SIRT1 decelerates morphological processing of oligodendrocyte cell lines and regulates the expression of cytoskeleton-related oligodendrocyte proteins

Hisahara, Shin; Iwahara, Naotoshi; Matsushita, T.; Suzuki, Syuuichirou; Matsumura, Akihiro; Fujikura, Mai; Yokokawa, Kazuki; Saito, Taro; Manabe, Tatsuo; Kawamata, Jun; Horio, Yoshiyuki; Shimohama, Shun

doi:10.1016/j.bbrc.2021.01.095

Cited by 11 publications

(8 citation statements)

References 27 publications

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“…There are two types of pain being most characteristic in patients with NMOSD: evoked pain most often caused by painful tonic muscle spasms, and ongoing neuropathic pain. 30 What’s more, pain due to excess loading and pain as a side effect of immunotherapy and in the context of comorbidities are also not rare in NMOSD patients. 31 Neuropathic pain is defined by the International Association for the Study of Pain (IASP) as a chronic pain state initiated or caused by a lesion or disease of the central or peripheral somatosensory nervous system.…”

Section: Discussionmentioning

confidence: 99%

Association of Pain with Plasma C5a in Patients with Neuromyelitis Optica Spectrum Disorders During Remission

Tong¹,

Liu²,

Yang³

et al. 2022

NDT

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Objective To investigate the association of pain with plasma C5a levels and other related inflammatory cytokines in neuromyelitis optica spectrum disorders (NMOSD) patients during remission. Participants and Methods NMOSD patients (n = 87) and healthy controls (HC; n = 44) were consecutively recruited between January 2017 and April 2018. Plasma complement 5 (C5), C5a, interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β levels were detected. Visual Analogue Scale (VAS), ID pain scale, 24-item Hamilton Depression Scale (HAMD), Multiple Sclerosis Impact Scale (MSIS-29), and Kurtzke Expanded Disability Status Scale (EDSS) were used to evaluate the degree and types of pain, the existence of depression and anxiety, and the life quality and disability status of patients. Binary logistic regression equation was used to assess the association of pain with plasma C5a levels. Results Among the 87 NMOSD patients, 40 complained of pain that in 67.5% (27/40) of cases had a neuropathic component (ID pain ≥2). Plasma C5a, IL-6, TNF-α, and IL-1β levels were significantly elevated in NMOSD patients than in HC. Plasma C5 levels were negatively correlated with the time from sampling to the last relapse or disease onset. NMOSD patients with pain had higher plasma C5a levels, and they suffered from a higher disability, more anxiety, and worse life quality compared to those patients without pain. In NMOSD patients with pain, there were not significant differences between plasma levels of C5, C5a, IL-6, TNF-α, or IL-1β, regardless of neuropathic pain or not. Binary logistic regression showed that the OR of plasma C5a level was 1.002, with gender and EDSS score were identified as independent factors associated with pain in NMOSD. Conclusion NMOSD patients during remission had elevated C5a and related inflammatory cytokines levels in peripheral blood. Elevated C5a may have a unique role in the pathogenesis of pain in NMOSD patients.

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Section: Discussionmentioning

confidence: 99%

Association of Pain with Plasma C5a in Patients with Neuromyelitis Optica Spectrum Disorders During Remission

Tong¹,

Liu²,

Yang³

et al. 2022

NDT

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“…We also detected reciprocal expression of the sirtuin signaling pathway between MS WMLs and GMLs. Although sirtuins have been involved in immune activity and metabolic regulations, SIRT1, a NAD-dependent protein deacetylase, has been implicated in the pathogenesis of various neurodegenerative diseases including MS (24,49,50). Activation of this pathway may also be associated with localization of SIRT3, SIRT4, and SIRT7 in mitochondria (51), which is already affected due to ongoing demyelination, and thus, leads to differential activation in WMLs and GMLs in progressive MS brains, respectively.…”

Section: Discussionmentioning

confidence: 99%

Comparative Proteomic Profiling Identifies Reciprocal Expression of Mitochondrial Proteins Between White and Gray Matter Lesions From Multiple Sclerosis Brains

Kumar

Singh

et al. 2021

Front. Neurol.

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Multiple sclerosis (MS) is a chronic inflammatory and demyelinating disease of the central nervous system, where ongoing demyelination and remyelination failure are the major factors for progressive neurological disability. In this report, we employed a comprehensive proteomic approach and immunohistochemical validation to gain insight into the pathobiological mechanisms that may be associated with the progressive phase of MS. Isolated proteins from myelinated regions, demyelinated white-matter lesions (WMLs), and gray-matter lesions (GMLs) from well-characterized progressive MS brain tissues were subjected to label-free quantitative mass spectrometry. Using a system-biology approach, we detected increased expression of proteins belonging to mitochondrial electron transport complexes and oxidative phosphorylation pathway in WMLs. Intriguingly, many of these proteins and pathways had opposite expression patterns and were downregulated in GMLs of progressive MS brains. A comparison to the human MitoCarta database mapped the mitochondrial proteins to mitochondrial subunits in both WMLs and GMLs. Taken together, we provide evidence of opposite expression of mitochondrial proteins in response to demyelination of white- and gray-matter regions in progressive MS brain.

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“…SYN is expressed endogenously in neurons and it is involved in neurological processes such as neurotransmitter release and synaptic plasticity; nevertheless, its precise role in these processes is still unknown [31,32]. TPPP is a key player in the differentiation of the dividing progenitor oligodendrocytes (OLGs) by stabilizing the microtubule network, which provides differentiated cells for the myelination in the central nervous system [33][34][35]. TPPP regulates the microtubule network by its bundling and acetylation promoting activities, it inhibits the tubulin deacetylase enzymes histone deacetylase 6 (HDAC6) and sirtuin-2 (SIRT2) [36].…”

Section: Simulation: a Ppdp Constrains Phenotype Spacementioning

confidence: 99%

The Sherpa hypothesis: Phenotype-Protecting Disordered Proteins stabilize the phenotypes of neurons and oligodendrocytes

Norris

Oláh

Krylov

et al. 2023

Preprint

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Intrinsically disordered proteins (IDPs) are central to many physiological functions and to various pathologies that include neurodegeneration. They can interact with numerous partner proteins. Here, we introduce the Sherpa hypothesis, according to which a subset of stable IDPs, which we term Phenotype-Preserving Disordered Proteins (PPDP), play a central role in protecting cell phenotypes from perturbations. To illustrate and test this hypothesis, we computer-simulate some salient features of how cells evolve and differentiate in the presence of either a single PPDP or two incompatible PPDPs. We relate this virtual experiment to the pathological interactions between two PPDPs, α-synuclein and Tubulin Polymerization Promoting Protein/p25, in neurodegenerative disorders. Finally, we discuss the implications of the Sherpa hypothesis for aptamer-based therapies of such disorders.

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SIRT1 decelerates morphological processing of oligodendrocyte cell lines and regulates the expression of cytoskeleton-related oligodendrocyte proteins

Cited by 11 publications

References 27 publications

Association of Pain with Plasma C5a in Patients with Neuromyelitis Optica Spectrum Disorders During Remission

Association of Pain with Plasma C5a in Patients with Neuromyelitis Optica Spectrum Disorders During Remission

Comparative Proteomic Profiling Identifies Reciprocal Expression of Mitochondrial Proteins Between White and Gray Matter Lesions From Multiple Sclerosis Brains

The Sherpa hypothesis: Phenotype-Protecting Disordered Proteins stabilize the phenotypes of neurons and oligodendrocytes

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