Background: This study investigated the effects of the long non-coding (lnc) RNA MT1DP on the apoptosis of nucleus pulposus (NP) cells. The interactions between MT1DP and the microRNA miR-365, and its effects on the anti-oxidant activity of nuclear factor erythroid 2-related factor 2 (NRF-2) were investigated in lumbar disc herniation (LDH).
Methods: Human degenerative intervertebral disc NP tissues were obtained from 10 patients with LDH who underwent lumbar spine surgery. Normal intervertebral disc NP tissues were obtained from 10 patients with lumbar vertebrae fractures and used as negative controls (NCs).
Results: The gene expressions of MT1DP and miR-365 in human degenerative disc NP tissues and nucleus pulposus cells (NPCs) were significantly increased, while the level of NRF-2 was significantly decreased. Overexpression of MT1DP and miR-365 (MT1DP + miR-365) and inhibition of NRF-2 suppressed NP cell viability and induced apoptosis. MT1DP + miR-365 caused inflammation in NP cells by damaging the mitochondrial membrane. The combination of lnc-MT1DP and miR-365 reduced cell mitochondrial function and led to a decrease in the ability of cells to elimination reactive oxygen species (ROS).
Conclusions: The combination of lnc-MT1DP and miR-365 damaged the cell mitochondrial membrane, reduced mitochondrial function and the ability to eliminate ROS, increased cell apoptosis, and caused LDH.
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http://dx.doi.org/10.21037/atm-20-8123 | DOI Listing |
Ann Transl Med
January 2021
Department of Orthopedics, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Background: This study investigated the effects of the long non-coding (lnc) RNA MT1DP on the apoptosis of nucleus pulposus (NP) cells. The interactions between MT1DP and the microRNA miR-365, and its effects on the anti-oxidant activity of nuclear factor erythroid 2-related factor 2 (NRF-2) were investigated in lumbar disc herniation (LDH).
Methods: Human degenerative intervertebral disc NP tissues were obtained from 10 patients with LDH who underwent lumbar spine surgery.
Although cadmium (Cd)-induced hepatoxicity is well established, pronounced knowledge gaps remain existed regarding the inherent cellular signaling that dictates Cd toxicity. Specifically, the molecular basis for determining the equilibrium between prosurvival and proapoptotic signaling remains poorly understood. Thus, it is recently revealed that long non-coding RNA (lncRNA) MT1DP, a pseudogene in the metallothionein (MT) family, promoted Cd-induced cell death through activating the RhoC-CCN1/2-AKT pathway and modulating MT1H induction.
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