Sirt1: Role Under the Condition of Ischemia/Hypoxia

Meng, Xiaofei; Tan, Jin; Li, Mengmeng; Song, Shuling; Miao, Yuyang; Zhang, Qiang

doi:10.1007/s10571-016-0355-2

Cited by 133 publications

(103 citation statements)

References 93 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interestingly, in the present study, we demonstrated that Sirt1 could also regulate miRNA expression. Recently, accumulating evidence has strongly implied that SIRT1, a highly conserved NAD‐dependent deacetylase that promotes cell survival under oxidative stress could deacetylate various transcription factors including NF‐κB, which in turn regulate downstream cellular pathways associated with oxidative stress . Therefore, activation of SIRT1‐mediated NF‐κB deacetylation to suppress oxidative stress and inflammation represents a potentially treatment strategy for RA.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol ameliorates rheumatoid arthritis via activation of SIRT1‐Nrf2 signaling pathway

et al. 2019

View full text Add to dashboard Cite

The present study was designed to explore the biological role of resveratrol (RES) in rheumatoid arthritis (RA) and the underlying mechanism. The adjuvant‐induced arthritic rats were administered RES on the 12th day after model establishment, and then arthritis assessment, oxidative stress measurement, histological examination, and immunohistochemical staining were performed. The primary rat fibroblast‐like synoviocytes (FLS) were isolated and treated with RES in vitro and then cell proliferation and apoptosis assay were examined. Chromatin immunoprecipitation assay, luciferase reporter assay, intracellular reactive oxygen species (ROS) determination, western blot, and quantitative real time‐polymerase chain reaction (qRT‐PCR) were performed to investigate the mechanisms. RES administration decreased arthritis scores and serum levels of antioxidant enzymes, attenuated paw swelling, synovial hyperplasia, inflammatory cell infiltration, and cartilage degradation, as well as inhibited synoviocyte proliferation in synovial tissues. Further investigation indicated that RES inhibited ROS production and FLS proliferation through activating the silent information regulator 1 (SIRT1)/nuclear factor erythroid 2‐related factor 2 (Nrf2) signaling pathway. NF‐κB was confirmed to negatively regulate miR‐29a‐3p and miR‐23a‐3p expression by directly binding to its promoter. Mechanistic analyses further revealed that Kelch‐like erythroid cell‐derived protein with CNC homology (ECH)‐associated protein 1 (Keap1), a negative regulator of Nrf2, was a downstream target of miR‐29a‐3p, while miR‐23a‐3p directly targeted cullin3 (cul3), a master regulator of ubiquitination and degradation of Nrf2. Together, the present study provided evidence that RES ameliorated RA through activation of Nrf2‐ARE signaling pathway via SIRT1/NF‐κB/miR‐29a‐3p/Keap1 and SIRT1/NF‐κB/miR‐23a‐3p/cul3 signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Resveratrol ameliorates rheumatoid arthritis via activation of SIRT1‐Nrf2 signaling pathway

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Sirt1 deficiency or knockdown attenuated the neuroprotection of NAD + in ischemic stroke 13, 42 . Sirt1 mediated deacetylation of p53, reducing its pro-apoptotic effects; and it also deacetylated NF-κB, reducing its pro-inflammatory effects 43 . p53 mediates apoptosis through several pathways and results in activation of caspase-3, the executor of cell death 44 .…”

Section: Discussionmentioning

confidence: 99%

Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD ⁺ /Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats

Manaenko

Bian

et al. 2017

Stroke

View full text Add to dashboard Cite

Background and purpose Energy depletion is a critical factor leading to cell death and brain dysfunction after ischemic stroke. In this study we investigated whether energy depletion is involved in hyperglycemia-induced hemorrhagic transformation (HT) after ischemic stroke and determined the pathway underlying the beneficial effects of hyperbaric oxygen (HBO). Methods After 2 hours MCAO, hyperglycemia was induced by injecting of 50% dextrose (6 ml/kg) intraperitoneally at the onset of reperfusion. Immediately after it rats were exposed to HBO at 2 atmospheres absolutes (ATA) for 1 hour. ATP synthase inhibitor Oligomycin A (Olig A), NAMPT inhibitor FK866 or Sirt1 siRNA was administrated for interventions. Infarct volume, hemorrhagic volume, neurobehavioral deficits were recorded; the level of blood glucose, ATP and NAD+ and the activity of NAMPT were monitored; the expression of Sirt1, acetylated P53, acetylated NF-κB and cleaved caspase 3 were detected by western blots; the activity of MMP-9 was assayed by zymography. Results Hyperglycemia deteriorated energy metabolism and reduced the level of ATP and NAD+, exaggerated hemorrhagic transformation, blood-brain barrier disruption and neurological deficits after MCAO. HBO treatment increased the levels of the ATP and NAD+ and consequently increased Sirt1, resulting in attenuation of hemorrhagic transformation, brain infarction as well as improvement of neurological function in hyperglycemic MCAO rats. Conclusion HBO induced activation of ATP/NAD+/Sirt1 pathway and protected blood-brain barrier in hyperglycemic MCAO rats. HBO might be promising approach for treatment of acute ischemic stroke patients, especially patients with diabetes or treated with rtPA.

show abstract

“…Sirt1 is another deacetylase that modulates transcriptional activation in ischaemia/hypoxia (Meng et al . ).…”

Section: Hypoxia‐responsive Transcriptional Regulationmentioning

confidence: 97%

Respiratory gases and the regulation of transcription

Cummins

Keogh

2016

Experimental Physiology

View full text Add to dashboard Cite

Eoin obtained a bachelor's degree in Pharmacology (2002) and a PhD (2007) from University College Dublin (UCD). During his postdoctoral career, Eoin became interested in the potential role for carbon dioxide as a modulator of inflammatory and immune signalling, in particular in relation to nuclear factor-κB signalling. The first paper on this work was published in the Journal of Immunology in 2010. In 2013, Eoin obtained his first faculty position as a Lecturer/Assistant Professor in Physiology in the School of Medicine UCD, and he currently leads a research group focused on the effects of hypercapnia on inflammation and immunity. New Findings r What is the topic of this review? This review highlights the transcriptional consequences for decreased cellular O 2 levels (hypoxia) and increased cellular CO 2 levels (hypercapnia). r What advances does it highlight?We discuss recent advances in our understanding of the cellular response to hypoxia and consider the potential cross-talk between O 2 -and CO 2 -dependent transcriptional regulation.Oxygen and carbon dioxide are the substrate and product of aerobic metabolism, respectively. Thus, the levels of these physiological gases are inextricably linked in physiological and pathophysiological conditions. Increased mitochondrial consumption of O 2 (to produce ATP) will produce more CO 2 . Furthermore, in lung pathologies such as chronic obstructive pulmonary disease, sleep apnoea and central hypoventilation syndrome, hypoxia and hypercapnia are co-incident. Acute responses to hypoxia involve carotid body-mediated changes in the rate and depth of breathing. Chronic adaptation to hypoxia involves a multitude of changes on a transcriptional level, which simultaneously increases oxygen utilization (via hypoxia-inducible factor and others), while suppressing superfluous energy-demanding processes. Acute responses to CO 2 affect breathing primarily via central chemoreceptors. The nature of hypercapnia-dependent transcriptional regulation is an emerging area of research, but at present the mechanisms underpinning this response are not fully characterized and understood. Thus, given the juxtaposition of hypoxia and hypercapnia in health and disease, this manuscript reviews the current evidence for transcriptional responses to hypoxia and hypercapnia. Finally, we discuss the potential cross-talk between hypoxia and hypercapnia on a transcriptional level.

show abstract

Sirt1: Role Under the Condition of Ischemia/Hypoxia

Cited by 133 publications

References 93 publications

Resveratrol ameliorates rheumatoid arthritis via activation of SIRT1‐Nrf2 signaling pathway

Resveratrol ameliorates rheumatoid arthritis via activation of SIRT1‐Nrf2 signaling pathway

Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD ⁺ /Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats

Respiratory gases and the regulation of transcription

Contact Info

Product

Resources

About

Sirt1: Role Under the Condition of Ischemia/Hypoxia

Cited by 133 publications

References 93 publications

Resveratrol ameliorates rheumatoid arthritis via activation of SIRT1‐Nrf2 signaling pathway

Resveratrol ameliorates rheumatoid arthritis via activation of SIRT1‐Nrf2 signaling pathway

Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD + /Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats

Respiratory gases and the regulation of transcription

Contact Info

Product

Resources

About

Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD ⁺ /Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats