5d, a novel analogue of 3-n-butylphthalide, decreases NADPH oxidase activity through the positive regulation of CK2 after ischemia/reperfusion injury

Zhou, Jia; Zhang, Yihua; Song, Huizhu; Ji, Hui; Wang, Xiaoli; Wang, Lei; Qian, Jun; Ling, Jingjing; Ping, Fengfeng

doi:10.18632/oncotarget.8548

Cited by 11 publications

(7 citation statements)

References 28 publications

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“…CK2 binds and phosphorylates Per2, which supports nuclear accumulation of Per2 and affects stability of Per2 in mouse fibroblasts, and inhibition of CK2 activity disrupts circadian rhythm [144,145] (Table 1). Notably, CK2 suppresses activation of A 2A R and D1R associated G αs [146], Rac1 [147,148] and NOX [149] thereby downregulates PKA signaling (Table 1).…”

Section: Sequential Activation Of Ck2 and Pka Controls Circadian Rhythmmentioning

confidence: 99%

Circadian control of p75 neurotrophin receptor leads to alternate activation of Nrf2 and c-Rel to reset energy metabolism in astrocytes via brain-derived neurotrophic factor

Ishii

Warabi

Mann

2018

Free Radical Biology and Medicine

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Circadian clock genes regulate energy metabolism partly through neurotrophins in the body. The low affinity neurotrophin receptor p75 is a clock component directly regulated by the transcriptional factor Clock:Bmal1 complex. Brain-derived neurotrophic factor (BDNF) is expressed in the brain and plays a key role in coordinating metabolic interactions between neurons and astrocytes. BDNF transduces signals through TrkB and p75 receptors. This review highlights a novel molecular mechanism by which BDNF via circadian control of p75 leads to daily resetting of glucose and glycogen metabolism in brain astrocytes to accommodate their functional interaction with neurons. Astrocytes store glycogen as an energy reservoir to provide active neurons with the glycolytic metabolite lactate. Astrocytes predominantly express the truncated receptor TrkB.T1 which lacks an intracellular receptor tyrosine kinase domain. TrkB.T1 retains the capacity to regulate cell morphology through regulation of Rho GTPases. In contrast, p75 mediates generation of the bioactive lipid ceramide upon stimulation with BDNF and inhibits PKA activation. As ceramide directly activates PKCζ, we discuss the importance of the TrkB.T1-p75-ceramide-PKCζ signaling axis in the stimulation of glycogen and lipid synthesis and activation of RhoA. Ceramide-PKCζ-casein kinase 2 signaling activates Nrf2 to support oxidative phosphorylation via upregulation of antioxidant enzymes. In the absence of p75, TrkB.T1 functionally interacts with adenosine AR and dopamine D1R receptors to enhance cAMP-PKA signaling and activate Rac1 and NF-κB c-Rel, favoring glycogen hydrolysis, gluconeogenesis and aerobic glycolysis. Thus, diurnal changes in p75 levels in astrocytes resets energy metabolism via BDNF to accommodate their metabolic interaction with neurons.

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Section: Sequential Activation Of Ck2 and Pka Controls Circadian Rhythmmentioning

confidence: 99%

Circadian control of p75 neurotrophin receptor leads to alternate activation of Nrf2 and c-Rel to reset energy metabolism in astrocytes via brain-derived neurotrophic factor

Ishii

Warabi

Mann

2018

Free Radical Biology and Medicine

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“…p22(phox) is a polymorphic subunit of NAD(P)H oxidase that plays a critical role in its activation and stabilization. NAD(P)H oxidase is involved in the production of superoxide that triggers the inflammation in ischaemic kidneys [ 43 , 16 ]. Mandegary et al .…”

Section: Resultsmentioning

confidence: 99%

Genetic susceptibility to delayed graft function following kidney transplantation: a systematic review of the literature

Huart

Krzesinski

Jouret

2018

Clinical Kidney Journal

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Delayed graft function (DGF) is defined as the need for dialysis within 7 days following kidney transplantation (KTx). DGF is associated with increased costs, higher risk for acute rejection and decreased long-term graft function. Renal ischaemia/reperfusion (I/R) injury plays a major role in DGF occurrence. Single nucleotide polymorphisms (SNPs) in certain genes may aggravate kidney susceptibility to I/R injury, thereby worsening post-transplant outcomes. The present article proposes an extensive review of the literature about the putative impact of donor or recipient SNPs on DGF occurrence in kidney transplant recipients (KTRs). Among 30 relevant PubMed reports, 16 articles identified an association between 18 SNPs and DGF. These polymorphisms concern 14 different well-known genes and one not-yet-identified gene located on chromosome 18. They have been categorized into five groups according to the role of the corresponding proteins in I/R cascade: (i) oxidative stress, (ii) telomere shortening, (iii) chemokines, (iv) T-cell homeostasis and (v) metabolism of anti-inflammatory molecules. The remaining 14 studies failed to demonstrate any association between the studied SNPs and the occurrence of DGF. A better understanding of the genetic susceptibility to renal I/R injury may help prevent DGF and improve clinical outcomes in KTRs.

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“…For instance, ATM inhibition was shown to increase NOX4 expression in normal fibroblasts [ 129 ]. Moreover, CK2 was described as a negative modulator of NOX4 [ 130 ]. Collectively, these data suggest that the ATM/CK2 kinases and NOX4-generated ROS might be functionally connected.…”

Section: Discussionmentioning

confidence: 99%

Cooperative Blockade of CK2 and ATM Kinases Drives Apoptosis in VHL-Deficient Renal Carcinoma Cells through ROS Overproduction

Giacosa

Pillet

Séraudie

et al. 2021

Cancers

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Kinase-targeted agents demonstrate antitumor activity in advanced metastatic clear cell renal cell carcinoma (ccRCC), which remains largely incurable. Integration of genomic approaches through small-molecules and genetically based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. The 786-O cell line represents a model for most ccRCC that have a loss of functional pVHL (von Hippel-Lindau). A multiplexed assay was used to study the cellular fitness of a panel of engineered ccRCC isogenic 786-O VHL− cell lines in response to a collection of targeted cancer therapeutics including kinase inhibitors, allowing the interrogation of over 2880 drug–gene pairs. Among diverse patterns of drug sensitivities, investigation of the mechanistic effect of one selected drug combination on tumor spheroids and ex vivo renal tumor slice cultures showed that VHL-defective ccRCC cells were more vulnerable to the combined inhibition of the CK2 and ATM kinases than wild-type VHL cells. Importantly, we found that HIF-2α acts as a key mediator that potentiates the response to combined CK2/ATM inhibition by triggering ROS-dependent apoptosis. Importantly, our findings reveal a selective killing of VHL-deficient renal carcinoma cells and provide a rationale for a mechanism-based use of combined CK2/ATM inhibitors for improved patient care in metastatic VHL-ccRCC.

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5d, a novel analogue of 3-n-butylphthalide, decreases NADPH oxidase activity through the positive regulation of CK2 after ischemia/reperfusion injury

Cited by 11 publications

References 28 publications

Circadian control of p75 neurotrophin receptor leads to alternate activation of Nrf2 and c-Rel to reset energy metabolism in astrocytes via brain-derived neurotrophic factor

Circadian control of p75 neurotrophin receptor leads to alternate activation of Nrf2 and c-Rel to reset energy metabolism in astrocytes via brain-derived neurotrophic factor

Genetic susceptibility to delayed graft function following kidney transplantation: a systematic review of the literature

Cooperative Blockade of CK2 and ATM Kinases Drives Apoptosis in VHL-Deficient Renal Carcinoma Cells through ROS Overproduction

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