MicroRNA339 Targeting PDXK Improves Motor Dysfunction and Promotes Neurite Growth in the Remote Cortex Subjected to Spinal Cord Transection

Xiong, Liu‐Lin; Qin, Yanxia; Xiao, Qiu‐Xia; Yuan, Jing; Al‐Hawwas, Mohammed; Ma, Zheng; Wang, You‐Cui; Belegu, Visar; Zhou, Xin‐Fu; Xue, Lu‐Lu; Du, Ruo‐Lan; Liu, Jia; Bai, Xue; Wang, Ting‐Hua

doi:10.3389/fcell.2020.00577

Cited by 8 publications

(2 citation statements)

References 63 publications

(80 reference statements)

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“…The four-min evaluation on each rat was made and scores of hindlimb movement were recorded by three experienced researchers. The average score was the final score [ 54 ].…”

Section: Methodsmentioning

confidence: 99%

METTL14 promotes apoptosis of spinal cord neurons by inducing EEF1A2 m6A methylation in spinal cord injury

et al. 2022

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Spinal cord injury (SCI) is a devastating traumatic condition. METTL14-mediated m6A modification is associated with SCI. This study was intended to investigate the functional mechanism of RNA methyltransferase METTL14 in spinal cord neuron apoptosis during SCI. The SCI rat model was established, followed by evaluation of pathological conditions, apoptosis, and viability of spinal cord neurons. The neuronal function of primary cultured spinal motoneurons of rats was assessed after hypoxia/reoxygenation treatment. Expressions of EEF1A2, Akt/mTOR pathway-related proteins, inflammatory cytokines, and apoptosis-related proteins were detected. EEF1A2 was weakly expressed and Akt/mTOR pathway was inhibited in SCI rat models. Hypoxia/Reoxygenation decreased the viability of spinal cord neurons, promoted LDH release and neuronal apoptosis. EEF1A2 overexpression promoted the viability of spinal cord neurons, inhibited neuronal apoptosis, and decreased inflammatory cytokine levels. Silencing METTL14 inhibited m6A modification of EEF1A2 and increased EEF1A2 expression while METTL14 overexpression showed reverse results. EEF1A2 overexpression promoted viability and inhibited apoptosis of spinal cord neurons and inflammation by activating the Akt/mTOR pathway. In conclusion, silencing METTL14 repressed apoptosis of spinal cord neurons and attenuated SCI by inhibiting m6A modification of EEF1A2 and activating the Akt/mTOR pathway.

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“…The four-min evaluation on each rat was made and scores of hindlimb movement were recorded by three experienced researchers. The average score was the final score [ 54 ].…”

Section: Methodsmentioning

confidence: 99%

METTL14 promotes apoptosis of spinal cord neurons by inducing EEF1A2 m6A methylation in spinal cord injury

et al. 2022

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“…In the same study, knockout of the microRNA (MiR339) that blocks PDXK translation was shown to decrease apoptosis of cortical neurons, thereby increasing neurite outgrowth [72].…”

Section: The Shared Genetic Origin Of the Vitamin-related Forms Of Cm...mentioning

confidence: 88%

The Therapeutic Potential of Vitamins B1, B3 and B6 in Charcot–Marie–Tooth Disease with the Compromised Status of Vitamin-Dependent Processes

Bunik

2023

Biology

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Understanding the molecular mechanisms of neurological disorders is necessary for the development of personalized medicine. When the diagnosis considers not only the disease symptoms, but also their molecular basis, treatments tailored to individual patients may be suggested. Vitamin-responsive neurological disorders are induced by deficiencies in vitamin-dependent processes. These deficiencies may occur due to genetic impairments of proteins whose functions are involved with the vitamins. This review considers the enzymes encoded by the DHTKD1, PDK3 and PDXK genes, whose mutations are observed in patients with Charcot–Marie–Tooth (CMT) disease. The enzymes bind or produce the coenzyme forms of vitamins B1 (thiamine diphosphate, ThDP) and B6 (pyridoxal-5′-phosphate, PLP). Alleviation of such disorders through administration of the lacking vitamin or its derivative calls for a better introduction of mechanistic knowledge to medical diagnostics and therapies. Recent data on lower levels of the vitamin B3 derivative, NAD+, in the blood of patients with CMT disease vs. control subjects are also considered in view of the NAD-dependent mechanisms of pathological axonal degeneration, suggesting the therapeutic potential of vitamin B3 in these patients. Thus, improved diagnostics of the underlying causes of CMT disease may allow patients with vitamin-responsive disease forms to benefit from the administration of the vitamins B1, B3, B6, their natural derivatives, or their pharmacological forms.

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Proteomic characterization of spontaneously regrowing spinal cord following injury in the teleost fish Apteronotus leptorhynchus, a regeneration-competent vertebrate

et al. 2022

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MicroRNA339 Targeting PDXK Improves Motor Dysfunction and Promotes Neurite Growth in the Remote Cortex Subjected to Spinal Cord Transection

Cited by 8 publications

References 63 publications

METTL14 promotes apoptosis of spinal cord neurons by inducing EEF1A2 m6A methylation in spinal cord injury

METTL14 promotes apoptosis of spinal cord neurons by inducing EEF1A2 m6A methylation in spinal cord injury

The Therapeutic Potential of Vitamins B1, B3 and B6 in Charcot–Marie–Tooth Disease with the Compromised Status of Vitamin-Dependent Processes

Proteomic characterization of spontaneously regrowing spinal cord following injury in the teleost fish Apteronotus leptorhynchus, a regeneration-competent vertebrate

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