microRNA–SIRT‐1 interactions: key regulators of adult skeletal muscle homeostasis?

McCormick, Rachel; Goljanek‐Whysall, Katarzyna

doi:10.1113/jp274233

Cited by 4 publications

(3 citation statements)

References 4 publications

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“…The sirtuin (SIRT) family, consisting of seven members (SIRT1-7), are a conserved superfamily of nicotinamide adenine dinucleotide + -dependent deacetylases that are involved in the regulation of energy metabolism, aging, cell apoptosis, gene transcription, tumor development, autoimmune inflammation and epigenetics (6). SIRTs serve notable functions in metabolic and inflammatory processes.…”

Section: Introductionmentioning

confidence: 99%

Abnormal expression of SIRTs in psoriasis: Decreased expression of SIRT 1-5 and increased expression of SIRT 6 and 7

et al. 2019

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The prevalence of psoriasis is increasing, and poses a serious risk to human health and quality of life. Psoriasis, a chronic immune-mediated skin disease with epidermal hyperkeratosis and parakeratosis, is associated with numerous complications, including metabolic syndromes that are regulated by sirtuins (SIRTs) via deacetylation. As they serve a necessary function in inflammation and metabolism, SIRTs are considered to link inflammation and metabolic syndrome. Previous studies have indicated that SIRTs serve a function in the pathophysiology of psoriasis, but to date no detailed research has been conducted investigating the expression levels and patterns of SIRTs in psoriasis. The present study investigated the abnormal expression of SIRTs in psoriasis and provided a theoretical foundation for the treatment and prognosis of psoriasis. Tumor necrosis factor (TNF)-α-stimulated HaCaT cells and an imiquimod-induced psoriasis mouse model were used to produce in vitro and in vivo models, respectively. Psoriasis clinical specimens (psoriasis area and severity index >10; n=22) and normal group specimens (n=22) were obtained from human subjects. The mRNA and protein expression levels in human and mouse skin lesions and TNF-α-stimulated HaCaT cells were detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting, and compared with the control groups. The expression patterns of SIRT proteins were investigated using immunofluorescence (IF) staining. The expression levels of SIRT1, SIRT2, SIRT3, SIRT4 and SIRT5 were downregulated while those of SIRT6 and SIRT7 were upregulated in skin lesions and TNF-α-stimulated HaCaT cells compared with the control group as determined by RT-qPCR, western blotting and IF. Statistically significant differences were observed in vivo and in vitro . P-values of SIRT1-7 mRNA are less than 0.05 in RT-qPCR, and the P-values of SIRT1-7 proteins are less than 0.05 except for SIRT4 in the western blot analysis. SIRTs serve notable functions in severe psoriasis dermatitis, with the overexpression of SIRT6 and SIRT7 potentially induced by the adaptive immune response, and the downregulation of SIRT1, SIRT2, SIRT3, SIRT4 and SIRT5 may be a result of an internal environment imbalance in vivo . Psoriasis is an inflammation and metabolism-associated disease mediated by the SIRT family. The present results provide a novel potential mechanism and strategy for the treatment of psoriasis by modulating the function and expression of SIRTs.

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Section: Introductionmentioning

confidence: 99%

Abnormal expression of SIRTs in psoriasis: Decreased expression of SIRT 1-5 and increased expression of SIRT 6 and 7

et al. 2019

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“…Sirtuin (SIRT) is a family of (NAD + )-dependent deacetylases, involved in cell apoptosis, gene transcription, tumor development, autoimmune inflammation and epigenetic modification processes. Specifically, SIRT1 regulates inflammation-associated signaling pathways [ 91 , 92 ]. Hwang et al showed that HDAC-1 is overexpressed and SIRT1 displays a decreased expression in skin biopsies of patients with PsO [ 93 ].…”

Section: Histone Modificationsmentioning

confidence: 99%

Contribution of the Environment, Epigenetic Mechanisms and Non-Coding RNAs in Psoriasis

et al. 2022

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Despite the increasing research and clinical interest in the predisposition of psoriasis, a chronic inflammatory skin disease, the multitude of genetic and environmental factors involved in its pathogenesis remain unclear. This complexity is further exacerbated by the several cell types that are implicated in Psoriasis’s progression, including keratinocytes, melanocytes and various immune cell types. The observed interactions between the genetic substrate and the environment lead to epigenetic alterations that directly or indirectly affect gene expression. Changes in DNA methylation and histone modifications that alter DNA-binding site accessibility, as well as non-coding RNAs implicated in the post-transcriptional regulation, are mechanisms of gene transcriptional activity modification and therefore affect the pathways involved in the pathogenesis of Psoriasis. In this review, we summarize the research conducted on the environmental factors contributing to the disease onset, epigenetic modifications and non-coding RNAs exhibiting deregulation in Psoriasis, and we further categorize them based on the under-study cell types. We also assess the recent literature considering therapeutic applications targeting molecules that compromise the epigenome, as a way to suppress the inflammatory cutaneous cascade.

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“…It is homologous to yeast Sir2, and the SIRT1 gene is located at chromosome 10q21.3 5,6 . SIRT1 is primarily located at the nucleus and is involved in regulation of skeletal muscle formation and atrophy 7 . The role of SIRT1 in some metabolism‐related diseases has been discussed.…”

Section: Introductionmentioning

confidence: 99%

Gene polymorphisms of SIRT1 in patients with rheumatoid arthritis

Zhou

et al. 2021

Int J of Rheum Dis

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Aim Previous studies have shown that silent information regulator 1 (SIRT1) expression is elevated in rheumatoid arthritis (RA) patients. However, whether gene polymorphisms in SIRT1 gene associated with RA in a Chinese Han population remains to be discussed. Method In this case‐control study, 529 RA patients and 700 healthy controls were selected, and association of 11 SIRT1 gene polymorphisms (rs12415800, rs3740051, rs932658, rs3740053, rs7895833, rs10509291, rs33957861, rs7069102, rs2273773, rs3818292, rs1467568) with RA susceptibility was evaluated. Results Frequency of GA+GG genotype of rs3740051 in RA patients was significantly lower than that in healthy controls (P = .037). Frequencies of GC and GC+GG genotypes of rs7069102 were significantly lower than those in healthy controls (P = .036, P = .047). Frequencies of GA and GA+GG genotypes of rs1467568 were lower in RA patients as compared to those in healthy controls (P = .011, P = .013). For rs2273773, RA patients who carried the T allele had higher number of tender joints than patients who carried the C allele (P = .033). Other polymorphisms did not associate with RA risk. Conclusion The findings suggest that rs3740051, rs7069102 and rs1467568 variants in SIRT1 gene are related to RA susceptibility in a Chinese Han population.

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microRNA–SIRT‐1 interactions: key regulators of adult skeletal muscle homeostasis?

Cited by 4 publications

References 4 publications

Abnormal expression of SIRTs in psoriasis: Decreased expression of SIRT 1-5 and increased expression of SIRT 6 and 7

Abnormal expression of SIRTs in psoriasis: Decreased expression of SIRT 1-5 and increased expression of SIRT 6 and 7

Contribution of the Environment, Epigenetic Mechanisms and Non-Coding RNAs in Psoriasis

Gene polymorphisms of SIRT1 in patients with rheumatoid arthritis

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