Emerging role of non-coding RNAs in neuroinflammation mediated by microglia and astrocytes

Abstract

Neuroinflammation has been implicated in the initiation and progression of several central nervous system (CNS) disorders, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, multiple sclerosis, ischemic stroke, traumatic brain injury, spinal cord injury, viral encephalitis, and bacterial encephalitis. Microglia and astrocytes are essential in neural development, maintenance of synaptic connections, and homeostasis in a healthy brain. The activation of astrocytes and microglia is a defense mechanism of the brain against damaged tissues and harmful pathogens. However, their activation triggers neuroinflammation, which can exacerbate or induce CNS injury. Non-coding RNAs (ncRNAs) are functional RNA molecules that lack coding capabilities but can actively regulate mRNA expression and function through various mechanisms. ncRNAs are highly expressed in astrocytes and microglia and are potential mediators of neuroinflammation. We reviewed the recent research progress on the role of miRNAs, lncRNAs, and circRNAs in regulating neuroinflammation in various CNS diseases. Understanding how these ncRNAs affect neuroinflammation will provide important therapeutic insights for preventing and managing CNS dysfunction.

Impaired meningeal lymphatic drainage in Listeria monocytogenes infection

“…and found that levels of VEGF-C were moderately elevated ( Figures 2A-C ). Microglia and astrocyte also play important roles in inflammation and neurological disorders, as their activation and release of inflammatory mediators can influence disease progression ( 26 ). Subsequently, we traced the source of VEGF-C and explored its connection with microglia and astrocyte.…”

Profiling of long non-coding RNAs in hippocampal–entorhinal system subfields: impact of RN7SL1 on neuroimmune response modulation in Alzheimer’s disease

“…Notably, microglial proliferation and activation within the brain, particularly around Aβ plaques, are prominent characteristics of AD [ 24 ]. Astrocytes contribute directly to neuroinflammatory and neurodegenerative processes in AD [ 61 ], and lncRNAs mediate neuroinflammation in glial cells [ 62 ]. For example, MEG3 overexpression has been reported to inhibit astrocyte activation, reduce inflammatory injury, and alleviate neuronal damage [ 63 ].…”

TGFβ1-induced hedgehog signaling suppresses the immune response of brain microvascular endothelial cells elicited by meningitic Escherichia coli

“…MicroRNAs (miRNAs) are endogenous ~ 22 nt RNAs targeting mRNAs for cleavage or translational repression, which played a regulatory role in the immunity process, particularly in BBB and CNS inflammatory reaction [ 39 , 40 ]. For instance, miR-17-5p mediated leukemia inhibitory factor modulation of reactive astrocyte proliferation [ 41 ], and astrocytic miR-19b-3p participated in promoting the production of inflammatory cytokines in JEV infection [ 42 ].…”