Treadmill exercise induces selective changes in hippocampal histone acetylation during the aging process in rats

Meireles, Louisiana Carolina Ferreira de; Bertoldi, Karine; Cechinel, Laura Reck; Schallenberger, Bruna; Silva, Vanessa Kappel da; Schröder, Nadja; Siqueira, Ionara Rodrigues

doi:10.1016/j.neulet.2016.10.008

Cited by 22 publications

(10 citation statements)

References 26 publications

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“…Growing evidence suggests that the microenvironment changes the posttranscriptional modification of histones via acetylation 18–20 , which subsequently influences the function of cells 12 . Consequently, we compared the expression patterns of HDAC families between the C2C12 cultured under normoxic conditions and the C2C12 cultured under hypoxic conditions.…”

Section: Resultsmentioning

confidence: 99%

Increase in HDAC9 suppresses myoblast differentiation via epigenetic regulation of autophagy in hypoxia

Zhang

Zhou

et al. 2019

Cell Death Dis

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Extremely reduced oxygen (O 2 ) levels are detrimental to myogenic differentiation and multinucleated myotube formation, and chronic exposure to high-altitude hypoxia has been reported to be an important factor in skeletal muscle atrophy. However, how chronic hypoxia causes muscle dysfunction remains unknown. In the present study, we found that severe hypoxia (1% O 2 ) significantly inhibited the function of C2C12 cells (from a myoblast cell line). Importantly, the impairment was continuously manifested even during culture under normoxic conditions for several passages. Mechanistically, we revealed that histone deacetylases 9 (HDAC9), a member of the histone deacetylase family, was significantly increased in C2C12 cells under hypoxic conditions, thereby inhibiting intracellular autophagy levels by directly binding to the promoter regions of Atg7 , Beclin1 , and LC3 . This phenomenon resulted in the sequential dephosphorylation of GSK3β and inactivation of the canonical Wnt pathway, impairing the function of the C2C12 cells. Taken together, our results suggest that hypoxia-induced myoblast dysfunction is due to aberrant epigenetic regulation of autophagy, and our experimental evidence reveals the possible molecular pathogenesis responsible for some muscle diseases caused by chronic hypoxia and suggests a potential therapeutic option.

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Section: Resultsmentioning

confidence: 99%

Increase in HDAC9 suppresses myoblast differentiation via epigenetic regulation of autophagy in hypoxia

Zhang

Zhou

et al. 2019

Cell Death Dis

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“…Notably, restoration of H4K12 acetylation levels promoted by a HDACi (Peleg et al, 2010) or by physical exercise (Zhong et al, 2016) attenuated the cognitive deficits observed in these animals. Moreover, 2 weeks of treadmill exercise improved memory performance in the inhibitory avoidance task and increased hippocampal H4K12ac levels in young adult and aged rats (de Meireles et al, 2016). Using the same exercise paradigm, this research group also demonstrated the ability of physical exercise to increase the histone H4 acetylation in the prefrontal cortex of aged rats (Cechinel et al, 2016), and to restore the aversive memory-induced reduction in H3K14ac levels in the hippocampus of adult rats (de Meireles et al, 2014).…”

Section: Epigenetics Mechanisms and Brainmentioning

confidence: 99%

Physical exercise as an epigenetic modulator of brain plasticity and cognition

Fernandes

Arida

Gómez‐Pinilla

2017

Neuroscience & Biobehavioral Reviews

241

172

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A large amount of evidence has demonstrated the power of exercise to support cognitive function, the effects of which can last for considerable time. An emerging line of scientific evidence indicates that the effects of exercise are longer lasting than previously thought up to the point to affect future generations. The action of exercise on epigenetic regulation of gene expression seem central to building an “epigenetic memory” to influence long-term brain function and behavior. In this review article, we discuss new developments in the epigenetic field connecting exercise with changes in cognitive function, including DNA methylation, histone modifications and microRNAs (miRNAs). The understanding of how exercise promotes long-term cognitive effects is crucial for directing the power of exercise to reduce the burden of neurological and psychiatric disorders.

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“…Epigenetic regulation could mediate crucial factors of aging and degenerative diseases like Alzheimer's disease. Studies have shown that exercise modifies the epigenetic mechanism in the hippocampus [25][26][27][28] and may prevent epigenetic changes due to aging or CNS disorders [29][30][31] . Specifically, acetylation of histones (histone 3 and histone 4) enhances gene expression, including hippocampal BDNF.…”

Section: Exercise Increases the Expression Of Bdnf In The Hippocampusmentioning

confidence: 99%

“…Activated HATs or inhibited HDACs increase acetylated histones and enhance total gene transcriptions. Previous literature has shown that exercise increases histone acetylation associated with the increase of beneficial proteins for learning and memory, including hippocampal BDNF 27,[29][30][31][32] . In addition, exercise reduces the expression 29,32) and activity level of HDACs 25 ) , and it increases the activity level of HATs in the hippocampus [23][24][25]33) .…”

Section: Exercise Increases the Expression Of Bdnf In The Hippocampusmentioning

confidence: 99%

Therapeutic exercise accompanied by neuronal modulation to enhance neurotrophic factors in the brain with central nervous system disorders

2019

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Exercise is a primary therapeutic regimen in physical therapy to rehabilitate the motor function of patients with central nervous system (CNS) disorders such as cerebrovascular accident (CVA). Furthermore, exercise positively contributes to cognitive function related to neuroplasticity and neuroprotection in the hippocampus. Neurotrophins play a crucial role in neuroplasticity, neurogenesis, and neuroprotection in the CNS. Exercise enhances the expression of neurotrophins in the brain. Thus, novel regimens for kinesiotherapy in CNS disorders to further enhance exercise-induced expression are expected. In this review, we described three novel regimens for kinesiotherapy in CNS disorders based on the interaction between exercise and pharmacological treatment with the idea of "inhibition of inhibition" in the CNS.

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Treadmill exercise induces selective changes in hippocampal histone acetylation during the aging process in rats

Cited by 22 publications

References 26 publications

Increase in HDAC9 suppresses myoblast differentiation via epigenetic regulation of autophagy in hypoxia

Increase in HDAC9 suppresses myoblast differentiation via epigenetic regulation of autophagy in hypoxia

Physical exercise as an epigenetic modulator of brain plasticity and cognition

Therapeutic exercise accompanied by neuronal modulation to enhance neurotrophic factors in the brain with central nervous system disorders

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