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RASSF7 expression and its regulatory roles on apoptosis in human intervertebral disc degeneration.
- Source :
-
International journal of clinical and experimental pathology [Int J Clin Exp Pathol] 2015 Dec 01; Vol. 8 (12), pp. 16097-103. Date of Electronic Publication: 2015 Dec 01 (Print Publication: 2015). - Publication Year :
- 2015
-
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.
- Subjects :
- Adult
Cadaver
Case-Control Studies
Cells, Cultured
Female
Gene Expression Regulation
Humans
Intervertebral Disc pathology
Intervertebral Disc Degeneration genetics
Intervertebral Disc Degeneration pathology
Male
Middle Aged
Signal Transduction
Transcription Factors genetics
Transfection
Apoptosis
Intervertebral Disc metabolism
Intervertebral Disc Degeneration metabolism
Transcription Factors metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1936-2625
- Volume :
- 8
- Issue :
- 12
- Database :
- MEDLINE
- Journal :
- International journal of clinical and experimental pathology
- Publication Type :
- Academic Journal
- Accession number :
- 26884887