SIRT1 activator ameliorates the renal tubular injury induced by hyperglycemia in vivo and in vitro via inhibiting apoptosis

Wang, Xueling; Wu, Liyan; Zhao, Liang; Sun, Lina; Liu, Haiying; Liu, Gang; Guan, Guangju

doi:10.1016/j.biopha.2016.06.009

Cited by 46 publications

(39 citation statements)

References 45 publications

(49 reference statements)

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“…Santos et al (2017) found that the addition of resveratrol to in vitro maturation (IVM) medium can enhance the developmental potential of vitrified porcine oocytes, and Giaretta et al (2013) demonstrated that resveratrol supplementation could exert antiapoptotic effects and decrease vitrification-induced damage in porcine oocytes. Additionally, resveratrol was reported to be an activator of SIRT1 in vivo and in vitro (X. L. Wang et al, 2016), suggesting that it is multifunctional. We could not exclude the possibility that resveratrol reduces γ-H2AX accumulation via its F I G U R E 5 Effect of resveratrol on γH2AX accumulation and the developmental rate in oocytes and preimplantation embryos.…”

Section: Discussionmentioning

confidence: 99%

Effect of oocyte vitrification on DNA damage in metaphase II oocytes and the resulting preimplantation embryos

Chang

Chen

Zhang

et al. 2019

Molecular Reproduction Devel

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As an assisted reproduction technology, vitrification has been widely used for oocyte and embryo cryopreservation. Many studies have indicated that vitrification affects ultrastructure, gene expression, and epigenetic status. However, it is still controversial whether oocyte vitrification could induce DNA damage in metaphase II (MII) oocytes and the resulting early embryos. This study determined whether mouse oocytes vitrification induce DNA damage in MII oocytes and the resulting preimplantation embryos, and causes for vitrification‐induced DNA damage. The effects of oocyte vitrification on reactive oxygen species (ROS) levels, γ‐H2AX accumulation, apoptosis, early embryonic development, and the expression of DNA damage‐related genes in early embryos derived by in vitro fertilization were examined. The results indicated that vitrification significantly increased the number of γ‐H2AX foci in zygotes and two‐cell embryos. Trp53bp1 was upregulated in zygotes, two‐cell embryos and four‐cell embryos in the vitrified group, and Brca1 was increased in two‐cell embryos after vitrification. Vitrification also increased the ROS levels in MII oocytes, zygotes, and two‐cell embryos and the apoptotic rate in blastocysts. Resveratrol (3,5,4′‐trihydroxystilbene) treatment decreased the ROS levels and the accumulation of γ‐H2AX foci in zygotes and two‐cell embryos and the apoptotic rate in blastocysts after vitrification. Overall, vitrification‐induced abnormal ROS generation, γ‐H2AX accumulation, an increase in the apoptotic rate and the disruption of early embryonic development. Resveratrol treatment could decrease ROS levels, γ‐H2AX accumulation, and the apoptotic rate and improve early embryonic development. Vitrification‐associated γ‐H2AX accumulation is at least partially due to abnormal ROS generation.

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Section: Discussionmentioning

confidence: 99%

Effect of oocyte vitrification on DNA damage in metaphase II oocytes and the resulting preimplantation embryos

Chang

Chen

Zhang

et al. 2019

Molecular Reproduction Devel

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“…Other studies have reported that SIRT1 expression was decreased in rats with gentamicin or cisplatin-induced nephrotoxicity [19,20]. Moreover, reduced SIRT1 expression has been found in mouse cortical collecting duct cells [14], in human kidney proximal tubule epithelial cells [21], and in rats with AKI induced by severe burns [22] and renal ischaemia-reperfusion injury [23]. Therefore, these findings imply that the decrease in SIRT1 expression is involved in renal injury processes in vivo and in vitro .…”

Section: Discussionmentioning

confidence: 99%

Sirtuin1 (SIRT1) Regulates Tumor Necrosis Factor-alpha (TNF-α-Induced) Aquaporin-2 (AQP2) Expression in Renal Medullary Collecting Duct Cells Through Inhibiting the NF-κB Pathway

Lin¹,

Geng²,

Lin³

et al. 2016

Med Sci Monit Basic Res

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BackgroundAquaporin-2 (AQP2) plays a major role in water reabsorption in the renal collecting duct, and is involved in a variety of renal disease. Recent studies have indicate that sirtuin1 (SIRT1) exerts renoprotective properties against kidney diseases. This study aimed to determine the potential role of SIRT1 in AQP2 expression induced by tumor necrosis factor-alpha (TNF-α) and to disclose the underlying mechanism in renal inner medullary collecting duct (IMCD) cells.Material/MethodsQuantitative real-time PCR and Western blotting were respectively identified mRNA and protein expression. Immunofluorescence staining was used to detect the localization of AQP2. Small-interfering RNA (siRNA) was carried out for mechanism study.ResultsResults showed that AQP2 was clearly increased in the plasma membrane and decreased in the cytoplasm of IMCD cells treated with AVP. TNF-α treatment in IMCD cells significantly reduced SIRT1 and AQP2 expression, and increased acetylated NF-κBp65 protein level in time- and concentration-dependent manners. Moreover, SIRT1 overexpression or the activator SRT1720 augmented AQP2 expression and reduced the acetylation of NF-κBp65, which was reversed by SIRT1 siRNA or the inhibitors Ex527 and sirtinol in TNF-α-induced IMCD cells. Knockdown of NF-κBp65 or NF-κBp65 inhibition by pyrrolidine dithiocarbamate (PDTC) enhanced AQP2 expression in IMCD cells exposed to TNF-α. Importantly, knockdown of NF-κBp65 augmented the up-regulation of SIRT1 on AQP2 expression in IMCD cells induced by TNF-α.ConclusionsThese findings indicate that SIRT1 increases AQP2 expression in TNF-α-induced IMCD cells via the NF-κB-dependent signalling pathway, which might provide novel insight to understanding the renoprotective effects of SIRT1 in kidney diseases.

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“…3 Hyperglycaemia in kidney also causes morphological changes, including glomerular hypertrophy, basement membrane thickening, and the accumulation of mesangial matrix. 1,9 Adiponectin (APN), an adipocyte-derived hormone, is a 30-KDa polypeptide with 244 amino acids 10,11 participating in the protection of different organs against oxidative stress. 5 mTOR pathway is essential for podocyte homeostasis.…”

Section: Introductionmentioning

confidence: 99%

“…In addition, DN is considered as a major form of chronic kidney disease, which can lead to endstage renal disease (ESRD). 1,2 Hyperglycaemia initiates the generation of free radical and oxidative stress in renal cells. It has been observed that hyperglycaemia can induce apoptosis in different cell lines, including tubular cells.…”

Section: Introductionmentioning

confidence: 99%

“…2,9 Activation of SIRT1 alleviated DN by reducing renal cell apoptosis, relieving renal inflammation and fibrosis. 1,9 Adiponectin (APN), an adipocyte-derived hormone, is a 30-KDa polypeptide with 244 amino acids 10,11 participating in the protection of different organs against oxidative stress. 12,13 APN regulates energy, lipid, and glucose metabolism via binding to APN receptors (adipoR1 and aipoR2) and activating 5´adenosine monophosphate-activated protein kinase (AMPK), 14 which results in mTOR inhibition 15 and SIRT1 activation.…”

Section: Introductionmentioning

confidence: 99%

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Prevention of kidney cell damage in hyperglycaemia condition by adiponectin

Esmaeili

Motamedrad

Hemmati

et al. 2019

Cell Biochemistry & Function

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Adiponectin (APN) is an adipocytokine, secreted from adipose tissue and has antiinflammatory, anti-ageing, and antidiabetic properties. Hyperglycaemia can damage the renal cells, and mammalian target of rapamycin (mTOR), along with Sirtuin 1 (SIRT1), have an important role in kidney cell response to hyperglycaemia. Therefore, understanding the relationship between adiponectin, mTOR, and SIRT1 proteins is beneficial for deciphering the mechanism of adiponectin function. In this study, Human Embryonic Kidney-293 (HEK-293) cells were cultured under normal and high-glucose condition, with and without APN (1, 10, and 100 ng/mL) for 48 hours. mTOR protein expression was evaluated by western blot analysis, and SIRT1 protein was assessed using ELISA method. To evaluate hyperglycaemia-mediated cytotoxicity, cell viability was determined using MTT assay. Data showed that APN in high dose (100 ng/mL) significantly reduced the expression of mTOR and p-mTOR, increased SIRT1 protein, and also improved cell viability compared with the control high glucose (p ≤ 0.05). According to this results, APN can be useful in preventing renal cell damage, by affecting on the expression of mTOR and SIRT1 proteins, as well as increasing the survival of kidney cells in hyperglycaemia conditions. Significance of the study: Adiponectin triggered mTOR/p-mTOR/SIRT1 pathway and decreased cell death in human kidney cells. Our findings provide preliminary experimental data that support further studies on the potential therapeutic role of adiponectin in diabetes and diabetic-induced metabolic complications.

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SIRT1 activator ameliorates the renal tubular injury induced by hyperglycemia in vivo and in vitro via inhibiting apoptosis

Cited by 46 publications

References 45 publications

Effect of oocyte vitrification on DNA damage in metaphase II oocytes and the resulting preimplantation embryos

Effect of oocyte vitrification on DNA damage in metaphase II oocytes and the resulting preimplantation embryos

Sirtuin1 (SIRT1) Regulates Tumor Necrosis Factor-alpha (TNF-α-Induced) Aquaporin-2 (AQP2) Expression in Renal Medullary Collecting Duct Cells Through Inhibiting the NF-κB Pathway

Prevention of kidney cell damage in hyperglycaemia condition by adiponectin

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