SIRT1 negatively regulates amyloid-beta-induced inflammation via the NF-κB pathway

Cao, Lining; Liu, Chao; Wang, F.; Wang, H.

doi:10.1590/1414-431x20132903

Cited by 54 publications

(40 citation statements)

References 38 publications

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“…SIRT1 is a NAD(+)‐dependent deacetylase and a critical regulator in various metabolic processes. SIRT1 can directly interact with RelA/P65, subunits of NF‐κB, and inhibit NF‐κB by deacetylating RelA/P65 at lysine 310, leading to the IκBa‐dependent nuclear export of NF‐κB . In addition to the SIRT1/ NFκB pathway, Atr also influences microglial activation.…”

Section: Discussionmentioning

confidence: 99%

Attractylone attenuates sepsis‐associated encephalopathy and cognitive dysfunction by inhibiting microglial activation and neuroinflammation

Tian

Liu

et al. 2019

J of Cellular Biochemistry

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Multiple studies demonstrated that sepsis is a life‐threatening state of organ dysfunction caused by infection and can induce neuroinflammation and cognitive impairment. The aim of this study was to evaluate the protective effects of attractylone (Atr) on sepsis‐associated encephalopathy (SAE) and cognitive dysfunction. Moreover, we studied the underlying molecular mechanisms. We used an LPS‐induced sepsis mouse model and evaluated the cognitive function with the Morris water maze and open field test. Neuronal damage in the hippocampus was assessed by immunohistochemical analysis. BV2 cells were used to identify the protective mechanism of Atr. The result showed that Atr attenuated LPS‐induced cognitive impairment, neural apoptosis, inflammatory factors, and microglial activation. The in vitro experiment showed that Atr promoted silent information regulator 1 (SIRT1) expression and suppressed NFκB expression. Downregulation of SIRT1 reversed the protective effect of Atr in the LPS condition. Moreover, Atr‐induced SIRT1 expression promoted BV2 from LPS‐induced M1 to M2 phenotype. Taken together, these results indicated that Atr was a potential therapeutic agent for SAE and cognitive dysfunction.

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Section: Discussionmentioning

confidence: 99%

Attractylone attenuates sepsis‐associated encephalopathy and cognitive dysfunction by inhibiting microglial activation and neuroinflammation

Tian

Liu

et al. 2019

J of Cellular Biochemistry

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“…Chronic inflammation caused by Ab has been widely reported. 52 RelA is a subunit of nuclear factorkappa B (NF-jB), a key regulator of the inflammation response. 53 The IjB kinase inhibitor of jB kinase epsilon (IKBKE) is an IjB kinase family member that can also activate the AKT and NF-jB pathways; IKBKE is also involved in the interleukin-1 (IL-1) signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA Expression Patterns Involved in Amyloid Beta–Induced Retinal Degeneration

Huang

Sun

Wang

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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Citation: Huang P, Sun J, Wang F, et al. MicroRNA expression patterns involved in amyloid beta-induced retinal degeneration. Invest Ophthalmol Vis Sci. 2017;58:172658: -173558: . DOI: 10.1167 PURPOSE. Dry age-related macular degeneration (AMD) is characterized by the accumulation of drusen under Bruch's membrane, and amyloid beta (Ab) is speculated to be one of the key pathologic factors. While the detrimental effects of Ab on retinas have been widely explored, Ab-induced epigenetic regulatory changes have yet to be fully investigated. We therefore aimed to identify the microRNA (miRNA) expression profiles in an Ab-induced mouse model of retinal degeneration.METHODS. C57BL/6 mice were intravitreally injected with Ab 1-40 or PBS and the eye tissues were collected for hematoxylin and eosin (H&E) staining, apoptosis immunofluorescence staining, and miRNA profiling. After filtering, 10 miRNAs and their target genes were chosen for quantitative RT-PCR (qRT-PCR) confirmations. Pathway analyses were employed for further bioinformatic analyses.RESULTS. Hematoxylin and eosin-stained sections of retinal pigment epithelium (RPE)/neural retina tissue demonstrated degenerative alterations, and immunofluorescence testing revealed apoptosis within the retina after Ab treatments. MicroRNA profiling revealed 61 miRNAs that were differentially expressed between the model and the control group. Among these, 38 miRNAs were upregulated (fold change > 1.5, P < 0.05) and 23 miRNAs were downregulated (fold change < 0.667, P < 0.05). Five of the 10 selected miRNAs (miR-142, miR-216, miR-155, miR-223, and miR-433) as well as several key target genes (CFH, IGF-1R, c-MET, and ABCA1) were confirmed by qRT-PCR analyses.CONCLUSIONS. Our study is the first to profile the miRNA expression patterns and suggests that Ab accumulation could lead to relevant biochemical alternations such as complement activation, barrier impairment, apoptosis, and positive feedback of Ab production.

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“…They were first discovered in yeast as a transcriptional repressor called silent information regulator 2 protein (Sir2) (Klar et al , 1979; Rine and Herskowitz, 1987). All eukaryotes encode sirtuins in their genomes as sirtuins have important functions in regulating cellular stress responses (Brunet et al , 2004; Dai et al , 2014; Maksin-Matveev et al , 2015), mitochondrial biogenesis (Brenmoehl and Hoeflich, 2013), apoptosis (Alcendor et al , 2004; Motta et al , 2004), metabolism (Purushotham et al , 2009), fatty acid oxidation (Hirschey et al , 2010), and inflammation (Cao et al , 2013; Liu and McCall, 2013). …”

Section: Pharmacologic Therapiesmentioning

confidence: 99%

Mitochondrial function in hypoxic ischemic injury and influence of aging

Ham

Raju

2017

Progress in Neurobiology

270

218

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Mitochondria are a major target in hypoxic/ischemic injury. Mitochondrial impairment increases with age leading to dysregulation of molecular pathways linked to mitochondria. The perturbation of mitochondrial homeostasis and cellular energetics worsens outcome following hypoxic-ischemic insults in elderly individuals. In response to acute injury conditions, cellular machinery relies on rapid adaptations by modulating posttranslational modifications. Therefore, post-translational regulation of molecular mediators such as hypoxia-inducible factor 1α (HIF-1α), peroxisome proliferator-activated receptor γ coactivator α (PGC-1α), c-MYC, SIRT1 and AMPK play a critical role in the control of the glycolytic-mitochondrial energy axis in response to hypoxic-ischemic conditions. The deficiency of oxygen and nutrients leads to decreased energetic reliance on mitochondria, promoting glycolysis. The combination of pseudohypoxia, declining autophagy, and dysregulation of stress responses with aging adds to impaired host response to hypoxic-ischemic injury. Furthermore, intermitochondrial signal propagation and tissue wide oscillations in mitochondrial metabolism in response to oxidative stress are emerging as vital to cellular energetics. Recently reported intercellular transport of mitochondria through tunneling nanotubes also play a role in the response to and treatments for ischemic injury. In this review we attempt to provide an overview of some of the molecular mechanisms and potential therapies involved in the alteration of cellular energetics with aging and injury with a neurobiological perspective.

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SIRT1 negatively regulates amyloid-beta-induced inflammation via the NF-κB pathway

Cited by 54 publications

References 38 publications

Attractylone attenuates sepsis‐associated encephalopathy and cognitive dysfunction by inhibiting microglial activation and neuroinflammation

Attractylone attenuates sepsis‐associated encephalopathy and cognitive dysfunction by inhibiting microglial activation and neuroinflammation

MicroRNA Expression Patterns Involved in Amyloid Beta–Induced Retinal Degeneration

Mitochondrial function in hypoxic ischemic injury and influence of aging

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