SIRT1 and NAD as regulators of ageing

Rehan, Leopold; Laszki-Szcząchor, Krystyna; Sobieszczańska, Małgorzata; Polak−Jonkisz, Dorota

doi:10.1016/j.lfs.2014.03.015

Cited by 47 publications

(25 citation statements)

References 39 publications

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“…MicroRNA-138 (miR-138) is reported to participate in oncogenesis and axon regeneration, but it is not clear whether miR-138 plays a role in inflammation or sepsis [15,16]. Silence information regulator 1 (SIRT1) is an NAD+ dependent class III histone deacetylase that modulates intracellular activities through transcription regulation in several separate cellular functions [17,18]. Recently, SIRT1 was demonstrated to inhibit inflammatory reactions 6.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-138 Aggravates Inflammatory Responses of Macrophages by Targeting SIRT1 and Regulating the NF-κB and AKT Pathways

Bai

Zhang

Yang

et al. 2018

Cell Physiol Biochem

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Background/Aims: With increased understanding of sepsis, mortality is decreasing. However, there is still a lack of effective therapeutic strategy. The inflammatory response of macrophages is critical during sepsis. Methods: Macrophages were stimulated with LPS. Western blotting and qRT-PCR were used to detect inflammatory responses. Then, the inhibitor of microRNA-138 was transfected and Western blotting, qRT-PCR, H&E staining and ELISA were used to verify the role of microRNA-138 in inflammation. Then target gene prediction databases were used to predict the potential target of microRNA-138. Both animal and cell models under LPS challenges were established to verify the regulation of SIRT1 and microRNA-138 during inflammation. Results: The present study showed that microRNA-138 was increased in macrophages stimulated with LPS. Additionally, the NF-κB and AKT pathways were both activated. The pre-treatment of microRNA-138 inhibitor decreased inflammatory factors, downregulated the NF-κB pathway, activated the AKT pathway and protected against organ damage in mice challenged with LPS. SIRT1 was demonstrated as a potential target of microRNA-138In macrophages stimulated with LPS, the inhibition effect of microRNA-138 inhibitor on inflammation was lost by SIRT1 siRNA pre-treatment. In the animal model, the protective effect of microRNA-138 antagomir disappeared in SIRT1 knockout mice. Conclusion: We demonstrated that miR-138 participated in the inflammatory process by inhibiting SIRT1 and activating the NF-κB pathway.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-138 Aggravates Inflammatory Responses of Macrophages by Targeting SIRT1 and Regulating the NF-κB and AKT Pathways

Bai

Zhang

Yang

et al. 2018

Cell Physiol Biochem

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“…In addition, SIRT1 activation with resveratrol has been linked to protection against oxidative stress, metabolic decline and inflammation, while conferring cardiovascular and neural protection against nutrient stressors in rodents and non-human primates [13]. Furthermore, SIRT1 is shown to attenuate AD pathogenesis, synaptic plasticity, and learning and memory [14,15], and a reduction in SIRT1 activity in neurons is suggested as an early prognostic marker for AD [16,17]. However, it is unclear whether SIRT1 signaling provides the mechanism basis by which hUC-MSCs and resveratrol offer neuroprotection in the setting of AD.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol promotes hUC-MSCs engraftment and neural repair in a mouse model of Alzheimer’s disease

Wang

Yang

et al. 2018

Behavioural Brain Research

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Mesenchymal stem cell transplantation is a promising therapeutic approach for Alzheimer’s disease (AD). However, poor engraftment and limited survival rates are major obstacles for its clinical application. Resveratrol, an activator of silent information regulator 2, homolog 1 (SIRT1), regulates cell destiny and is beneficial for neurodegenerative disorders. The present study is designed to explore whether resveratrol regulates the fate of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) and whether hUC-MSCs combined with resveratrol would be efficacious in the treatment of neurodegeneration in a mouse model of AD through SIRT1 signaling. Herein, we report that resveratrol facilitates hUC-MSCs engraftment in the hippocampus of AD mice and resveratrol enhances the therapeutic effects of hUC-MSCs in this model as demonstrated by improved learning and memory in the Morris water maze, enhanced neurogenesis and alleviated neural apoptosis in the hippocampus of the AD mice. Moreover, hUC-MSCs and resveratrol jointly regulate expression of hippocampal SIRT1, PCNA, p53, ac-p53, p21, and p16. These data strongly suggests that hUC-MSCs transplantation combined with resveratrol may be an effective therapy for AD.

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“…SIRT1 is a NAD+-dependent protein deacetylase, which regulates energy, longevity, and circadian clock rhythm [16,17]. SIRT1 is closely related with nervous system [18,19].…”

Section: Introductionmentioning

confidence: 99%

Paliperidone Protects SH-SY5Y Cells Against MK-801-Induced Neuronal Damage Through Inhibition of Ca2+ Influx and Regulation of SIRT1/miR-134 Signal Pathway

Zhu

Zhang

et al. 2015

Mol Neurobiol

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Schizophrenia is a serious psychotic disease. Recently, increasing evidences support that neurodegeneration occurs in the brain of schizophrenia patients with progressive morphological changes. Paliperidone, an atypical antipsychotic drug, could attenuate psychotic symptom and protect neurons from different stressors. However, the underlying mechanisms are largely unknown. In this study, we used SH-SY5Y cells to evaluate the neuroprotective capability of paliperidone against the neurotoxicity induced by N-methyl-D-aspartate receptor antagonist, MK-801. And, we also explored the possible molecular mechanism. Neurotoxicity of 100 μM MK-801, which reduced the cell viability, was diminished by 100 μM paliperidone using MTT and LDH assays (both p < 0.05). Analysis with Hoechst 33342/PI double staining demonstrated that exposure to MK-801 (100 μM) for 24 h led to the death of 30 % of cultured cells (p < 0.05). Moreover, the patch clamp technique was employed to detect voltage calcium channel changes; the results showed that paliperidone effectively blocked the Ca(2+) influx through inhibiting the voltage-gated calcium channels (p < 0.05). Furthermore, paliperidone significantly reversed MK-801 induced increase of SIRT1 and decrease of miR-134 expression (both p < 0.05). Finally, SIRT1 inhibitor nicotinamide blocked MK-801 injury effects and suppressed miR-134 expression. Taken together, our results demonstrated that paliperidone could protect SH-SY5Y cells against MK-801 induced neurotoxicity via inhibition of Ca(2+) influx and regulation of SIRT1/miR-134 pathway, providing a promising and potential therapeutic target for schizophrenia.

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SIRT1 and NAD as regulators of ageing

Cited by 47 publications

References 39 publications

MicroRNA-138 Aggravates Inflammatory Responses of Macrophages by Targeting SIRT1 and Regulating the NF-κB and AKT Pathways

MicroRNA-138 Aggravates Inflammatory Responses of Macrophages by Targeting SIRT1 and Regulating the NF-κB and AKT Pathways

Resveratrol promotes hUC-MSCs engraftment and neural repair in a mouse model of Alzheimer’s disease

Paliperidone Protects SH-SY5Y Cells Against MK-801-Induced Neuronal Damage Through Inhibition of Ca2+ Influx and Regulation of SIRT1/miR-134 Signal Pathway

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