Regulation of the tubulin polymerization-promoting protein by Ca2+/S100 proteins

Doi, Seita; Fujioka, Naoki; Ohtsuka, Satomi; Kondo, Rina; Yamamoto, Maho; Denda, Miwako; Kanayama, Naoki; Hatano, Naoya; Morishita, Ryo; Hasegawa, Takafumi; Tokumitsu, Hiroshi

doi:10.1016/j.ceca.2021.102404

Cited by 9 publications

(9 citation statements)

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“…What factors may lead to weakened functional connectivity in hippocampal circuits in response to repeated stress? Earlier studies have reported that chronic, but not acute stress, causes dendritic shortening and debranching and synaptic loss on apical branches of pyramidal cells in areas CA3 and CA1 (Magariños and McEwen, 1995;Conrad et al, 1999;Sousa et al, 2000;Sandi et al, 2003). Hitherto, the functional consequences of these structural changes have not been well understood.…”

Section: Discussionmentioning

confidence: 99%

“…This dichotomy in the impact of acute and chronic stress has also been observed in the hippocampus, a brain region crucial for the acquisition and consolidation of declarative memory. At the cellular level, chronic, but not acute stress, causes dendritic shrinkage and debranching (Watanabe et al, 1992;Sousa et al, 2000) and decreases the number of synaptic contacts (spines) on principal hippocampal pyramidal neurons (Magariños et al, 1997;Sandi et al, 2003). Further, earlier studies employing both ex vivo electrophysiology and in vivo tetrode recordings report that chronic stress also alters the functionality of hippocampal pyramidal cells.…”

Section: Introductionmentioning

confidence: 98%

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Differential Impact of Acute and Chronic Stress on CA1 Spatial Coding and Gamma Oscillations

Tomar

Polygalov

McHugh

2021

Front. Behav. Neurosci.

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Chronic and acute stress differentially affect behavior as well as the structural integrity of the hippocampus, a key brain region involved in cognition and memory. However, it remains unclear if and how the facilitatory effects of acute stress on hippocampal information coding are disrupted as the stress becomes chronic. To examine this, we compared the impact of acute and chronic stress on neural activity in the CA1 subregion of male mice subjected to a chronic immobilization stress (CIS) paradigm. We observed that following first exposure to stress (acute stress), the spatial information encoded in the hippocampus sharpened, and the neurons became increasingly tuned to the underlying theta oscillations in the local field potential (LFP). However, following repeated exposure to the same stress (chronic stress), spatial tuning was poorer and the power of both the slow-gamma (30–50 Hz) and fast-gamma (55–90 Hz) oscillations, which correlate with excitatory inputs into the region, decreased. These results support the idea that acute and chronic stress differentially affect neural computations carried out by hippocampal circuits and suggest that acute stress may improve cognitive processing.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Differential Impact of Acute and Chronic Stress on CA1 Spatial Coding and Gamma Oscillations

Tomar

Polygalov

McHugh

2021

Front. Behav. Neurosci.

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“…These dualities in the functions of specific isoforms appears to rely on complex and mechanistically still unclear bidirectional interplay of S100 isoforms with key cellular factors and cancer drivers, e.g., p53 [ 84 ], Wnt/β-catenin [ 85 ], p38 Mitogen-Activated Protein Kinases (p38 MAPK) [ 86 ], ERK [ 87 ], AKT [ 88 ], p21 [ 89 ] or NFκB [ 90 ], among others. Cell migration is also affected by numerous S100 proteins, which modulate the cytoskeleton dynamic and integrity [ 91 , 92 , 93 , 94 ], thereby also impacting the secretory pathways and the integrity of cell–cell junctions. Further supporting the importance of S100 specific members in cell motility and cancer metastasis, matrix metalloproteinase (MMP) expression/activity and degradation of the extra-cellular matrix (ECM) is also under the control of S100 proteins such as S100A4, S100A8, S100A9, S100A10 and S100A14 [ 95 , 96 , 97 , 98 ].…”

Section: General Overview Of S100 Proteins Functionsmentioning

confidence: 99%

S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma

Delangre

Oppliger

Berkcan

et al. 2022

IJMS

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Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent and slow progressing hepatic pathology characterized by different stages of increasing severity which can ultimately give rise to the development of hepatocellular carcinoma (HCC). Besides drastic lifestyle changes, few drugs are effective to some extent alleviate NAFLD and HCC remains a poorly curable cancer. Among the deregulated molecular mechanisms promoting NAFLD and HCC, several members of the S100 proteins family appear to play an important role in the development of hepatic steatosis, non-alcoholic steatohepatitis (NASH) and HCC. Specific members of this Ca2+-binding protein family are indeed significantly overexpressed in either parenchymal or non-parenchymal liver cells, where they exert pleiotropic pathological functions driving NAFLD/NASH to severe stages and/or cancer development. The aberrant activity of S100 specific isoforms has also been reported to drive malignancy in liver cancers. Herein, we discuss the implication of several key members of this family, e.g., S100A4, S100A6, S100A8, S100A9 and S100A11, in NAFLD and HCC, with a particular focus on their intracellular versus extracellular functions in different hepatic cell types. Their clinical relevance as non-invasive diagnostic/prognostic biomarkers for the different stages of NAFLD and HCC, or their pharmacological targeting for therapeutic purpose, is further debated.

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“…Expression of the tubulin chaperone TBCA has been found to be altered in PD dementia patients, suggesting that defects in synaptic transmission and axonal function are early events in the pathogenesis of PD. 27 Interestingly, two long intergenic non-protein coding RNA genes (lincRNAs; LINC01262 and LINC01375) were nominated as potential subtop hits. Recent studies have shown that lincRNAs might alter the expression of PD-linked genes, such as PINK1, LRRK2, and SNCA.…”

Section: Discussionmentioning

confidence: 99%

Polygenic Resilience Modulates the Penetrance of Parkinson Disease Genetic Risk Factors

Liu

Dehestani

Blauwendraat

et al. 2022

Annals of Neurology

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The aim of the current study is to understand why some individuals avoid developing Parkinson disease (PD) despite being at relatively high genetic risk, using the largest datasets of individual-level genetic data available. Methods: We calculated polygenic risk score to identify controls and matched PD cases with the highest burden of genetic risk for PD in the discovery cohort (International Parkinson's Disease Genomics Consortium, 7,204 PD cases and 9,412 controls) and validation cohorts (Comprehensive Unbiased Risk Factor Assessment for Genetics and Environment in Parkinson's Disease, 8,968 cases and 7,598 controls; UK Biobank, 2,639 PD cases and 14,301 controls; Accelerating Medicines Partnership-Parkinson's Disease Initiative, 2,248 cases and 2,817 controls). A genome-wide association study meta-analysis was performed on these individuals to understand genetic variation associated with resistance to disease. We further constructed a polygenic resilience score, and performed multimarker analysis of genomic annotation (MAGMA) gene-based analyses and functional enrichment analyses. Results: A higher polygenic resilience score was associated with a lower risk for PD (β = À0.054, standard error [SE] = 0.022, p = 0.013). Although no single locus reached genome-wide significance, MAGMA gene-based analyses nominated TBCA as a putative gene. Furthermore, we estimated the narrow-sense heritability associated with resilience to PD (h 2 = 0.081, SE = 0.035, p = 0.0003). Subsequent functional enrichment analysis highlighted histone methylation as a potential pathway harboring resilience alleles that could mitigate the effects of PD risk loci. Interpretation: The present study represents a novel and comprehensive assessment of heritable genetic variation contributing to PD resistance. We show that a genetic resilience score can modify the penetrance of PD genetic risk factors and therefore protect individuals carrying a high-risk genetic burden from developing PD.

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Regulation of the tubulin polymerization-promoting protein by Ca2+/S100 proteins

Cited by 9 publications

References 50 publications

Differential Impact of Acute and Chronic Stress on CA1 Spatial Coding and Gamma Oscillations

Differential Impact of Acute and Chronic Stress on CA1 Spatial Coding and Gamma Oscillations

S100 Proteins in Fatty Liver Disease and Hepatocellular Carcinoma

Polygenic Resilience Modulates the Penetrance of Parkinson Disease Genetic Risk Factors

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