IRF9 promotes apoptosis and innate immunity by inhibiting SIRT1-p53 axis in fish

Jiang, Zeyin; Weng, Panwei; Xu, Xiaowen; Li, Meifeng; Li, Yinping; Lv, Yangfeng; Chang, Kaile; Wang, Shanghong; Lin, Gang; Hu, Chengyu

doi:10.1016/j.fsi.2020.05.038

Cited by 13 publications

(4 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several inflammation-related proteins have been found to mediate Sirt1, such as NF-κB [60]. Thus, the data indicate that the specific inhibitor of Sirt1, EX-527, increased the activation of inflammatory pathways in mice, while SAC pretreatment in mice effectively reversed these inflammatory response changes compared to the cisplatin-treated group in mice.…”

Section: Discussionmentioning

confidence: 85%

Salvianolic Acid C Protects against Cisplatin-Induced Acute Kidney Injury through Attenuation of Inflammation, Oxidative Stress and Apoptotic Effects and Activation of the CaMKK–AMPK–Sirt1-Associated Signaling Pathway in Mouse Models

Chien

Deng

et al. 2021

Antioxidants

View full text Add to dashboard Cite

Acute kidney injury (AKI) is a sudden reduction in kidney activity and has a high mortality rate. Salvianolic acid C (SAC), one of the main polyphenolic components of Salvia miltiorrhiza, displays significant pharmacologically active effects. An animal model of cisplatin-induced kidney injury was used to study the potential of SAC to improve AKI. First, SAC was administered intraperitoneally in mice for 10 consecutive days, and then cisplatin was administered intraperitoneally on day 7 to establish a nephrotoxicity mouse model. SAC mitigated renal histological changes, blood creatinine (CRE) and blood urea nitrogen (BUN) production and the levels of inflammatory mediators in the cisplatin-induced AKI. Furthermore, malondialdehyde (MDA) levels were reduced and glutathione (GSH) was increased after intraperitoneal injection (i.p.) administration of SAC. In addition, based on Western blot data, SAC reduced the expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) activation in mouse renal tissues. Finally, SAC diminished the level of TLR-4 expression and enhanced the production of several antioxidative enzymes (superoxidase dismutase (SOD1), glutathione peroxidase (GPx3), catalase, nuclear-factor-erythroid-2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1)), Sirtuin 1 (Sirt1), p-AMP-activated protein kinase (AMPK) and p-Ca2+/calmodulin-dependent protein kinase kinase (CaMKK). In addition, Sirt1 inhibition (EX 527) inverted the effect of SAC against cisplatin-induced nephrotoxicity. Collectively, SAC provides a therapeutic target with promising clinical potential after cisplatin treatment by attenuating oxidative stress and inflammation.

show abstract

Section: Discussionmentioning

confidence: 85%

Salvianolic Acid C Protects against Cisplatin-Induced Acute Kidney Injury through Attenuation of Inflammation, Oxidative Stress and Apoptotic Effects and Activation of the CaMKK–AMPK–Sirt1-Associated Signaling Pathway in Mouse Models

Chien

Deng

et al. 2021

Antioxidants

View full text Add to dashboard Cite

show abstract

“…NAD + -dependent class 3 histone deacetylase modulates cell metabolism, particularly in terms of inflammation, apoptosis, senescence, tumorigenesis, and cellular stress and age-related autophagy. Silent information regulator factor 2-related enzyme 1 (Sirt1), which belongs to the family of NAD + -dependent class 3 histone deacetylase, also has the effect mentioned above. − Besides, some studies reported Sirt1 plays its positive role via activating deacetylation of non-histone proteins, such as, p53, NF-κB, and STAT. − Numerous studies confirmed the influence of Sirt1 against OS and ER stress in various cell types. , Moreover, Sirt1 also plays an essential role in maintaining chondrocyte homeostasis in OA. It eliminates free radicals and suppresses OS in order to alleviate cell apoptosis and ECM degeneration, , which, ultimately, delays OA progression. ,, …”

Section: Introductionmentioning

confidence: 99%

Safranal Treatment Induces Sirt1 Expression and Inhibits Endoplasmic Reticulum Stress in Mouse Chondrocytes and Alleviates Osteoarthritis Progression in a Mouse Model

Zhang

Chen

et al. 2022

J. Agric. Food Chem.

View full text Add to dashboard Cite

Osteoarthritis (OA) is an age-related degenerative disease. Oxidative stress (OS) modulates OA pathogenesis by enhancing chondrocyte apoptosis and extracellular matrix (ECM) degeneration via activation of the endoplasmic reticulum (ER) stress. Prior studies revealed that safranal plays a critical role in multiple diseases treatments, but there are no reports on its effect on OA. Therefore, investigating the effect of safranal on OA is needed. As a compound that can lead excessive reactive oxygen species (ROS) accumulation, tert-butyl hydroperoxide (TBHP) was used to induce OS and OS-mediated endoplasmic reticulum (ER) stress for imitating OA in vitro. Besides, the bilateral medial meniscus was removed to induce joint instability and excessive friction of the joint surface to establish destabilization of medial meniscus for imitating the initiation and progression of OA in vivo. We, next, conducted Western blot and RT-PCR analyses to identify biomarkers of the underlying signaling pathway. Our results demonstrated that 30 μM safranal strongly upregulated Sirt1 expression, suppressed TBHP-mediated ER stress, and, in turn, prevented chondrocyte apoptosis and ECM degeneration. Furthermore, compared with the other two classic signaling pathways of ER stress, safranal can inhibit the PERK-eIF2α-CHOP axis at the lower concentration (5 and 15 μM). In vivo, using Safranin O staining, X-ray, immunofluorescence (IF), and immunohistochemical (IHC) staining, we demonstrated that OA progression can be postponed with intraperitoneal injection of 90 and 180 mg/kg safranal in an OA mouse model. Taken together, our analyses revealed that safranal can potentially prevent OA development.

show abstract

“…A previous study showed that p53 acetylation is crucial for p53-mediated antiviral responses [ 20 ]. p53 is the first non-histone deacetylation target of SIRT1 and the SIRT1-p53 axis plays a crucial role in a variety of cellular processes [ 44 ]. Therefore, in this study, it was further explored whether RV infection affects the acetylation of p53 caused by SIRT1.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-194-3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1

Huang,

Liao,

Zhou

et al. 2023

Virol J

View full text Add to dashboard Cite

Background Rotavirus (RV) is the main cause of serious diarrhea in infants and young children worldwide. Numerous studies have demonstrated that RV use host cell mechanisms to motivate their own stabilization and multiplication by degrading, enhancing, or hijacking microRNAs (miRNAs). Therefore, exploring the molecular mechanisms by which miRNAs motivate or restrain RV replication by controlling different biological processes, including autophagy, will help to better understand the pathogenesis of RV development. This study mainly explored the effect of miR-194-3p on autophagy after RV infection and its underlying mechanism of the regulation of RV replication. Methods Caco-2 cells were infected with RV and used to measure the expression levels of miR-194-3p and silent information regulator 1 (SIRT1). After transfection with plasmids and RV infection, viral structural proteins, RV titer, cell viability, and autophagy-linked proteins were tested. The degree of acetylation of p53 was further investigated. A RV-infected neonatal mouse model was constructed in vivo and was evaluated for diarrhea symptoms and lipid droplet formation. Results The results showed that miR-194-3p was reduced but SIRT1 was elevated after RV infection. Elevation of miR-194-3p or repression of SIRT1 inhibited RV replication through the regulation of autophagy. The overexpression of SIRT1 reversed the effects of miR-194-3p on RV replication. The upregulation of miR-194-3p or the downregulation of SIRT1 repressed RV replication in vivo. MiR-194-3p targeted SIRT1 to decrease p53 acetylation. Conclusion These results were used to determine the mechanism of miR-194-3p in RV replication, and identified a novel therapeutic small RNA molecule that can be used against RV.

show abstract

IRF9 promotes apoptosis and innate immunity by inhibiting SIRT1-p53 axis in fish

Cited by 13 publications

References 41 publications

Salvianolic Acid C Protects against Cisplatin-Induced Acute Kidney Injury through Attenuation of Inflammation, Oxidative Stress and Apoptotic Effects and Activation of the CaMKK–AMPK–Sirt1-Associated Signaling Pathway in Mouse Models

Salvianolic Acid C Protects against Cisplatin-Induced Acute Kidney Injury through Attenuation of Inflammation, Oxidative Stress and Apoptotic Effects and Activation of the CaMKK–AMPK–Sirt1-Associated Signaling Pathway in Mouse Models

Safranal Treatment Induces Sirt1 Expression and Inhibits Endoplasmic Reticulum Stress in Mouse Chondrocytes and Alleviates Osteoarthritis Progression in a Mouse Model

MicroRNA-194-3p impacts autophagy and represses rotavirus replication via targeting silent information regulator 1

Contact Info

Product

Resources

About