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Compensatory Upregulation Of MT2A Alleviates Neurogenic Intermittent Claudication Through Inhibiting Activated P38 MAPK-Mediated Neuronal Apoptosis London Spine Lumbar Stenosis

The article discusses the relationship between metallothionein 2A (MT2A) and neurogenic intermittent claudication (NIC), a common symptom of lumbar spinal stenosis. Researchers used a rat model to study the role of MT2A in NIC progression and found that increased MT2A expression in dorsal root ganglion (DRG) tissues may be linked to NIC development. Further analysis indicated that MT2A may regulate the p38 MAPK pathway to inhibit neuronal apoptosis in DRG tissues. Through experiments on hypoxia-exposed neurons, researchers confirmed that MT2A overexpression could protect against NIC by inhibiting p38 MAPK-mediated cell apoptosis. This study suggests that targeting MT2A could be a potential therapeutic strategy for treating NIC associated with lumbar spinal stenosis

Summarised by Mr Mo Akmal – Lead Spinal Surgeon
The London Spine Unit : most specialised day surgery hospital in UK

Published article

Neurogenic intermittent claudication (NIC), a classic symptom of lumbar spinal stenosis (LSS), is associated with neuronal apoptosis. To explore the novel therapeutic target of NIC treatment, we constructed the rat model of NIC by cauda equina compression (CEC) method and collected dorsal root ganglion (DRG) tissues, a region responsible for sensory and motor function, for mRNA sequencing. Bioinformatic analysis of mRNA sequencing indicated that upregulated metallothionein 2A (MT2A), an…

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Abstract Neurogenic intermittent claudication (NIC), a classic symptom of lumbar spinal stenosis (LSS), is associated with neuronal apoptosis. To explore the novel therapeutic target of NIC treatment, we constructed the rat model of NIC by cauda equina compression (CEC) method and collected dorsal root ganglion (DRG) tissues, a region responsible for sensory and motor function,

Abstract

Neurogenic intermittent claudication (NIC), a classic symptom of lumbar spinal stenosis (LSS), is associated with neuronal apoptosis. To explore the novel therapeutic target of NIC treatment, we constructed the rat model of NIC by cauda equina compression (CEC) method and collected dorsal root ganglion (DRG) tissues, a region responsible for sensory and motor function, for mRNA sequencing. Bioinformatic analysis of mRNA sequencing indicated that upregulated metallothionein 2A (MT2A), an apoptosis-regulating gene belonging to the metallothionein family, might participate in NIC progression. Activated p38 MAPK mediated motor dysfunction following LSS and it was also found in DRG tissues of rats with NIC. Therefore, we supposed that MT2A might affect NIC progression by regulating p38 MAPK pathway. Then the rat model of NIC was used to explore the exact role of MT2A. Rats at day 7 post-CEC exhibited poorer motor function and had two-fold MT2A expression in DRG tissues compared with rats with sham operation. Co-localization analysis showed that MT2A was highly expressed in neurons, but not in microglia or astrocytes. Subsequently, neurons isolated from DRG tissues of rats were exposed to hypoxia condition (3% O292% N25% CO2) to induce cell damage. Gain of MT2A function in neurons was performed by lentivirus-mediated overexpression. MT2A overexpression inhibited apoptosis by inactivating p38 MAPK in hypoxia-exposed neurons. Our findings indicated that high MT2A expression was related to NIC progression, and MT2A overexpression protected against NIC through inhibiting activated p38 MAPK-mediated neuronal apoptosis in DRG tissues.

Keywords: Cell apoptosis; Metallothionein 2A; Neurogenic intermittent claudication; Neuron; p38 MAPK.

The London Spine Unit : most specialised day surgery hospital in UK

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Compensatory upregulation of MT2A alleviates neurogenic intermittent claudication through inhibiting activated p38 MAPK-mediated neuronal apoptosis

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Abstract Neurogenic intermittent claudication (NIC), a classic symptom of lumbar spinal stenosis (LSS), is associated with neuronal apoptosis. To explore the novel therapeutic target of NIC treatment, we constructed the rat model of NIC by cauda equina compression (CEC) method and collected dorsal root ganglion (DRG) tissues, a region responsible for sensory and motor function

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