SOCS-1 rescues IL-1β-mediated suppression of epithelial sodium channel in mouse lung epithelial cells via ASK-1

Galam, Lakshmi; Soundararajan, Ramani; Breitzig, Mason; Rajan, Ashna; Yeruva, Rajashekar Reddy; Czachor, Alexander; Harris, Francine; Lockey, Richard F.; Kolliputi, Narasaiah

doi:10.18632/oncotarget.8543

Cited by 13 publications

(21 citation statements)

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“…Galam et al found that SOCS-1 exhibits its protective role against ALI by suppressing pro-inflammatory cytokines production [42]. Zhang et al showed that SOCS-1 ameliorated smoke inhalation-induced ALI through inhibition of apoptosis,…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of miR-let-7e attenuates LPS-induced acute lung injury in mice via inhibiting pulmonary inflammation by targeting SCOS1/NF-κB pathway

Zhang

et al. 2021

Bioscience Reports

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Excessive pulmonary inflammatory response is critical in the development of acute lung injury (ALI). Previously, microRNAs (miRNAs) have been recognized as an important regulator of inflammation in various diseases. However, the effects and mechanisms of miRNAs on inflammatory response in ALI remain unclear. Herein, we tried to screen miRNAs in the processes of ALI and elucidate the potential mechanism. Using a microarray assay, microRNA let-7e (let-7e) was chose as our target for its reported suppressive roles in several inflammatory diseases. Downregulation of let-7e by antagomiR-let-7e injection attenuated LPS-induced acute lung injury. We also found that antagomiR-let-7e could obviously improve the survival rate in ALI mice. Moreover, let-7e inhibition reduced LPS-induced the production of pro-inflammatory cytokines (i.e., TNF-α, IL-1β and IL-6) in bronchoalveolar lavage fluid (BALF). Luciferase reporter assays confirmed that suppressor of cytokine signaling 1 (SOCS1), a powerful attenuator of nuclear factor kappa B (NF-κB) signaling pathway, was directly targeted and suppressed by let-7e in RAW264.7 cells. In addition, it was further observed that SOCS1 was downregulated, and inversely correlated with let-7e expression levels in lung tissues of ALI mice. Finally, downregulation of let-7e suppressed the activation of NF-κB pathway, as evidenced by the reduction of p-IκBα, and nuclear p-p65 expressions in ALI mice. Collectively, our findings indicate that let-7e antagomir protects mice against LPS-induced lung injury via repressing the pulmonary inﬂammation though regulation of SOCS1/NF-κB pathway, and let-7e may act as a potential therapeutic target for ALI.

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Section: Discussionmentioning

confidence: 99%

Down-regulation of miR-let-7e attenuates LPS-induced acute lung injury in mice via inhibiting pulmonary inflammation by targeting SCOS1/NF-κB pathway

Zhang

et al. 2021

Bioscience Reports

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“…It has also been pointed out that SOCS-1 exerts cytoprotection against apoptosis initiated by tumor necrosis factor-α, IFN-γ and apoptosis-inducing chemicals in tissue injury [9]. SOCS-1 overexpression rescues alveolar epithelial cells from apoptosis in hyperoxia-induced ALI through apoptosis signal-regulating kinase 1 (ASK-1) degradation [8,9]. Consistently, our previous study demonstrates that overexpression of SOCS-1 protects alveolar epithelial cells from reduction of cellular viability and inhibits apoptosis induced by smoke via degradation of ASK-1 [33].…”

Section: Discussionmentioning

confidence: 99%

“…Suppressor of cytokine signaling 1 (SOCS-1), also known as STAT-induced STAT inhibitor 1 (SSI-1) and JAB, is a member of cytokine signaling inhibitor family, which regulate the production of several cytokines associated with inflammation [7]. Several studies indicate that SOCS-1 is an important regulator in pulmonary inflammation [7,8]. Earlier experiments show that SOCS-1 restores majority of interleukin-1β (IL-1β)-mediated cellular damage during hyperoxic lung injury [8,9].…”

Section: Introductionmentioning

confidence: 99%

“…Several studies indicate that SOCS-1 is an important regulator in pulmonary inflammation [7,8]. Earlier experiments show that SOCS-1 restores majority of interleukin-1β (IL-1β)-mediated cellular damage during hyperoxic lung injury [8,9]. Exogenous SOCS-1 adenovirus (Ad-SOCS-1) administration exhibits protective effect against bleomycin-induced pulmonary inflammation and fibrosis as well as hyperoxic acute lung injury [7,10].…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1

et al. 2020

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Smoke inhalation causes acute lung injury (ALI), a severe clinical disease with high mortality. Accumulating evidence indicates that microRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS-1), as mediators of inflammatory response, are involved in the pathogenesis of ALI. In this paper, we explored the proinflammatory mechanism of miR-155 in smoke-inhalation-induced ALI. Our data revealed that smoke inhalation induces miR-155 expression, and miR-155 knockout (KO) significantly ameliorates smoke-inhalation-induced lung injury in mice. Neutrophil infiltration and myeloperoxidase (MPO), macrophage inflammatory protein 2 (MIP-2) and keratinocyte chemoattractant (KC) expressions were decreased in miR-155–/– mice after smoke inhalation as well. Real-time RT-PCR and immunoblotting results showed that SOCS-1 level was remarkably increased in miR-155–/– mice after smoke exposure. Furthermore, the experiments performed in isolated miR-155 KO pulmonary neutrophils demonstrated that the lack of SOCS-1 enhanced inflammatory cytokines (MIP-2 and KC) secretion in response to smoke stimulation. In conclusion, smoke induces increased expression of miR-155, and miR-155 is involved in inflammatory response to smoke-inhalation-induced lung injury by inhibiting the expression of SOCS-1.

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“…Current research suggests that pulmonary edema may be attributed to the flammatory response during ALI. Several inflammatory cytokines, including TNF-α and IL-1β may affect ENaC expression [9][10][11]. Many studies have indicated that inhibiting the release of inflammatory cytokines may promote AFC by increasing the expression of ENaC [12].…”

Section: Introductionmentioning

confidence: 99%

Dexmedetomidine alleviates pulmonary edema through epithelial sodium channel (ENaC) via the PI3K/Akt/Nedd4-2 pathway in LPS- induced acute lung injury

Jiang¹,

Huang

et al. 2020

Preprint

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Background: Pulmonary edema is a hallmark in acute lung injury(ALI). Researchers have also revealed that dexmedetomidine (Dex) alleviate pulmonary edema following ALI, but the mechanism is unclear.The alveolar epithelial sodium channel (ENaC)-mediated alveolar fluid clearance (AFC) plays an important role in reducing pulmonary edema. In this study, we attempted to investigate the effect of Dex on ENaC in modulating AFC and its mechanism. Methods: LipopolysacchAride (LPS) was used to induce ALI in rat and alveolar epithelial cell injury in A549 cell. The rats were randomly allotted into the following groups: control, LPS, LPS+Dex, LPS+Dex+LY294002 (n = 6 per group). In vitro, cells (1×10 6 cells/cm 2 ) were subcultured in six-well plates, then cells were allotted into the following groups: control, LPS, LPS+Dex, LPS+Dex+LY294002. Results: In vivo, Dex markedly reduced pulmonary edema induced by LPS through promoting AFC.Moreover, Dex prevented LPS-induced downregulation of α-, β- and γ-ENaC expression. In A549 cells stimulated with LPS, Dex attanuated LPS-mediated cell injury and the downregulation of α-, β- and γ-ENaC expression. Howere, all of which was blocked by PI3K inhibitor LY294002,suggesting that the protective role of Dex is PI3K dependent. Additionaly, Dex increases the expression of phosphorylated Akt and reduces the expression of Need4-2 in vivo and vitro, while the LY294002 reverses the effect of Dex, indicating that Dex activates the PI3K/Akt/Nedd4-2 signaling pathway. C onclusio ns: Dex alleviates pulmonary edema by promoting AFC, and the mechanism is partly related to up-regulation of ENaC expression via PI3K/Akt/Nedd4-2 signaling pathway.

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SOCS-1 rescues IL-1β-mediated suppression of epithelial sodium channel in mouse lung epithelial cells via ASK-1

Cited by 13 publications

References 50 publications

Down-regulation of miR-let-7e attenuates LPS-induced acute lung injury in mice via inhibiting pulmonary inflammation by targeting SCOS1/NF-κB pathway

Down-regulation of miR-let-7e attenuates LPS-induced acute lung injury in mice via inhibiting pulmonary inflammation by targeting SCOS1/NF-κB pathway

MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1

Dexmedetomidine alleviates pulmonary edema through epithelial sodium channel (ENaC) via the PI3K/Akt/Nedd4-2 pathway in LPS- induced acute lung injury

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