Who watches the watchmen? Regulation of the expression and activity of sirtuins

Buler, Marcin; Andersson, Ulf; Hakkola, Jukka

doi:10.1096/fj.201600410rr

Cited by 78 publications

(73 citation statements)

References 237 publications

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“…SIRT1 is a nicotinamide adenine dinucleotide- (NAD + -) dependent deacetylase that regulates crucial cellular functions and is associated with aging and longevity. It mediates stress resistance and its expression levels decline in aging organisms, where OS occurs [90]. A variety of miRNAs regulate SIRT1 expression [90].…”

Section: Mirnas Regulating Os In Cellular Senescencementioning

confidence: 99%

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MicroRNA Regulation of Oxidative Stress‐Induced Cellular Senescence

Wedel

Cavinato

et al. 2017

Oxidative Medicine and Cellular Longevity

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Aging is a time-related process of functional deterioration at cellular, tissue, organelle, and organismal level that ultimately brings life to end. Cellular senescence, a state of permanent cell growth arrest in response to cellular stress, is believed to be the driver of the aging process and age-related disorders. The free radical theory of aging, referred to as oxidative stress (OS) theory below, is one of the most studied aging promoting mechanisms. In addition, genetics and epigenetics also play large roles in accelerating and/or delaying the onset of aging and aging-related diseases. Among various epigenetic events, microRNAs (miRNAs) turned out to be important players in controlling OS, aging, and cellular senescence. miRNAs can generate rapid and reversible responses and, therefore, are ideal players for mediating an adaptive response against stress through their capacity to fine-tune gene expression. However, the importance of miRNAs in regulating OS in the context of aging and cellular senescence is largely unknown. The purpose of our article is to highlight recent advancements in the regulatory role of miRNAs in OS-induced cellular senescence.

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Section: Mirnas Regulating Os In Cellular Senescencementioning

confidence: 99%

“…It mediates stress resistance and its expression levels decline in aging organisms, where OS occurs [90]. A variety of miRNAs regulate SIRT1 expression [90]. Of note, miR-34a was found to induce cellular senescence by targeting SIRT1 in different tissues [89, 91–93].…”

Section: Mirnas Regulating Os In Cellular Senescencementioning

confidence: 99%

MicroRNA Regulation of Oxidative Stress‐Induced Cellular Senescence

Wedel

Cavinato

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…In fact, treatment with BCH increased expression and activities of various SIRTs, such as SIRT1, SIRT3 and SIRT5, which are involved in metabolism of FAO and ATP generation. The report that fasting and calorie restriction induced expression of cytosolic/nuclear SIRT1 and mitochondrial SIRT3 and SIRT5 suggests that BCH treatment induce fasting and calorie restriction state in liver40. In particular, SIRT1 activation is likely to be an important mediator for BCH-induced improvement in insulin resistance since SIRT1 inhibitor prevented BCH-induced beneficial effect on hepatic insulin resistance in HF/HFr-fed mice.…”

Section: Discussionmentioning

confidence: 99%

Glutamate dehydrogenase activator BCH stimulating reductive amination prevents high fat/high fructose diet-induced steatohepatitis and hyperglycemia in C57BL/6J mice

Han

Choi

et al. 2016

Sci Rep

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Individuals with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2D) induced by high calorie western diet are characterized by enhanced lipogenesis and gluconeogenesis in the liver. Stimulation of reductive amination may shift tricarboxylic acid cycle metabolism for lipogenesis and gluconeogenesis toward glutamate synthesis with increase of NAD+/NADH ratio and thus, ameliorate high calorie diet-induced fatty liver and hyperglycemia. Stimulation of reductive amination through glutamate dehydrogenase (GDH) activator 2-aminobicyclo-(2,2,1)-heptane-2-carboxylic acid (BCH) reduced both de novo lipogenesis and gluconeogenesis but increased the activities of sirtuins and AMP-activated kinase in primary hepatocytes. Long-term BCH treatment improved most metabolic alterations induced by high fat/high fructose (HF/HFr) diet in C57BL/6J mice. BCH prevented HF/HFr-induced fat accumulation and activation of stress/inflammation signals such as phospho-JNK, phospho-PERK, phospho-p38, and phospho-NFκB in liver tissues. Furthermore, BCH treatment reduced the expression levels of inflammatory cytokines such as TNF-α and IL-1β in HF/HFr-fed mouse liver. BCH also reduced liver collagen and plasma levels of alanine transaminase and aspartate transaminase. On the other hand, BCH significantly improved fasting hyperglycemia and glucose tolerance in HF/HFr-fed mice. In conclusion, stimulation of reductive amination through GDH activation can be used as a strategy to prevent high calorie western diet-induced NAFLD and T2D.

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“…Resveratrol is an activator of Sirt1 [33][34][35][36][37][38]. Whether does resveratrol activate the Shh signaling via Sirt1?…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Activated Sonic Hedgehog Signaling to Enhance Viability of NIH3T3 Cells in Vitro via Regulation of Sirt1

Guo¹,

Liao²,

Liu³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Injuries of the brain and spinal cord result in the formation of glial (reactive gliosis) and fibrotic (formed by fibroblasts) scars. Recent studies have shown that the fibrotic scar was much more important for hindering regeneration after brain or spinal cord injury than the astrocytic scar. However, it has been given much less attention for effects and mechanism of fibroblasts during formation of the fibrotic scar. Resveratrol may be a potential anti-scarring agent in burn-related scarring and keloid fibroblasts. However, it is unclear whether and how resveratrol affects formation of the fibrotic scar after brain or spinal cord injury. Earlier studies have shown that the activated Shh signaling has anti-apoptosis, anti-oxidation, anti-inflammation properties. Moreover, resveratrol can activate the Shh signaling. However, it is unclear how resveratrol activates the Shh signaling. Resveratrol is a activator of Sirt1. It is unknown whether resveratrol activates the Shh signaling via Sirt1. Methods: NIH3T3 cells, a fibroblast cell line, were used as model cells and treated with drugs. Cell viability was assessed by Cell Counting Kit 8. The expressions and activity of Shh signaling pathway proteins were evaluated by immunocytochemistry and Western blotting. Transcriptional activity of Gli-1 was detected with Dual-Luciferase Reporter Gene Assay Kit. Results: Resveratrol, Sirt1 agonist STR1720 and recombinant mouse Shh protein, an activator of hedgehog signaling, enhanced the viability of NIH3T3 cells, promoted Smo to translocated to the primary cilia and Gli-1 entered into the nuclei from cytoplasm, and upregulated expressions of Shh, Ptc-1, Smo, and Gli-1 proteins, which can be reversed by Smo antagonist cyclopamine and Sirt1 antagonist Sirtinol. Additionally, resveratrol increased transcriptional activity of Gli-1. Conclusion: We indicate in the first time that it may be mediated by Sirt1 for resveratrol activating the Shh signaling to enhance viability of NIH3T3 cells, and Sirt1 may be a regulator for upstream of the Shh signaling pathway.This study provides a basis for further investigating effects and mechanism of resveratrol during the formation of fibrous scar after brain or spinal cord injury.

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Who watches the watchmen? Regulation of the expression and activity of sirtuins

Cited by 78 publications

References 237 publications

MicroRNA Regulation of Oxidative Stress‐Induced Cellular Senescence

MicroRNA Regulation of Oxidative Stress‐Induced Cellular Senescence

Glutamate dehydrogenase activator BCH stimulating reductive amination prevents high fat/high fructose diet-induced steatohepatitis and hyperglycemia in C57BL/6J mice

Resveratrol Activated Sonic Hedgehog Signaling to Enhance Viability of NIH3T3 Cells in Vitro via Regulation of Sirt1

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