MicroRNA: A Key Player for the Interplay of Circadian Rhythm Abnormalities, Sleep Disorders and Neurodegenerative Diseases

Abstract

Circadian rhythms are endogenous 24-h oscillators that regulate the sleep/wake cycles and the timing of biological systems to optimize physiology and behavior for the environmental day/night cycles. The systems are basically generated by transcription–translation feedback loops combined with post-transcriptional and post-translational modification. Recently, evidence is emerging that additional non-coding RNA-based mechanisms are also required to maintain proper clock function. MicroRNA is an especially important factor that plays critical roles in regulating circadian rhythm as well as many other physiological functions. Circadian misalignment not only disturbs the sleep/wake cycle and rhythmic physiological activity but also contributes to the development of various diseases, such as sleep disorders and neurodegenerative diseases. The patient with neurodegenerative diseases often experiences profound disruptions in their circadian rhythms and/or sleep/wake cycles. In addition, a growing body of recent evidence implicates sleep disorders as an early symptom of neurodegenerative diseases, and also suggests that abnormalities in the circadian system lead to the onset and expression of neurodegenerative diseases. The genetic mutations which cause the pathogenesis of familial neurodegenerative diseases have been well studied; however, with the exception of Huntington’s disease, the majority of neurodegenerative diseases are sporadic. Interestingly, the dysfunction of microRNA is increasingly recognized as a cause of sporadic neurodegenerative diseases through the deregulated genes related to the pathogenesis of neurodegenerative disease, some of which are the causative genes of familial neurodegenerative diseases. Here we review the interplay of circadian rhythm disruption, sleep disorders and neurodegenerative disease, and its relation to microRNA, a key regulator of cellular processes.

Diurnal Variation of Plasma Extracellular Vesicle Is Disrupted in People Living with HIV

“…Evidence shows that the expressions of the mature or precursor forms of some miRNAs exhibit circadian and/or diurnal rhythms and are suggested to be involved in circadian rhythm regulation and physiological function [ 69 , 70 ]. The miRNAs miR-155, miR-27b-3p, miR-211, and miR-142 have been described to regulate the rhythmic expression of Bmal1 mRNA and protein levels [ 69 , 71 , 72 ]. HIV infection has been associated with irregularities in physiological functions related to circadian rhythm [ 37 , 73 ].…”

Curcumin Reinforces MiR-29a Expression, Reducing Mesangial Fibrosis in a Model of Diabetic Fibrotic Kidney via Modulation of CB1R Signaling

“…Thus, intraperitoneal injection of curcumin in animals was chosen in the present study.In the future, improving bioavailability of curcuminand selectinga proper administration routewould be important for its application in treating diabetic kidney disease. Second, growing evidence has shown that the sleep circadian rhythm significantly associates withthe expression of mircoRNA including mir-29a [46]. Due to the fact that miR-29a is rhythmically expressed and involves the regulation of core clock components, mice that were intraperitoneally injected with curcumin or were sacrificed at different Zeitgeber times (ZT) or circadian times (CT) may probably lead to differential outcomes.…”

Regulation of microRNA Expression in Sleep Disorders in Patients with Epilepsy

“…In particular, the levels of microRNA-125a, microRNA-126, and microRNA-146a are significantly lower in short-sleep compared with normal sleep groups. Dysregulated miRNA-146A in patients with fatal familial insomnia causes increased tau hyperphosphorylation [ 6 ].…”

“…MicroRNAs whose regulation affects sleep homeostasis and circadian rhythm include microRNA-107, microRNA-124, micorRNA-125a-3p, microRNA-132, microRNA-182, microRNA-126, and microRNA-146a [ 6 , 7 ]. MicroRNA-124 regulates the development of neurons by controlling key differentiation factors such as REST (repressor element-1 silencing transcription factor) and PTBP1 (polypyrimidine tract-binding protein 1) as well as maturation through effects on CREB (CRE binding protein―cAMP response element).…”