Long-term chronic caloric restriction alters miRNA profiles in the brain of ageing mice

Özorhan, Ümit; Tuna, Bilge Güvenç; Cicekdal, Munevver Burcu; Kuşkucu, Ayşegül; Bayrak, Ömer Faruk; Yılmaz, Bayram; Demirel, Pınar; Cleary, Margot P.; Doğan, Soner

doi:10.1017/s0007114521001239

Cited by 7 publications

(3 citation statements)

References 52 publications

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“…The abnormal regulation of miRNA may participate in the progression of the disease by affecting the expression and function of target genes [ 43 ]. MiR-184 has been shown to play a role in neurogenesis, chromatin, and histone regulation, which may be a potential target for neurodegenerative diseases [ 44 ]. This study showed that the levels of miR-184 in urinary exosomes from PD patients were significantly higher than those of matched healthy control subjects, which were inconsistent with the plasma miR-184 levels in PD patients reported by Na Li et al [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-184 Mediated the Expression of ZNF865 in Exosome to Promote Procession in the PD Model

Liu,

Wang,

et al. 2023

Mol Neurobiol

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Exosomes are nanoscale small vesicles (EVs) secreted by cells that carry important bio information, including proteins, miRNAs, and more. Exosome contents are readily present in body fluids, including blood, and urine of humans and animals, and thereby act as markers of diseases. In patients with Parkinson’s disease (PD), exosomes may spread alpha-synuclein and miR-184 between the cells contributing to dopaminergic neuronal loss. In this study, we detected the levels of miR-184 in urine-excreted neuronal exosomes between PD patients and age-matched healthy subjects by qRT-PCR analysis. Transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA) were also used to determine the ultracellular structures of exosomes nanoparticles. MPP + and MPTP were used to construct the cell and animal PD model. Behavioral tests were used to detect motor performance. Furthermore, the cytological experiments were measured to examine the relationship between miR-184 and ZNF865. We found that the levels of miR-184 in urine-derived neuronal exosomes from PD patients were higher, compared to aged-matched normal people. The exosomes from PD patients were larger with greater numbers than those from the age-matched healthy subjects. The difference in miR-184 in urinary exosomes between PD patients and normal people may provide a novel perspective for early diagnosis of PD. However, no difference in CD63 level was observed in Exo-control and Exo-PD groups (exosome from control or PD groups). Moreover, ZNF865 was detected as the targeted gene of miR-184. In addition, miR-184 ASO (miR-184 antisense oligodeoxynucleotide, miR-184 ASO) could rescue the damage of neuronal apoptosis and motor performance in PD mice. Our results showed the miR-184 potential to function as a diagnostic marker of PD. Graphical Abstract

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Section: Discussionmentioning

confidence: 99%

MiR-184 Mediated the Expression of ZNF865 in Exosome to Promote Procession in the PD Model

Liu,

Wang,

et al. 2023

Mol Neurobiol

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“…NK cell aging [282,283] , age-related loss of muscle cells [284] , and skeletal cell aging [285] ; downregulated in peripheral blood and associated with all-cause mortality and agerelated traits [286] 7 miR-184 Downregulated in calorie-restricted mouse brain [287] , older adults with major depressive disorder [288] , downregulated in aging heart [278] 8 miR-222-5p…”

Section: Mir-200cmentioning

confidence: 99%

Hypertrophic cardiomyopathy in MYBPC3 carriers in aging

Ananthamohan,

Stelzer,

Sadayappan

2024

J Cardiovasc Aging

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Hypertrophic cardiomyopathy (HCM) is characterized by abnormal thickening of the myocardium, leading to arrhythmias, heart failure, and elevated risk of sudden cardiac death, particularly among the young. This inherited disease is predominantly caused by mutations in sarcomeric genes, among which those in the cardiac myosin binding protein-C3 (MYBPC3 ) gene are major contributors. HCM associated with MYBPC3 mutations usually presents in the elderly and ranges from asymptomatic to symptomatic forms, affecting numerous cardiac functions and presenting significant health risks with a spectrum of clinical manifestations. Regulation of MYBPC3 expression involves various transcriptional and translational mechanisms, yet the destiny of mutant MYBPC3 mRNA and protein in late-onset HCM remains unclear. Pathogenesis related to MYBPC3 mutations includes nonsense-mediated decay, alternative splicing, and ubiquitin-proteasome system events, leading to allelic imbalance and haploinsufficiency. Aging further exacerbates the severity of HCM in carriers of MYBPC3 mutations. Advancements in high-throughput omics techniques have identified crucial molecular events and regulatory disruptions in cardiomyocytes expressing MYBPC3 variants. This review assesses the pathogenic mechanisms that promote late-onset HCM through the lens of transcriptional, post-transcriptional, and post-translational modulation of MYBPC3 , underscoring its significance in HCM across carriers. The review also evaluates the influence of aging on these processes and MYBPC3 levels during HCM pathogenesis in the elderly. While pinpointing targets for novel medical interventions to conserve cardiac function remains challenging, the emergence of personalized omics offers promising avenues for future HCM treatments, particularly for late-onset cases.

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“…Таким образом, по мнению авторов, режим CCR может оказывать защитные эффекты, модулируя специфические miRNA, поскольку они играют роль в нейрогенезе, регуляции хроматина и гистонов. Эти три группы miRNA могут быть потенциальными мишенями для нейродегенеративных и связанных со старением заболеваний и могут играть важную роль в защитных эффектах ограничения калорийности пищи в головном мозге [106].…”

Section: Reviewunclassified

Effect of caloric restriction on aging and neurodegenerative diseases

Фефелова¹,

Мурашев²

2022

Zhurnal «Patologicheskaia Fiziologiia I Eksperimental`naia Terapiia»

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Исследования на моделях млекопитающих демонстрируют, что ограничение калорийности питания замедляет процессы старения, увеличивает продолжительность жизни и отодвигает начало ряда возрастных заболеваний, в том числе нейродегенеративных. При ограничении калорийности питания организм переходит в режим поддержания жизнеспособности, что реализуется за счет включения программ стрессоустойчивости и замедления процессов роста и репродукции. К реализации данных программ приводят выраженные изменения внутриклеточных процессов: активация репарации макромолекул и восстановление длины теломер хромосом, что способствует поддержанию стабильности генома и протеома, выживаемости стволовых клеток. Кроме того, происходит перепрограммирование метаболических процессов и изменение их скорости, в том числе через влияние рестрикции питания на эпигенетические механизмы контроля. Ограничение калорий - это диетическая стратегия, которая может оказать влияние на скорость развития нейродегенерации. Таким образом, диета и питание являются одними из наиболее значимых модифицируемых внешних факторов, регулирующих метаболизм клеток, что определяет перспективные траектории изучения их влияния на механизмы развития нейровоспалительных и нейродегенеративных процессов. В обзоре обсуждаются механизмы, посредством которых клетки переходят на иные программы жизнеобеспечения при рестрикции питания, что проявляется изменениями процессов нейровоспаления, нейрогенеза в ответ на реализацию эпигенетических программ, запуска ответа сиртуинов, изменений в митохондриальном биогенезе. Research using mammalian models has shown that calorie restriction slows the aging process, increases life expectancy, and delays the onset of a number of age-related diseases, including neurodegenerative diseases. During caloric restriction, the organism goes into a viability maintenance mode, which is realized by the activation of stress resistance programs and the slowing of growth and reproduction processes. Very pronounced changes in intracellular processes lead to the realization of these programs, which include activation of mechanisms for repair of macromolecules and for restoration of the length of chromosome telomeres. This contributes to maintaining the stability of the genome and proteome, and the survival of stem cells. In addition, metabolic processes are reprogrammed, and their rate changes due to the influence of nutritional restriction on epigenetic control mechanisms. Caloric restriction is a dietary strategy that may have an impact on the rate of neurodegeneration. Therefore, diet and nutrition are among the most significant modifiable external factors that regulate cell metabolism. This approach offers promising ways for studying the influence of diet and nutrition on the mechanisms of neuroinflammatory and neurodegenerative processes. This article discusses mechanisms that change cellular function such that cells switch to life support programs during nutritional restriction. This is manifested by changes in the processes of neuroinflammation and neurogenesis in response to epigenetic programs that trigger the sirtuin response and change mitochondrial biogenesis.

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Long-term chronic caloric restriction alters miRNA profiles in the brain of ageing mice

Cited by 7 publications

References 52 publications

MiR-184 Mediated the Expression of ZNF865 in Exosome to Promote Procession in the PD Model

MiR-184 Mediated the Expression of ZNF865 in Exosome to Promote Procession in the PD Model

Hypertrophic cardiomyopathy in MYBPC3 carriers in aging

Effect of caloric restriction on aging and neurodegenerative diseases

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