The crosstalk between Sirt1 and Keap1/Nrf2/ARE anti-oxidative pathway forms a positive feedback loop to inhibit FN and TGF-β1 expressions in rat glomerular mesangial cells

Huang, Kaipeng; Gao, Xiang; Wei, Wenhong

doi:10.1016/j.yexcr.2017.09.042

Cited by 133 publications

(67 citation statements)

References 42 publications

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“…SIRT‐1 is a nicotinamide adenosine dinucleotide (NAD + )‐dependent protein deacetylase that possesses remarkable antioxidant capacity by deacetylating numerous substrates. Thus, these pathways are usually up‐regulated to protect the organisms from ROS damage . However, in our study, the expression of these proteins was not increased with ETS.…”

Section: Discussioncontrasting

confidence: 70%

Spondias mombin supplementation attenuated cardiac remodelling process induced by tobacco smoke

Lourenço

Braz

Aun

et al. 2018

J Cellular Molecular Medi

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The objective of this study was to investigate the influence of Spondias mombin (SM) supplementation on the cardiac remodelling process induced by exposure to tobacco smoke (ETS) in rats. Male Wistar rats were divided into 4 groups: group C (control, n = 20) comprised animals not exposed to cigarette smoke and received standard chow; group ETS (n = 20) comprised animals exposed to cigarette smoke and received standard chow; group ETS100 (n = 20) received standard chow supplemented with 100 mg/kg body weight/d of SM; and group ETS250 (n = 20) received standard chow supplemented with 250 mg/kg body weight/d of SM. The observation period was 2 months. The ETS animals had higher values of left cardiac chamber diameters and of left ventricular mass index. SM supplementation attenuated these changes. In addition, the myocyte cross‐sectional area (CSA) was lower in group C compared with the ETS groups; however, the ETS250 group had lower values of CSA compared with the ETS group. The ETS group also showed higher cardiac levels of lipid hydroperoxide (LH) compared with group C; and, groups ETS100 and ETS250 had lower concentrations of LH compared with the ETS group. Regarding energy metabolism, SM supplementation decreased glycolysis and increased the β‐oxidation and the oxidative phosphorylation. There were no differences in the expression of Nrf‐2, SIRT‐1, NF‐κB, interferon‐gamma and interleukin 10. In conclusion, our results suggest that ETS induced the cardiac remodelling process. In addition, SM supplementation attenuated this process, along with oxidative stress reduction and energy metabolism modulation.

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Section: Discussioncontrasting

confidence: 70%

Spondias mombin supplementation attenuated cardiac remodelling process induced by tobacco smoke

Lourenço

Braz

Aun

et al. 2018

J Cellular Molecular Medi

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“…Other experiments studied in advanced glycation-end products (AGEs) treated glomerular mesangial cells (GMCs), crosstalk between Sirt1 and Keap1/Nrf2/ARE anti-oxidative pathway forms a positive feedback loop to inhibit the protein expressions of FN and TGF-β1 [23]. In our experiments, we found that Sirt1 expression and activity were inhibited by HG, and mitochondrial dysfunction and podocyte damage were more severe when we lowered Sirt1 in podocytes exposed to HG.…”

Section: Cellular Physiology and Biochemistrysupporting

confidence: 46%

“…As a pivotal protein in cellular metabolism, the regulatory effect of Sirt1 on mitochondrial dynamics has been established [22]. Huang et al have demonstrated that crosstalk between Sirt1 and the Keap1/Nrf2/ARE anti-oxidative pathway forms a positive feedback loop to inhibit protein expression of fibronectin and transforming growth factor-β1 in advanced glycation-end products-treated in rat glomerular mesangial cells treated with advanced glycation end products [23]. However, it remains to be determined if Sirt1 plays a role in activation of the Nrf2-ARE pathway.…”

Section: Introductionmentioning

confidence: 99%

Activation of the Nrf2-ARE Pathway Ameliorates Hyperglycemia-Mediated Mitochondrial Dysfunction in Podocytes Partly Through Sirt1

Zhang¹,

Deng²,

Zhang³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Previously we have shown that activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-antioxidant response element (ARE) attenuated hyperglycemia-induced damage in podocytes, but the molecular mechanism remains unknown. Methods: Tert-butylhydroquinone (t-BHQ) and small interfering RNAs (siRNAs) were used to regulate Nrf2 expression, while nicotinamide and siRNAs were used to regulate sirtuin 1 (Sirt1) activity and expression, respectively. Mitochondrial superoxide, membrane potential and ATP levels were measured to assess changes in mitochondrial function. Nephrin and synaptopodin expression were measured by western blot analysis. Human podocytes and db/db diabetic mice were used in this study. Results: t-BHQ pretreatment of human podocytes exposed to high glucose (HG) alleviated mitochondrial dysfunction, enhanced the expression of Sirt1, nephrin and synaptopodin and lowered BSA permeability compared with podocytes exposed to HG without t-BHQ pretreatment (p< 0.05). Human podocytes exposed to HG had more severe mitochondrial dysfunction, lower expression of Sirt1, synaptopodin and nephrin and higher BSA permeability than podocytes exposed to HG when Nrf2 expression was downregulated by siRNAs (p< 0.05). The protection provided by activation of the Nrf-ARE pathway in podocytes exposed to HG was partially diminished when Sirt1 expression or activity was decreased by siRNAs or inhibitor compared with podocytes exposed to HG and pretreated with t-BHQ (p< 0.05). When nicotinamide and t-BHQ were both administered to db/db mice, we observed higher levels of urinary albumin/creatinine, lower nephrin and synaptopodin expression, more severe mesangial matrix deposition, collagen deposition on pathological slides and mitochondrial structural damage in podocytes compared to db/db mice treated only with t-BHQ. Conclusions: Our findings suggest that crosstalk between Sirt1 and the Nrf2-ARE anti-oxidative pathway forms a positive feedback loop and that protection provided by t-BHQ activation of the Nrf2-ARE pathway in db/db mice is partly dependent on Sirt1.

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“…These results suggest that SIRT1 inhibits the NLRP3 inflammasome activation through inhibiting oxidative stress. Previous studies have shown bidirectional crosstalk between SIRT1 and nuclear factor erythroid 2-related factor 2 (Nrf2) in human renal proximal tubular and glomerular mesangial cells [57,58]. The upregulation of SIRT1 activates Nrf2 through the inhibition of p53 or activation of AMPK [59][60][61].…”

Section: Discussionmentioning

confidence: 99%

SIRT1 Alleviates LPS-Induced IL-1β Production by Suppressing NLRP3 Inflammasome Activation and ROS Production in Trophoblasts

Park

Shin

Bae

et al. 2020

Cells

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Emerging evidence indicates that aberrant maternal inflammation is associated with several pregnancy-related disorders such as preeclampsia, preterm birth, and intrauterine growth restriction. Sirtuin1 (SIRT1), a class III histone deacetylase, is involved in the regulation of various physiopathological processes including cellular inflammation and metabolism. However, the effect of SIRT1 on the placental proinflammatory environment remains to be elucidated. In this study, we investigated the effect of SIRT1 on lipopolysaccharide (LPS)-induced NLRP3 inflammasome activation and its underlying mechanisms in human first-trimester trophoblasts (Sw.71 and HTR-8/SVneo cells). Treatment with LPS elevated SIRT1 expression and induced NLRP3 inflammasome activation in mouse placental tissues and human trophoblasts. Knockdown of SIRT1 enhanced LPS-induced NLRP3 inflammasome activation, inflammatory signaling, and subsequent interleukin (IL)-1β secretion. Furthermore, knockdown of NLRP3 considerably attenuated the increase of IL-1β secretion in SIRT1-knockdown cells treated with LPS. Moreover, SIRT1 inhibited LPS-induced NLRP3 inflammasome activation by reducing oxidative stress. This study revealed a novel mechanism via which SIRT1 exerts anti-inflammatory effects, suggesting that SIRT1 is a potential therapeutic target for the prevention of inflammation-associated pregnancy-related complications.

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The crosstalk between Sirt1 and Keap1/Nrf2/ARE anti-oxidative pathway forms a positive feedback loop to inhibit FN and TGF-β1 expressions in rat glomerular mesangial cells

Cited by 133 publications

References 42 publications

Spondias mombin supplementation attenuated cardiac remodelling process induced by tobacco smoke

Spondias mombin supplementation attenuated cardiac remodelling process induced by tobacco smoke

Activation of the Nrf2-ARE Pathway Ameliorates Hyperglycemia-Mediated Mitochondrial Dysfunction in Podocytes Partly Through Sirt1

SIRT1 Alleviates LPS-Induced IL-1β Production by Suppressing NLRP3 Inflammasome Activation and ROS Production in Trophoblasts

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