Stable Expression of dmiR-283 in the Brain Promises Positive Effects in Endurance Exercise on Sleep-Wake Behavior in Aging Drosophila .
Qiufang LiLingxiao WangYurou CaoXiaoya WangChao TangLan ZhengPublished in: International journal of molecular sciences (2023)
Sleep-wake stability is imbalanced with natural aging, and microRNAs (miRNAs) play important roles in cell proliferation, apoptosis, and aging; however, the biological functions of miRNAs in regulating aging-related sleep-wake behavior remain unexplored. This study varied the expression pattern of dmiR-283 in Drosophila and the result showed that the aging decline in sleep-wake behavior was caused by the accumulation of brain dmiR-283 expression, whereas the core clock genes cwo and Notch signaling pathway might be suppressed, which regulate the aging process. In addition, to identify exercise intervention programs of Drosophila that promote healthy aging, mir-283 SP /+ and Pdf > mir-283 SP flies were driven to perform endurance exercise for a duration of 3 weeks starting at 10 and 30 days, respectively. The results showed that exercise starting in youth leads to an enhanced amplitude of sleep-wake rhythms, stable periods, increased activity frequency upon awakening, and the suppression of aging brain dmiR-283 expression in mir-283 SP /+ middle-aged flies. Conversely, exercise performed when the brain dmiR-283 reached a certain accumulation level showed ineffective or negative effects. In conclusion, the accumulation of dmiR-283 expression in the brain induced an age-dependent decline in sleep-wake behavior. Endurance exercise commencing in youth counteracts the increase in dmiR-283 in the aging brain, which ameliorates the deterioration of sleep-wake behavior during aging.
Keyphrases
- physical activity
- high intensity
- cell proliferation
- poor prognosis
- resting state
- resistance training
- long non coding rna
- sleep quality
- white matter
- signaling pathway
- functional connectivity
- randomized controlled trial
- skeletal muscle
- young adults
- binding protein
- cell death
- multiple sclerosis
- dna methylation
- cerebral ischemia
- pi k akt
- public health
- endoplasmic reticulum stress
- cell cycle
- blood brain barrier
- transcription factor
- subarachnoid hemorrhage
- stress induced