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  3. RASSF7 expression and its regulatory roles on apoptosis in human intervertebral disc degeneration

RASSF7 expression and its regulatory roles on apoptosis in human intervertebral disc degeneration

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Files
DOI
10.7892/boris.78898
Official URL
http://www.ijcep.com/files/ijcep0014013.pdf
PubMed ID
26884887
Abstract
Apoptosis plays an important role in intervertebral disc degeneration (IDD). Overwhelming evidence indicates that RASSF7 is essential for cell growth and apoptosis. Recently, it has been noted that the JNK signaling can be negatively regulated by suppressing phosphorylated-MKK7 activation during pro-apoptosis. We aimed to investigate the RASSF7 expression level in human degenerative nucleus pulposus (NP) cells and non-degenerative NP cells and the link between RASSF7-JNK with NP cells apoptosis. We harvested NP tissues from 20 IDD patients as disease group and 8 cadaveric donors as normal controls. We detected RASSF7 expression by Real-time-PCR and western blotting. Consequently, we found that the expression of RASSF7 was higher in non-degenerative group than in degenerative group (P<0.05). Overexpression of RASSF7 in degenerative NP cells led to decreased apoptosis rate than that in scramble group (P<0.05). Collectively, our findings suggest that RASSF7 plays an important role in human IDD and RASSF7 might be potentially developed as a curative agent.
Date Issued
2015
Publication Type
Article
Subject(s)
500 Science > 570 Life sciences; biology
600 Technology > 610 Medicine & health
Subjects
Intervertebral disc degeneration
•
JNK
•
RASSF7
•
apoptosis
•
nucleus pulposus
Language(s)
en
Author(s)
Liu, Zhi-Heng
Huo, Jun-Li
Wu, Zhi-Gang
Sun, Zhen
Bai, Feng
Samartzis, Dino
Gantenbein, Benjamin  orcid-logo
Institut für chirurgische Technologien und Biomechanik (ISTB)  
Fan, Shao-Di
Wang, Hai-Qiang
Additional Credits
Institut für chirurgische Technologien und Biomechanik (ISTB)  
Journal
International journal of clinical and experimental pathology
Publisher
e-Century Publishing
ISSN
1936-2625
Access(Rights)
open.access
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