NOV (CCN3) regulation in the growth plate and CCN family member expression in cartilage neoplasia

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

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Huiyan Gan ◽  
Wenqian Xue ◽  
Ya Gao ◽  
Guixia Zhu ◽  
Danny Chan ◽  
...  

Abstract Background The growth plate is a special region of the cartilage that drives longitudinal growth of long bones. Proliferating chondrocytes in the growth plate, arranged in columns, divide perpendicular to the long axis of the growth plate then intercalate to re-align with parental columns. Which molecular partners maintain growth plate columnar structures and chondrocyte cytokinesis has not been fully revealed. It is reported that kinesin family member 3A (KIF3A), a subunit of kinesin-2, plays an important role in maintaining columnar organization in growth plates via controlling primary cilia formation and cell proliferation. Result Here we identify kinesin family member 5B (KIF5B), the heavy chain of kinesin-1, a ubiquitously expressed motor protein for anterograde intracellular transport along the microtubule network, as a key modulator of cytokinesis in chondrocytes via maintenance of central spindle organization. We show that KIF5B is concentrated in the central spindle during cytokinesis in both primary chondrocytes and chondrogenic ATDC5 cells. Conclusion The failure of cytokinesis in KIF5B null chondrocytes leads to incomplete cell rotation, disrupting proliferation and differentiation, and results in a disorganized growth plate.


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.


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

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