Sirt1 gene confers Adriamycin resistance in DLBCL via activating the PCG-1α mitochondrial metabolic pathway

Zhou, Zhen; Ma, Dan; Li, Peifan; Wang, Ping; Liu, Ping; Wei, Danna; Wang, Jun; Fang, Qin; Wang, Jishi

doi:10.18632/aging.103174

Cited by 12 publications

(7 citation statements)

References 48 publications

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“…Previous studies have demonstrated that syringin regulated TLR4/NF-κB and SIRT3/PGC1α pathways. 31,32 As SIRT1 is upstream regulator of both pathways, [33][34][35] we hypothesized that syringin also could influence the expression of SIRT1. SIRT1 is expressed in all mammalian cell lines and was initially judged to be a nuclear protein.…”

Section: Discussionmentioning

confidence: 99%

Syringin exerts anti‐inflammatory and antioxidant effects by regulating SIRT1 signaling in rat and cell models of acute myocardial infarction

Zhao

Liu

Wang

et al. 2023

Immunity Inflam & Disease

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Introduction: This study aimed to investigate the role of syringin in improving heart function during myocardial ischemia/reperfusion (I/R) and to determine whether the sirtuin 1/peroxisome proliferator-activated receptor gamma coactivator 1 alpha (SIRT1/PGC-1α) pathway contributes to this cardioprotective effect in vivo and in vitro. Methods: H9c2 cells were incubated with H 2 O 2 for 12 h. The effect of syringin was assessed by measuring cell viability; the apoptotic rate; Keap1/NRF2/HO-1 activation; and the levels of proinflammatory cytokines, oxidative products, and antioxidative enzymes. In addition, SIRT1 was silenced via short hairpin RNA (shRNA)-SIRT1 transfection to evaluate its involvement in syringin-mediated protection. Syringin rescued cells from H 2 O 2 -induced reductions in viability, antioxidative enzyme levels, and NRF2/HO-1 activation; likewise, syringin inhibited apoptosis, inflammation, and oxidative stress. We also created a rat model of I/R by ligating the left anterior descending coronary artery for 30 min, followed by reperfusion for 12 min. Syringin was then intraperitoneally injected, and the effect on infarct size and cardiac function was examined after 7 days. NRF2/HO-1 activity and the levels of myocardial proinflammatory cytokines, oxidative products, and antioxidative enzymes were measured. Results:In comparison to the untreated I/R group, the syringin treatment group exhibited improved cardiac function and reduced cardiac lesion and infarct size. Syringin administration also markedly reduced the levels of proinflammatory cytokines and reactive oxygen species and promoted antioxidative enzyme expression and NRF2/HO-1 pathway activation.Conclusions: Syringin may serve a protective role in animal and cell models of I/R by improving cardiac function, inhibiting the inflammatory response, and activating the antioxidative response.

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Section: Discussionmentioning

confidence: 99%

Syringin exerts anti‐inflammatory and antioxidant effects by regulating SIRT1 signaling in rat and cell models of acute myocardial infarction

Zhao

Liu

Wang

et al. 2023

Immunity Inflam & Disease

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“…Whereas the deacetylation of MFN2 by Sirt1 has been previously reported ( 22 ), the mechanisms by which Sirt1 regulates MFN2 protein expression remain unclear. Previous research has revealed that PGC-1α is a target protein of Sirt1, and that the overexpression of Sirt1 can cause an increase in PGC-1α protein expression ( 36 ). Furthermore, PGC1α can regulate Mfn2 transcription by binding to its promoter region ( 37 ).…”

Section: Discussionmentioning

confidence: 99%

miR‑141 impairs mitochondrial function in cardiomyocytes subjected to hypoxia/reoxygenation by targeting Sirt1 and MFN2

Zhang

Wang

et al. 2022

Exp Ther Med

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Mitochondrial oxidative stress and dysfunction are major pathogenic features of cardiac injury induced by ischemia/reperfusion (I/R). has been implicated in the mitochondrial dysfunction in cell-based models of oxidant stress. Thus, the main aim of the present study was to systematically assess the role of miR-141 in cardiomyocyte injury induced by simulated I/R. The challenge of HL-1 cardiomyocytes with hypoxia/reoxygenation (H/R) decreased cell viability, which was also associated with an increase in miR-141 expression. The H/R-induced cell injury was mitigated by a miR-141 inhibitor and exacerbated by a miR-141 mimic. Furthermore, H/R induced mitochondrial superoxide production, dysfunction (decreased oxygen utilization and membrane depolarization), as well as ultrastructural damage. These mitochondrial effects were mitigated by a miR-141 inhibitor and intensified by a miR-141 mimic. Luciferase reporter assay, reverse transcription-quantitative PCR, and western blot analyses identified sirtuin-1 (Sirt1) and mitofusin-2 (MFN2) as targets of miR-141. The silencing of Sirt1 reduced the MFN2 cardiomyocyte levels and reversed the alleviating effects of miR-141 inhibitor on mitochondrial function during H/R. Collectively, these findings suggest that miR-141 functions as a causative agent in cardiomyocyte injury induced by I/R, primarily by interfering with two mitochondrial regulatory proteins, Sirt1 and MFN2.

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“…In the present study, a similar phenomenon was also observed after cryopreservation of mouse GV oocytes. Sirt1 mediated activation of Pgc-1α through Pgc-1α deacetylation (50,51), potentially regulating mitochondrial biogenesis and mitochondrial metabolism (52). Meanwhile, Pgc-1α could also activate Tfam, which is required for mtDNA transcription and mtDNA replication, through co-activation of nuclear respiratory factor 1 (Nrf1) (53).…”

Section: Discussionmentioning

confidence: 99%

Melatonin Promotes in vitro Development of Vitrified-Warmed Mouse GV Oocytes, Potentially by Modulating Phosphorylation of Drp1

et al. 2021

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Previous studies have shown that melatonin can mitigate cryopreservation-induced mitochondrial dysfunction in oocytes; however, the underlying molecular mechanism remains unclear. The objective of the present study was to investigate whether melatonin can improve the mitochondrial function during in vitro maturation of vitrified-warmed mouse germinal vesicle (GV) oocytes by modulating phosphorylation of dynamin related protein 1 (Drp1). Vitrification/warming procedures resulted in the following: (1) After cryopreservation of mouse GV oocytes, the phosphorylation level of Drp1 at Ser616 (p-Drp1 Ser616) in metaphase II (MII) oocytes was increased (P < 0.05). Furthermore, the rates of in vitro maturation, cleavage and blastocyst formation after parthenogenetic activation were decreased (P < 0.05). (2) In MII oocytes, the expression levels of translocase of the mitochondrial outer membrane 20 (TOMM20), mitochondrial membrane potential (MMP), adenosine triphosphate (ATP) content, and mRNA levels of mitochondrial biogenesis-related genes (Sirt1, Pgc-1α, Tfam) were all decreased (P < 0.05), and (3) Reactive oxygen species (ROS) level, early apoptosis level, Cytochrome C release and mRNA levels of pro-apoptotic related genes (Bax, Caspase9, Caspase3) in MII oocytes were all increased (P < 0.05). The results of this study further revealed that negative impacts of GV oocyte cryopreservation were mitigated by supplementation of warming and in vitro maturation media with 10−7mol /L melatonin or 2 x 10−5mol/L Mdivi-1 (Drp1 inhibitor). Therefore, we concluded that 10−7mol/L melatonin improved mitochondrial function, reduced oxidative stress and inhibited apoptosis by regulating phosphorylation of Drp1, thereby enhancing in vitro development of vitrified-warmed mouse GV oocytes.

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Sirt1 gene confers Adriamycin resistance in DLBCL via activating the PCG-1α mitochondrial metabolic pathway

Cited by 12 publications

References 48 publications

Syringin exerts anti‐inflammatory and antioxidant effects by regulating SIRT1 signaling in rat and cell models of acute myocardial infarction

Syringin exerts anti‐inflammatory and antioxidant effects by regulating SIRT1 signaling in rat and cell models of acute myocardial infarction

miR‑141 impairs mitochondrial function in cardiomyocytes subjected to hypoxia/reoxygenation by targeting Sirt1 and MFN2

Melatonin Promotes in vitro Development of Vitrified-Warmed Mouse GV Oocytes, Potentially by Modulating Phosphorylation of Drp1

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