Exogenous H2S Inhibits Autophagy in Unilateral Ureteral Obstruction Mouse Renal Tubule Cells by Regulating the ROS-AMPK Signaling Pathway

Chen, Qinghai; Yu, Song; Zhang, Kuo; Zhang, Zuobiao; Li, Chao; Gao, Bingpeng; Zhang, Weihua; Wang, Yan

doi:10.1159/000493824

Cited by 31 publications

(18 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In recent years, it has been found that autophagy is closely related to the protective effect of H 2 S. Pretreatment with NaHS could alleviate acute myocardial ischemia injury by suppressing autophagy under oxidative stress, significantly reducing brain damage and preserving the blood-brain barrier integrity after traumatic brain injury by inhibiting autophagy via activation of the PI3K/Akt/mTOR signaling pathway and mitigating acrylonitrile-induced decrease of cell viability through influencing autophagy (Bai et al, 2018; Xu et al, 2018; Yang et al, 2018). Exogenous H 2 S also might protect mouse kidney against unilateral ureteral obstruction by suppressing ROS-AMPK-mediated autophagy, ameliorating blood-spinal cord barrier disruption and improving functional recovery by suppressing endoplasmic reticulum stress-mediated autophagy and inducing the apoptosis of hepatocellular carcinoma cells through promoting autophagy via the PI3K/AKT/mTOR signaling pathway (Chen et al, 2018a,b; Wang et al, 2017, 2018). Autophagy has also been reported to be closely related to NLRP3 inflammasome-mediated inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…Exogenous H 2 S can significantly improve myocardial inflammatory injury induced by ischemia, reduce the release of inflammatory mediators, inhibit the production of inflammatory mediators in primary myocardial cells of rats induced by lipopolysaccharide (LPS) and alleviate inflammatory injury of gastric mucosal cells induced by ischemia-reperfusion (Sodha et al, 2009; Elrod et al, 2007; Toldo et al, 2014; Guo et al, 2014). Exogenous H 2 S also inhibits oxidative stress response and weakens LPS-induced acute renal inflammatory injury (Chen et al, 2018a,b), inhibits the activation of inflammasome by sodium urate crystallization and reduces the release of proinflammatory factors (Castelblanco et al, 2018). At present, the relationship between H 2 S and NLRP3 inflammasome has gradually become a research hotspot.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Exogenous hydrogen sulfide mitigates NLRP3 inflammasome-mediated inflammation through promoting autophagy via AMPK-mTOR pathway

2019

View full text Add to dashboard Cite

The aim of this study was to investigate whether exogenous hydrogen sulfide (H 2 S) could mitigate NLRP3 inflammasome-mediated inflammation through promoting autophagy via the AMPK-mTOR pathway in L02 cells. L02 cells were stimulated with different concentrations of oleic acid (OA), then cell viability and the protein expression of NLRP3 and pro-caspase-1 were detected by MTT and western blot, respectively, to determine appropriate OA concentration in this study. The cells were divided into four groups: the cells in the control group were cultured with RPMI-1640 for 24.5 h; the cells in the OA group were cultured with RPMI-1640 for 0.5 h, then were stimulated with 1.2 mmol/l OA for 24 h; the cells in the NaHS+OA group were pretreated with sodium hydrogen sulfide (NaHS, a donor of H 2 S) for 0.5 h before exposure to OA for 24 h; and the cells in the NaHS group were treated with NaHS 0.5 h, then were cultured with RPMI-1640 for 24 h. Subsequently, the cells in every group were collected and the protein expression of NLRP3, procaspase-1, cleaved caspase-1, P62, LC3, Beclin1, T-AMPK, P-AMPK, T-mTOR, P-mTOR and the level of IL-1β were detected by western blot and ElISA, respectively. Exogenous H 2 S reduced the level of NLRP3, caspase-1, P62, IL-1β and the ratio of P-mTOR/T-mTOR induced by OA and increased the ratio of LC3 II/I and the protein expression of Beclin1 suppressed by OA. This study demonstrates for the first time that H 2 S might suppress NLRP3 inflammasome-mediated inflammation induced by OA through promoting autophagy via the AMPK-mTOR pathway. It provides a theoretical basis for the further study of the anti-inflammatory mechanism of H 2 S.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Exogenous hydrogen sulfide mitigates NLRP3 inflammasome-mediated inflammation through promoting autophagy via AMPK-mTOR pathway

2019

View full text Add to dashboard Cite

show abstract

“…Change in intracellular ROS levels were by measuring the oxidative conversion of cell permeable 2′,7′-dichlorofluorescein diacetate (DCFH-DA, Sigma) to fluorospectro-photometer ( Chen et al, 2018 ). Cells were plated in 6 cm dish (1 × 10 6 cells/well) and allowed to attach overnight.…”

Section: Methodsmentioning

confidence: 99%

RSL3 Drives Ferroptosis Through GPX4 Inactivation and ROS Production in Colorectal Cancer

et al. 2018

View full text Add to dashboard Cite

Ferroptosis is an iron-dependent, oxidative cell death, and is characterized by iron-dependent accumulation of reactive oxygen species (ROS) within the cell. It has been implicated in various human diseases, including cancer. Recently, ferroptosis, as a non-apoptotic form of cell death, is emerging in specific cancer types; however, its relevance in colorectal cancer (CRC) is unexplored and remains unclear. Here, we showed that ferroptosis inducer RSL3 initiated cell death and ROS accumulation in HCT116, LoVo, and HT29 CRC cells over a 24 h time course. Furthermore, we found that ROS levels and transferrin expression were elevated in CRC cells treated with RSL3 accompanied by a decrease in the expression of glutathione peroxidase 4 (GPX4), indicating an iron-dependent cell death, ferroptosis. Overexpression GPX4 resulted in decreased cell death after RSL3 treatment. Therefore, RSL3 was able to induce ferroptosis on three different CRC cell lines in vitro in a dose- and time-dependent manner, which was due to increased ROS and an increase in the cellular labile iron pool. Moreover, this effect was able to be reversed by overexpression of GPX4. Taken together, our results suggest that the induction of ferroptosis contributed to RSL3-induced cell death in CRC cells and ferroptosis may be a pervasive and dynamic form of cell death for cancer treatment.

show abstract

“…Autophagy is induced in response to diverse stimuli of ALI, including bacterial infection, lipopolysaccharide (LPS) exposure, sepsis, trauma, hyperoxia, pharmaceutical exposure, and mechanical ventilation [ 241 ]. One of the major inducers of autophagy in ALI is increased oxidative stress, which has been shown to promote autophagy in a number of lung cell lines and animal models of lung injury [ [242] , [243] , [244] ]. However, the role of autophagy in ALI still remains controversial ( Fig.…”

Section: Autophagy and Ros In Pulmonary Diseasesmentioning

confidence: 99%

Complex interplay between autophagy and oxidative stress in the development of pulmonary disease

et al. 2020

View full text Add to dashboard Cite

The autophagic pathway involves the encapsulation of substrates in double-membraned vesicles, which are subsequently delivered to the lysosome for enzymatic degradation and recycling of metabolic precursors. Autophagy is a major cellular defense against oxidative stress, or related conditions that cause accumulation of damaged proteins or organelles. Selective forms of autophagy can maintain organelle populations or remove aggregated proteins. Dysregulation of redox homeostasis under pathological conditions results in excessive generation of reactive oxygen species (ROS), leading to oxidative stress and the associated oxidative damage of cellular components. Accumulating evidence indicates that autophagy is necessary to maintain redox homeostasis. ROS activates autophagy, which facilitates cellular adaptation and diminishes oxidative damage by degrading and recycling intracellular damaged macromolecules and dysfunctional organelles. The cellular responses triggered by oxidative stress include the altered regulation of signaling pathways that culminate in the regulation of autophagy. Current research suggests a central role for autophagy as a mammalian oxidative stress response and its interrelationship to other stress defense systems. Altered autophagy phenotypes have been observed in lung diseases such as chronic obstructive lung disease, acute lung injury, cystic fibrosis, idiopathic pulmonary fibrosis, and pulmonary arterial hypertension, and asthma. Understanding the mechanisms by which ROS regulate autophagy will provide novel therapeutic targets for lung diseases. This review highlights our current understanding on the interplay between ROS and autophagy in the development of pulmonary disease.

show abstract

Exogenous H2S Inhibits Autophagy in Unilateral Ureteral Obstruction Mouse Renal Tubule Cells by Regulating the ROS-AMPK Signaling Pathway

Cited by 31 publications

References 36 publications

Exogenous hydrogen sulfide mitigates NLRP3 inflammasome-mediated inflammation through promoting autophagy via AMPK-mTOR pathway

Exogenous hydrogen sulfide mitigates NLRP3 inflammasome-mediated inflammation through promoting autophagy via AMPK-mTOR pathway

RSL3 Drives Ferroptosis Through GPX4 Inactivation and ROS Production in Colorectal Cancer

Complex interplay between autophagy and oxidative stress in the development of pulmonary disease

Contact Info

Product

Resources

About