Kinase-independent role of nuclear RIPK1 in regulating parthanatos through physical interaction with PARP1 upon oxidative stress

Jang, Ki-Hong; Jang, Taeik; Son, Eunji; Choi, Soonjin; Kim, Eunhee

doi:10.1016/j.bbamcr.2017.10.004

Cited by 20 publications

(18 citation statements)

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“…OS has been reported to play an essential role in IRI . Among the predicted miRNAs regulating the RIPK1 gene, only miR‐590‐3p had the potential of suppressing OS, and RIPK1 gene was found to be associated with OS . Thus, a hypothesis was made that miR‐590‐3p could influence IRI by regulating RIPK1 gene.…”

Section: Resultsmentioning

confidence: 99%

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Zhao

Jiang

Wang

et al. 2018

J of Cellular Biochemistry

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Ischemic heart disease is widely considered as a major health threat, which causes a high number of deaths every year worldwide. Much evidence has shown that oxidative stress (OS) is implicated in the pathogenesis of ischemiareperfusion injury (IRI). This study aims to evaluate the effect of miR-590-3p on the OS of IRI mice through the nuclear factor kappa-B (NF-κB) signaling pathway by targeting receptor-interacting protein kinase 1 (RIPK1). IRI mouse models were established for extracting myocardial tissues and isolating myocardial cells. The expression of inflammatory related-factors was detected by enzyme-linked immunosorbent assay, and superoxide dismutase (SOD) and malondialdehyde (MDA) in tissues were determined. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were performed to assess the role of miR-590-3p in the expression of NF-κB-related factors and apoptosis-related factors. Besides, the regulatory effects of miR-590-3p on myocardial cell proliferation and apoptosis were also assessed. According to the obtained results, we found that IRI mice displayed higher expression of tumor necrosis factor-α, interleukin (IL)-6, and interferon-γ, lower expression of IL-10 in serum, a decreased SOD level, and an increased MDA level. In addition, RIPK1 was determined as a target gene of miR-590-3p. After transfection of overexpressed miR-590-3p or si-RIPK1, declined RIPK1, NF-κB, Toll-like receptor 4, caspase-3, FasL, p53, and c-myc levels, increased B-cell lymphoma-2 level, promoted cell proliferation, promoted cell cycle distribution and inhibited apoptosis of myocardial cells were found. Our study demonstrates that miR-590-3p can alleviate the OS of IRI mice through the inhibition of the RIPK1 and NF-κB signaling pathway. Thus, miR-590-3p represents a potential target for IRI repair. K E Y W O R D S microRNA-590-3p, myocardial ischemia/reperfusion injury, nuclear factor kappa-B (NF-κB), oxidative stress (OS), receptor-interacting protein kinase 1 (RIPK1) J Cell Biochem. 2019;120:3559-3573.wileyonlinelibrary.com/journal/jcb Overexpression of microRNA-590-3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF-κB signaling pathway by binding to RIPK1.

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Section: Resultsmentioning

confidence: 99%

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Zhao

Jiang

Wang

et al. 2018

J of Cellular Biochemistry

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“…In the present study, PSPC significantly restored the NAD + level in the livers of HFD-treated mouse. Oxidative stress is widely reported to be responsible for NAD + depletion by impairing NAD + biosynthesis and elevating NAD + breakdown under various pathological conditions including metabolic syndrome (51,52). Consistent with our previous works (17)(18)(19), our present results showed that PSPC markedly abated HFD-induced oxidative stress in mouse livers.…”

Section: Discussionsupporting

confidence: 93%

Purple sweet potato color protects against hepatocyte apoptosis through Sirt1 activation in high-fat-diet-treated mice

Su¹,

Zhang²,

Chen³

et al. 2020

Food & Nutrition Research

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Background: Recent evidence indicates that the inhibition of hepatocyte apoptosis is possible to develop a potential therapeutic strategy for nonalcoholic fatty liver disease (NAFLD). Our previous work suggested that purple sweet potato color (PSPC), a class of naturally occurring anthocyanins, effectively improved many features of high-fat diet (HFD)-induced NAFLD. However, whether PSPC ameliorates HFD-induced hepatocyte apoptosis has never been investigated. Objective: Here we investigated the effects of PSPC on HFD-induced hepatic apoptosis and the mechanisms underlying these effects. Design: Mice were divided into four groups: Control group, HFD group, HFD + PSPC group and PSPC group. PSPC was administered by daily oral gavage at doses of 700 mg/kg/day for 20 weeks. EX-527 (a SirT1-selective inhibitor) and Sirt1 siRNA were used to demonstrate the Sirt1 dependence of PSPC-mediated effects on apoptotic and survival signaling pathways in vivo and in vitro. Results: Our results showed that PSPC reduced body weights, hepatic triglyceride contents, histopathological lesions and serum ALT levels in a mouse model of NAFLD induced by HFD. Furthermore, PSPC attenuated HFD-induced hepatocyte apoptosis ratio from 7.27 ± 0.92% to 1.79 ± 0.27% in mouse livers, which is insignificant compared with that of controls. Moreover, PSPC activated Sirt1 by boosting NAD + level in HFD-treated mouse livers. Furthermore, PSPC promoted Sirt1-dependent suppression of P53-mediated apoptotic signaling and activation of Akt survival signaling pathway in HFD-treated mouse livers, which was confirmed by EX527 treatment. Moreover, Sirt1 knockdown abolished these ameliorative effects of PSPC on apoptosis and P53 acetylation and protein expression in PA-treated L02 cells. Ultimately, PSPC reduced Caspase-3 activation and Bax level, and elevated the Bcl-2 level in HFD-treated mouse livers. Conclusion: PSPC protected against HFD-induced hepatic apoptosis by promoting Sirt1-dependent inhibition of p53-apoptotic pathway and facilitation of Akt survival pathway. This study indicates that PSPC is a candidate for nutritional intervention of NAFLD.

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“…In order to elucidate the specific molecular pathways required for ZBP1-induced apoptosis in the context of VZV infection, we sought to determine whether RIPK3 was necessary for cell death. To this end, we performed infectious centre assays with ARPE-19 cells, a cell line known to be permissive to VZV infection that possesses a full complement of caspases but does not express RIPK3 (57). For this assay, only the VZV parent strain and the VZV-RHIMmut were compared, since we had established that the IQIG core tetrad is crucial for the prevention of ZBP1-induced cell death.…”

Section: Resultsmentioning

confidence: 99%

Varicella zoster virus encodes a viral decoy RHIM to inhibit cell death

Steain

Baker

Pham

et al. 2020

Preprint

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Author Summary: 43 44 Rip homotypic interaction motifs (RHIMs) are found in host proteins that can signal 45 for programmed cell death and in viral proteins that can prevent it. Complexes 46 stabilized by intermolecular interactions involving RHIMs have a fibrillar amyloid 47 how a decoy amyloid strategy is employed by pathogens to circumvent the host 55 response. 56 57 58 Viruses have evolved a diverse range of strategies to evade host intrinsic, innate and 59 adaptive immune responses. Members of the Herpesviridae family, Herpes simplex 60 virus (HSV) -1 and human and murine cytomegalovirus (HCMV/MCMV), are 61 masters at manipulating host cell death pathways such as apoptosis and necroptosis, in 62 order to successfully spread and establish latency (1-3). Although Varicella zoster 63 virus (VZV) causes a significant health burden (4-6), the mechanisms employed by 64 VZV to undermine host responses have not been fully elucidated. Primary infection 65with VZV leads to varicella, commonly known as chickenpox. During this infection 66 the virus establishes latency within sensory neurons, and when VZV-specific T cell 67 immunity wanes, the virus can reactivate to result in herpes zoster (shingles) (7). 68Complications arising from VZV reactivation include protracted pain termed post-69 herpetic neuralgia, encephalitis and VZV vasculopathy (reviewed in 8). 70VZV is a highly cell-associated virus and does not release cell-free virions into 71 culture (9), necessitating cell-associated propagation of the virus in vitro. VZV is also 72 highly species-specific, not progressing to productive infection in cells of non-human 73 origin (10). Therefore no animal model exists which re-capitulates the full spectrum 74 of VZV disease. Combined, these properties of VZV have largely hampered the 75 characterization of VZV pathogenesis. 76

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Kinase-independent role of nuclear RIPK1 in regulating parthanatos through physical interaction with PARP1 upon oxidative stress

Cited by 20 publications

References 50 publications

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Purple sweet potato color protects against hepatocyte apoptosis through Sirt1 activation in high-fat-diet-treated mice

Varicella zoster virus encodes a viral decoy RHIM to inhibit cell death

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