling : a Possible Role in the Pathogenesis of Pulmonary Arterial Hypertension |
| 言語 |
|
|
言語 |
eng |
| キーワード |
|
|
主題Scheme |
Other |
|
主題 |
Endothelin |
| キーワード |
|
|
主題Scheme |
Other |
|
主題 |
β-arrestin |
| キーワード |
|
|
主題Scheme |
Other |
|
主題 |
G-protein coupled receptor |
| キーワード |
|
|
主題Scheme |
Other |
|
主題 |
Pulmonary arterial hypertension |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 著者 |
Narita, Noritomo
Hanada, Kenji
Senoo, Maiko
Kato, Tomo
Kudo, Natsumi
Yokono, Yoshikazu
Tsushima, Michiko
Toyama, Yuichi
Narita, Masato
Tomita, Hirofumi
|
| 著者所属 |
|
|
値 |
Department of Cardiology, Hirosaki University Graduate School of Medicine, |
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Background: Endothelin （ET） is a strong vasoconstrictor that plays important roles in the pathogenesis and progression of cardiovascular remodeling. ET receptor（ ET-R） antagonists have recently become established as a drug essential for treating pulmonary arterial hypertension（ PAH）. β-arrestin was originally identified as a regulator of G-protein coupled receptor recycling, but it recently became apparent that β-arrestins act as scaffolds in their own signaling pathway. In this study, we examined the role of β-arrestin in ET-R signaling and explored its possible role in the pathogenesis of PAH.
Methods and Results: The knockdown of β-arrestin1 or β-arrestin2 in human kidney embryonic 293 cells resulted in nhanced extracellular signal-regulated kinase （ERK） 1/2 phosphorylation in response to ET. Confocal microscopy showed that, in the absence of stimulation, transiently transfected green fluorescent protein-tagged epidermal growth factor receptors（ EGFRs） were located on the plasma membrane, whereas they were internalized in response to ET, as shown by their redistribution into cellular aggregates. Pretreatment with Ro318425（ a protein kinase C inhibitor） or AG1478（ an EGFR antagonist） suppressed ERK1/2 phosphorylation in response to ET.
Conclusions: β-arrestins and EGFR transactivation are involved in ET-R signaling. These new insights may contribute to elucidating further layers in the pathogenesis of PAH. |
| 書誌情報 |
弘前医学
巻 69,
号 1-4,
p. 146-154,
発行日 2019-03-15
|
| ISSN |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
0439-1721 |
| 書誌レコードID |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AN00211444 |
| 著者版フラグ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 日本十進分類法 |
|
|
主題Scheme |
NDC |
|
主題 |
490 |
| 出版者 |
|
|
出版者 |
弘前大学大学院医学研究科・弘前医学会 |
HirosakiMedJ_69(1-4)_146.pdf (440.5 kB)
