SIRT1 Decreases Emotional Pain Vulnerability with Associated CaMKIIα Deacetylation in Central Amygdala

Zhou, Chenghua; Wu, Yuqing; Ding, Xiaobao; Shi, Naihao; Cai, Youqin; Pan, Zhizhong Z.

doi:10.1523/jneurosci.1259-19.2020

Cited by 25 publications

(21 citation statements)

References 78 publications

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“…However, individuals show considerable vulnerability to the development of chronic pain under similar pain conditions. In a study on male rat and mouse models of chronic neuropathic pain, it was identified SIRT1 in central amygdala is a key epigenetic regulator that controls the development of comorbid emotional disorders underlying the individual vulnerability to chronic pain (Zhou et al, 2020 ). In fact, researchers found that animals that were vulnerable to developing behaviors of anxiety and depression under the pain condition displayed reduced SIRT1 protein levels in their central amygdala, but not in those animals resistant to the emotional disorders.…”

Section: Estrogen Receptor As a Potential Example Of Biodynamic Inter...mentioning

confidence: 99%

On the Interplay Between the Medicine of Hildegard of Bingen and Modern Medicine: The Role of Estrogen Receptor as an Example of Biodynamic Interface for Studying the Chronic Disease's Complexity

Melino¹,

Mormone²

2022

Front. Neurosci.

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IntroductionHildegard of Bingen (1098-1179) interpreted the origins of chronic disease highlighting and anticipating, although only in a limited fashion, the importance that complex interactions among numerous genetic, internal milieu and external environmental factors have in determining the disease phenotype. Today, we recognize those factors, capable of mediating the transmission of messages between human body and environment and vice versa, as biodynamic interfaces.AimWe analyzed, in the light of modern scientific evidence, Hildegard of Bingen's medical approach and her original humoral theory in order to identify possible insights included in her medicine that could be referred to in the context of modern evidence-based medicine. In particular, the abbess's humoral theory suggests the identification of biodynamic interfaces with sex hormones and their receptors.FindingsWe found that the Hildegardian holistic vision of the organism-environment relationship can actually represent a visionary approach to modern endocrinology and that sex hormones, in particular estrogens, could represent an example of a biodynamic interface. Estrogen receptors are found in regions of the brain involved in emotional and cognitive regulation, controlling the molecular mechanism of brain function. Estrogen receptors are involved in the regulation of the hypothalamic-pituitary-adrenal axis and in the epigenetic regulation of responses to physiological, social, and hormonal stimuli. Furthermore, estrogen affects gene methylation on its own and related receptor promoters in discrete regions of the developing brain. This scenario was strikingly perceived by the abbess in the XIIth century, and depicted as a complex interplay among different humors and flegmata that she recognized to be sex specific and environmentally regulated.ViewpointConsidering the function played by hormones, analyzed through the last scientific evidence, and scientific literature on biodynamic interfaces, we could suggest Hildegardian insights and theories as the first attempt to describe the modern holistic, sex-based medicine.ConclusionHildegard anticipated a concept of pathogenesis that sees a central role for endocrinology in sex-specific disease. Furthermore, estrogens and estrogen receptors could represent a good example of molecular interfaces capable of modulating the interaction between the organism internal milieu and the environmental factors.

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Section: Estrogen Receptor As a Potential Example Of Biodynamic Inter...mentioning

confidence: 99%

On the Interplay Between the Medicine of Hildegard of Bingen and Modern Medicine: The Role of Estrogen Receptor as an Example of Biodynamic Interface for Studying the Chronic Disease's Complexity

Melino¹,

Mormone²

2022

Front. Neurosci.

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“…SIRT1 deacetylates RelA/p65 to inhibit the nuclear translocation of NF‐κB, thus inhibiting inflammation 24 . Intrathecal injection of a lentiviral vector overexpressing SIRT1 was shown to alleviate mechanical allodynia or thermal hyperalgesia 25 . SIRT1 overexpression mediated by the lentiviral vector suppressed interleukin (IL)‐1 beta‐induced extracellular matrix degradation and cell apoptosis, alleviating the low back pain caused by intervertebral disk degeneration 24 .…”

Section: Introductionmentioning

confidence: 99%

“…24 Intrathecal injection of a lentiviral vector overexpressing SIRT1 was shown to alleviate mechanical allodynia or thermal hyperalgesia. 25 SIRT1 overexpression mediated by the lentiviral vector suppressed interleukin (IL)-1 beta-induced extracellular matrix degradation and cell apoptosis, alleviating the low back pain caused by intervertebral disk degeneration. 24 Accumulating evidence has demonstrated that enhanced synaptic plasticity of nociceptive interneurons in the spinal dorsal horn is the basis of central sensitization in neuropathic pain.…”

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confidence: 99%

SIRT1: A promising therapeutic target for chronic pain

et al. 2022

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Chronic pain remains an unresolved problem. Current treatments have limited efficacy. Thus, novel therapeutic targets are urgently required for the development of more effective analgesics. An increasing number of studies have proved that sirtuin 1 (SIRT1) agonists can relieve chronic pain. In this review, we summarize recent progress in understanding the roles and mechanisms of SIRT1 in mediating chronic pain associated with peripheral nerve injury, chemotherapy‐induced peripheral neuropathy, spinal cord injury, bone cancer, and complete Freund's adjuvant injection. Emerging studies have indicated that SIRT1 activation may exert positive effects on chronic pain relief by regulating inflammation, oxidative stress, and mitochondrial dysfunction. Therefore, SIRT1 agonists may serve as potential therapeutic drugs for chronic pain.

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“…Interestingly, the notion that H3K9 global acetylation decreases in the Schwann cells in the trigeminal ganglia of a nerve injury mouse model induced by trigeminal inflammatory compression [ 6 ], whereas that histone deacetylase inhibitors (HDACi) can prevent the persistent hypersensitivity of neurons from neuropathic pain [ 7 ], which indicate that cells in different areas of trigeminal root entry zone and ganglion contain display a different response to TN. Moreover, various HDAC subclusters have also been found to exert varying effects on pain vulnerability and excitability of neurons [ 8 , 9 ]. Therefore, the epigenetic regulation of the gene expression in response to compressive stress-induced imbalanced homeostasis in the trigeminal ganglion and trigeminal root entry zone is still obscure.…”

Section: Introductionmentioning

confidence: 99%

Characterization of Acetylation of Histone H3 at Lysine 9 in the Trigeminal Ganglion of a Rat Trigeminal Neuralgia Model

Wei

Liu

Qiu

et al. 2022

Oxidative Medicine and Cellular Longevity

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Trigeminal neuralgia (TN) is a chronic neuropathic pain disorder characterized by spontaneous and elicited paroxysms of electric-shock-like or stabbing pain in a region of the face. The epigenetic regulation of TN is still obscure. In current study, a rat TN model subject to carbamazepine (CBZ) treatment was established, and transcriptome- and genome-scale profiling of H3K9ac and HDAC3 was performed by RNA-seq and ChIP-seq. We observed that H3K9ac levels in the trigeminal ganglion were lower in the TN rats compared with those in the control, and CBZ treatment led to recovery of H3K9ac levels. Further, we found that HDAC3 was overactivated, which interfered with H3K9 acetylation due to higher phosphorylation in TN compared with that in the control. Finally, the phosphokinase leucine-rich repeat kinase 2 (LRRK2) was demonstrated to contribute to HDAC3 activity via the MAPK signaling pathway. Taken together, we identified a regulatory mechanism in which the phosphate groups transferred from activated ERK and LRRK2 to HDAC3 caused genome-scale deacetylation at H3K9 and resulted in the silencing of a large number of genes in TN. The kinases or important enzymes within this regulatory axis may represent important targets for TN therapy and prevention.

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SIRT1 Decreases Emotional Pain Vulnerability with Associated CaMKIIα Deacetylation in Central Amygdala

Cited by 25 publications

References 78 publications

On the Interplay Between the Medicine of Hildegard of Bingen and Modern Medicine: The Role of Estrogen Receptor as an Example of Biodynamic Interface for Studying the Chronic Disease's Complexity

On the Interplay Between the Medicine of Hildegard of Bingen and Modern Medicine: The Role of Estrogen Receptor as an Example of Biodynamic Interface for Studying the Chronic Disease's Complexity

SIRT1: A promising therapeutic target for chronic pain

Characterization of Acetylation of Histone H3 at Lysine 9 in the Trigeminal Ganglion of a Rat Trigeminal Neuralgia Model

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