Abstract
The central nervous system can respond to threat via the induction of an inflammatory response. Under normal circumstances this response is tightly controlled, however uncontrolled neuroinflammation is a hallmark of many neurological disorders. MicroRNAs are small non-coding RNA molecules that are important for regulating many cellular processes. The ability of microRNAs to modulate inflammatory signaling is an area of ongoing research, which has gained much attention in recent years. MicroRNAs may either promote or restrict inflammatory signaling, and either exacerbate or ameliorate the pathological consequences of excessive neuroinflammation. The aim of this review is to summarize the mode of regulation for several important and well-studied microRNAs in the context of neuroinflammation, including miR-155, miR-146a, miR-124, miR-21 and let-7. Furthermore, the pathological consequences of miRNA deregulation during disorders that feature neuroinflammation are discussed, including Multiple Sclerosis, Alzheimer’s disease, Parkinson’s disease, Prion diseases, Japanese encephalitis, Herpes encephalitis, ischemic stroke and traumatic brain injury. There has also been considerable interest in the use of altered microRNA signatures as biomarkers for these disorders. The ability to modulate microRNA expression may even serve as the basis for future therapeutic strategies to help treat pathological neuroinflammation.
Highlights
The central nervous system (CNS) is traditionally thought of as an immune-privileged site, separated from peripheral immune cells that are unable to cross the blood brain barrier (BBB) under normal conditions [1]
Microglia express an array of pattern recognition receptors, cytokine receptors and neuronal receptors which can respond to a variety of pathogen associated molecular patterns (PAMPs), danger associated molecular patterns (DAMPs) and other molecular signatures, triggering signaling that leads to microglial activation [8]
Depending on the nature of the signals that lead to their activation, microglia may differentiate into either M1 or M2 phenotypes which resemble those seen in macrophages
Summary
The central nervous system (CNS) is traditionally thought of as an immune-privileged site, separated from peripheral immune cells that are unable to cross the blood brain barrier (BBB) under normal conditions [1]. Resident glial cells including microglia and astrocytes become activated and induce an inflammatory response through pro-inflammatory cytokines, chemokines, secondary messengers and reactive oxygen species (ROS) [2] This response, termed neuroinflammation, may be beneficial, by protecting the brain from pathogens and neurotoxic agents and promoting tissue repair processes [3,4]. M1 microglia release inflammatory mediators such as ROS, MMP-9 and pro-inflammatory cytokines such as TNFα, IL-6 and IL-1β [10] The balance between these different microglial phenotypic states may promote inflammation or tissue repair and influence the progression of neuroinflammatory disorders [10]. Among the central regulators of these processes are microRNAs (miRNAs), which may either become deregulated, contributing to disease progression, or may reflect a homeostatic attempt of the CNS to prevent excessive damage and restore normal conditions
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