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Epigenetic Alterations in Alzheimer’s Disease and Its Therapeutic and Dietary Interventions
Published in Atanu Bhattacharjee, Akula Ramakrishna, Magisetty Obulesu, Phytomedicine and Alzheimer’s Disease, 2020
P. M. Aswathy, C. M. Shafeeque, Moinak Banerjee
An investigation of the methylation status of DNA repair genes in AD subjects, compared with controls, did not find any increased promoter methylation in peripheral blood of AD patients (Coppedè et al. 2017). A cross-tissue analysis of methylomic variation in AD, using samples from four independent human post-mortem brain cohorts, identified a differentially hypermethylated region in the Ankyrin 1 (ANK1) gene, that was associated with neuropathology in the entorhinal cortex (and also in the superior temporal gyrus and prefrontal cortex), the primary site of AD manifestation (Lunnon et al. 2014). A dynamic regulation of DNA methylation in the human cerebral cortex has been reported throughout the lifespan, with hypermethylation of vinexin (encoding a cell adhesion molecule expressed in neurons and glia) (Ito et al. 2007) and hypomethylation of S100A2 (a member of the S100 family of calcium-binding proteins), compared with other non-AD subjects older than 60 years (Siegmund et al. 2007). Hypomethylation of CREB5, encoding a transcription factor implicated in synaptic plasticity and cognition, was reported in the prefrontal cortex from AD and normal subjects (Zukin 2009). Hypomethylation of the mitochondrial DNA (mtDNA) D-loop region was reported in peripheral blood DNA of LOAD patients (Stoccoro et al. 2017). Another study reported hypermethylation in the opioid receptor delta 1 (OPRD1, a member of the opioid family of G-protein-coupled receptors) promoter region, and discussed its role in influencing the risk of AD.
Mechanism of Action of Isotretinoin
Published in Ayse Serap Karadag, Berna Aksoy, Lawrence Charles Parish, Retinoids in Dermatology, 2019
Clinical observations suggest that wound healing may be altered in patients treated with systemic isotretinoin (194). Mechanical dermabrasion and fully ablative laser surgery are not recommended in the setting of systemic isotretinoin treatment (195). p53, which is upregulated by isotretinoin, impairs wound healing, whereas inhibition of p53 enhances wound healing (196,197). p53 is an inducer of S100A2 (198), which forms a complex with p53 that potentiates p53-mediated transcription and increases p53 expression (199). It has recently been demonstrated in epithelial-specific S100A2 transgenic mice that the p53-S100A2 positive feedback loop negatively regulates epithelialization in cutaneous wound healing (175).
Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
Many of the S100 protein genes are clustered in the epidermal differentiation complex in human chromosome 1q21, which includes the PSORS4 locus, and 13 S100 proteins (S100A2, S100A3, S100A4, S100A6, S100A7, S100A8, S100A9, S100A10, S100A11, S100A12, S100A15, S100B, and S100P) are expressed in normal and/or diseased epidermis (Eckert et al. 2004). Of these, the following are overexpressed in psoriasis; some are regulated under the aryl hydrocarbon receptor nuclear translocator (Arnt)/Hif1b and are known to have angiogenic properties:
A shotgun proteomic approach reveals novel potential salivary protein biomarkers for asthma
Published in Journal of Asthma, 2022
Orapan Poachanukoon, Sittiruk Roytrakul, Sittichai Koontongkaew
S100A2 is a member of a family of the S100/calgranulin Ca++‐binding proteins implicated in a number of inflammatory diseases (28). Little is known about the role of S100A2 in human asthmatics compared to S100A8/A9 (29,30) and S100A12 (31,32). S100A2 gene was less upregulated in bronchial epithelial cells of asthmatic patients than normal subjects in response to ozone exposure and virus infection (33). Little is known about the function of ZNF263, except that it may have a repressive effect on gene transcription and often binds intragenic regions (34). ZNF263 is involved in the development of the many complex diseases associated with stress and aging (35).
Integrative analysis identifies an immune-relevant epigenetic signature for prognostication of non-G-CIMP glioblastomas
Published in OncoImmunology, 2021
Anan Yin, Zhende Shang, Amandine Etcheverry, Yalong He, Marc Aubry, Nan Lu, Yuhe Liu, Jean Mosser, Wei Lin, Xiang Zhang, Yu Dong
In our study, the biological implications of the multimarker signature were preliminarily exemplified by one CpG component and its relevant gene S100A2. S100A2 is a member of S100 family, encoding an EF hand calcium-binding protein that regulates protein phosphorylation, cytoskeletal components, and calcium homeostasis. Aberrant alterations in DNA methylation and gene expression of S100A2 have been widely reported in various cancers,27,41,42 exhibiting a protumorigenic role with DNA hypomethylation-induced gene avtivation in some cancers (e.g., ovarian and pancreatic cancers) whist a tumor suppressor role with promoter hypermethylation-associated silencing of S100A2 in other cancers (e.g., prostate and breast cancers). In this study, S100A2 expression was found to be increased with glioma grade, and negatively correlated with the single CpG methylation at non-CGI region. It is also noted that S100A2 appear to be expressed with high variability in GBM cells or samples with unmethylated CpG, which indicates the permissive but not determinant role of non-CGI DNA hypomethylation in gene re-expression. In vitro experimental data showed that S100A2 knockdown reduced cell proliferation by arresting the cell cycle at the G2/M phase but not at the S phase, promoted cell apoptosis, and inhibited cell invasion and migration in GBM cell lines. All those data supported a potent GBM-promoting role of S100A2. Interestingly, reduced expression of S100A2 was found to be associated with reduced NF-κB activity in GBM cell lines. Increased evidence has shown that NF-κB activation is a major driver for malignant progression of GBMs. Therefore, the pro-tumor role of S100A2 might be due to its regulatory effects on NF-κB activity in GBMs.43 The cellular experiment results were mostly in consistent with GSEA results; high-risk tumors (with higher S100A2 expression; data not shown) in each dataset were mostly enriched with gene sets relevant to the regulation of cell-cell adhesion, cell migration, apoptotic pathway, and NF-κB activity. Considering the immune implications of the epigenetic signature, we also tested the transcriptional correlation of S100A2 on a reported set of glioma-related immunosuppressive factors, and identified a co-expression pattern of S100A2 and FGL2, a multimodality regulator of glioma-mediate immune suppression.27 FGL2 has been reported to have multiple roles in tumor immune suppression via modulating M2 polarization, T cell subpopulation and immune checkpoints.27 Despite not knowing the molecular mechanism of S100A2 on expression of FGL2, it is reasoned that the epigenetic signature may have impacts on GBM cell immunity partially via influencing FGL2 activity. Gene related to other identified CpGs have also been reported to have implications in immunity and cancer including gliomas such as COX4I2,44 ELMO3,45 TRIM40,46,47 and GATA4.48,49 Future studies will be needed to explore the biological relevance of the specific molecular mechanism of S100A2 on FGL2 expression and glioma immunity, and the biological relevance of other identified CpGs and relevant genes.