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Review
. 2017 Dec:111:12-22.
doi: 10.1016/j.neuint.2017.01.015. Epub 2017 Jan 26.

Non-coding RNAs and neuroprotection after acute CNS injuries

Affiliations
Review

Non-coding RNAs and neuroprotection after acute CNS injuries

Raghavendar Chandran et al. Neurochem Int. 2017 Dec.

Abstract

Accumulating evidence indicates that various classes of non-coding RNAs (ncRNAs) including microRNAs (miRNAs), PIWI-interacting RNAs (piRNAs) and long non-coding RNAs (lncRNAs) play important roles in normal state as well as the diseases of the CNS. Interestingly, ncRNAs have been shown to interact with messenger RNA, DNA and proteins, and these interactions could induce epigenetic modifications and control transcription and translation, thereby adding a new layer of genomic regulation. The ncRNA expression profiles are known to be altered after acute CNS injuries including stroke, traumatic brain injury and spinal cord injury that are major contributors of morbidity and mortality worldwide. Hence, a better understanding of the functional significance of ncRNAs following CNS injuries could help in developing potential therapeutic strategies to minimize the neuronal damage in those conditions. The potential of ncRNAs in blood and CSF as biomarkers for diagnosis and/or prognosis of acute CNS injuries has also gained importance in the recent years. This review highlighted the current progress in the understanding of the role of ncRNAs in initiation and progression of secondary neuronal damage and their application as biomarkers after acute CNS injuries.

Keywords: Hemorrhagic stroke; Ischemic stroke; Non-coding RNA; Spinal cord injury; Traumatic brain injury; lncRNA; microRNA; piRNA.

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Figures

Fig. 1
Fig. 1
NcRNAs mediate common molecular mechanisms associated with the different acute CNS injuries. Different studies have shown that ncRNAs like miRNAs and lncRNAs contribute to the pathophysiology of acute CNS injuries by mediating common pathophysiological mechanisms like apoptosis, inflammation and glutamate excitotoxicity as well as neuroprotective mechanisms like neuroprotection, neuroplasticity and angiogenesis.

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