LncRNA HOTAIR suppresses TNF-α induced apoptosis of nucleus pulposus cells by regulating miR-34a/Bcl-2 axis - 20/09/18
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Graphical abstract |
HOTAIR inhibits miR-34a expression.
Bcl-2 was a target of miR-34a, and miR-34a was negatively correlated with Bcl-2.
HOTAIR suppresses TNF-α induced apoptosis of NPCs by regulating miR-34a/Bcl-2 axis.
Highlights |
• | HOTAIR expression is down-regulated in nucleus pulposus tissues and cells. |
• | HOTAIR reduced miR-34a induced apoptosis of nucleus pulposus cell. |
• | Bcl-2 was a target of miR-34a and negatively related with miR-34a. |
Abstract |
Objective |
The aim of this study was to investigate the regulation mechanism of HOTAIR on nucleus pulposus cell (NPC) apoptosis induced by inflammatory cytokines.
Methods |
QRT-PCR was performed to analyze the expression of HOTAIR and miR-34a. Safranin O staining and immunohistochemical staining were measured to identify NPCs. ELISA assay was used to detect TNF-α level. Apoptosis was detected with TUNEL assay. Western blotting was measured to analyze the expression of caspase-3, Bax and Bcl-2. TargetScan was used to predict potential targets of miR-34a.
Results |
HOTAIR was significantly low-expressed in degenerative nucleus pulposus (NP) tissues and cells of IDD patients, overexpressing HOTAIR obviously inhibited TNF-α level, NPCs apoptosis and the expression of caspase-3 and Bax, while promoted the expression of Bcl-2. MiR-34a was obviously expressed in degenerative NP tissues and cells of IDD patients. HOTAIR reduced miR-34a induced apoptosis. Apoptotic inhibition gene Bcl-2 is the target gene of miR-34a, and showed a negative relationship with miR-34a.
Conclusion |
Our data suggest that lncRNA HOTAIR suppresses TNF-α induced NPCs apoptosis by regulating miR-34a/Bcl-2 axis in IDD patients.
Le texte complet de cet article est disponible en PDF.Keywords : HOTAIR, Nucleus pulposus cells, miR-34a, Bcl-2
Plan
Vol 107
P. 729-737 - novembre 2018 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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