CCN family member 1 deregulates cholesterol metabolism and aggravates atherosclerosis

2018 ◽  
Vol 225 (3) ◽  
Author(s):  
Jin‐Feng Zhao ◽  
Hsiang‐Ying Chen ◽  
Jeng Wei ◽  
Shr‐Jeng Jim Leu ◽  
Tzong‐Shyuan Lee
2009 ◽  
Vol 3 (2) ◽  
pp. 105-113 ◽  
Author(s):  
Yukio Nakamura ◽  
Yajun Cui ◽  
Carol Fernando ◽  
Wendy E. Kutz ◽  
Matthew L. Warman

2020 ◽  
Vol 40 (1) ◽  
Author(s):  
Yoshitaka Kase ◽  
Hideyuki Okano

Abstract It has been reported that coronavirus disease 2019 (COVID-19) causes not only pneumonia but also systemic inflammations including central nervous system (CNS) disorders. However, little is known about the mechanism that triggers the COVID-19-associated CNS disorders, due to the lack of appropriate experimental systems. Our present study showed that angiotensin-converting enzyme-2 (ACE2), a cellular receptor for SARS-CoV-2, is expressed in human induced pluripotent stem cell (iPSC)-derived neural stem/progenitor cells (hiPSC-NS/PCs) and young neurons. Furthermore, together with database analysis, we found that a viral virulent factor CCN family member 1 (CCN1), which is known to be induced by SARS-CoV-2 infection, is expressed in these cells at basal levels. Considering the role of CCN1 which is known to be involved in viral toxicity and inflammation, hiPSC-NS/PCs could provide an excellent model for COVID-19-associated CNS disorders from the aspect of SARS-CoV-2 infection-ACE2-CCN1 axis. In addition, we identified compounds that reduce CCN1 expression. Collectively, our study using hiPSC-NS/PCs may aid in the development of a therapeutic target for COVID-19-related CNS disorders.


2003 ◽  
Vol 201 (4) ◽  
pp. 609-615 ◽  
Author(s):  
Chunying Yu ◽  
Anh-Thy Le ◽  
Herman Yeger ◽  
Bernard Perbal ◽  
Benjamin A Alman

Author(s):  
Thabo Mahendiran ◽  
Roland Klingenberg ◽  
David Nanchen ◽  
Baris Gencer ◽  
David Meier ◽  
...  

2007 ◽  
Vol 117 (10) ◽  
pp. 3075-3086 ◽  
Author(s):  
Yukio Nakamura ◽  
Gilbert Weidinger ◽  
Jennifer O. Liang ◽  
Allisan Aquilina-Beck ◽  
Keiko Tamai ◽  
...  

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