miR-33 and RIP140 participate in LPS-induced  acute lung injury

Li, Hua; Hou, Huan; Liu, Shuang; Feng, Yangyang; Zhong, Wansi; Hu, Xiaojuan; Yan, Nianlong

doi:10.3906/sag-1804-173

Cited by 9 publications

(4 citation statements)

References 27 publications

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“…LPS or endotoxin is a proinflammatory cytokine with very high bioactivity. Li et al [ 22 ] found that LPS was able to directly act on PMVECs, induce the release of inflammatory factors, and lead to cell permeability change, cytoskeleton rearrangement, cell cycle arrest, and cell apoptosis. Currently, no radical measures have been found to directly prevent PMVECs from injury, and the research hotspots mainly focus on searching for suitable drugs to help PMVECs resist LPS-induced cell injury.…”

Section: Discussionmentioning

confidence: 99%

[Retracted] Ginkgolide A Participates in LPS‐Induced PMVEC Injury by Regulating miR‐224 and Inhibiting p21 in a Targeted Manner

Liu

Yang

2022

Contrast Media & Molecular Imaging

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Most studies have focused on the protective effects of ginkgolide A against ischemia/reperfusion-induced cardiomyopathy and injury of the brain, liver, and other organs, but there are few reports about the protection of lung tissues. This study was designed to clarify the protection of ginkgolide A against lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial cell (PMVEC) injury. PMVECs were extracted and fell into control, LPS, and ginkgolide A groups. Next, we delved into the growth activity and apoptosis rate of cells via the CCK-8 assay and Hoechst staining, independently. Beyond that, western blotting (WB) was implemented for measurement of the expressions of cyclin D1, cyclin-dependent kinase 4 (CDK4), and CDK inhibitor (p21) that pertained to the cell cycle. The target sites of ginkgolide A were confirmed by miRNA array and real-time quantitative PCR. The relationship between miR-224 and p21 was analyzed using dual-luciferase reporter gene assay. Compared with the control group, the LPS group and ginkgolide A group had significantly decreased cell growth activity and relative expressions of cyclin D1 and CDK4 and elevated apoptosis rate and p21 expression. Pronounced elevations were observable in the cell growth activity and expressions of cyclin D1, CDK4, and p21, while the ginkgolide A group presented with a reduced apoptosis rate in comparison with the LPS group ( P < 0.05 ). MiR-224 was the target of ginkgolide A, which had targeted regulatory effects on p21. Ginkgolide A can modulate miR-224 expression and regulate p21 expression in a targeted manner to enhance the resistance of PMVECs to LPS-induced cell apoptosis.

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Section: Discussionmentioning

confidence: 99%

[Retracted] Ginkgolide A Participates in LPS‐Induced PMVEC Injury by Regulating miR‐224 and Inhibiting p21 in a Targeted Manner

Liu

Yang

2022

Contrast Media & Molecular Imaging

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“…Li et al. also showed that MiR-33 is involved in acute lung injury provoked by LPS, too ( Li et al., 2019 ). Moreover, over-expression of MiR-146b could alleviate ARDS, both in mice and in cells ( He et al., 2019 ).…”

Section: Discussionmentioning

confidence: 99%

MiR-199a-3p-regulated alveolar macrophage-derived secretory autophagosomes exacerbate lipopolysaccharide-induced acute respiratory distress syndrome

Liu

Dong

et al. 2022

Front. Cell. Infect. Microbiol.

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PurposeAcute respiratory distress syndrome (ARDS) is a prevalent illness in intensive care units. Extracellular vesicles and particles released from activated alveolar macrophages (AMs) assist in ARDS lung injury and the inflammatory process through mechanisms that are unclear. This study investigated the role of AM-derived secretory autophagosomes (SAPs) in lung injury and microRNA (MiR)-199a-3p-regulated inflammation associated with ARDS in vitro and in a murine model.MethodsThe ARDS model in mouse was established by intratracheal LPS lipopolysaccharide (LPS) injection. The agomirs or antagomirs of MiR-199a-3p were injected into the caudal vein to figure out whether MiR-199a-3p could influence ARDS inflammation and lung injury, whereas the mimics or inhibitors of MiR-199a-3p, siRNA of Rab8a, or PAK4 inhibitor were transfected or applied to RAW264.7 cells to evaluate the mechanism of SAP release. Culture supernatants of RAW264.7 cells treated with LPS or bronchoalveolar lavage fluid from mice were collected for the isolation of SAPs.ResultsWe found that MiR-199a-3p was over-expressed in the lungs of ARDS mice. The MiR-199a-3p antagomir alleviated, whereas the MiR-199a-3p agomir exacerbated LPS-induced inflammation in mice by promoting AM-derived SAP secretion. In addition, MiR-199a-3p over-expression exacerbated LPS-induced ARDS via activating Rab8a, and Rab8a silencing significantly suppressed the promoting influence of the MiR-199a-3p mimic on SAP secretion. Furthermore, MiR-199a-3p mimic activated Rab8a by directly inhibiting PAK4 expression.ConclusionThe novel finding of this study is that MiR-199a-3p participated in the regulation of SAP secretion and the inflammatory process via targeting of PAK4/Rab8a, and is a potential therapeutic candidate for ARDS treatment.

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“…Experimental data represent the average and standard deviation of three biological replicates. The SMS2 expression level was normalized to the expression of GAPDH [ 46 ].…”

Section: Methodsmentioning

confidence: 99%

Sphingomyelin Synthase 2 Participate in the Regulation of Sperm Motility and Apoptosis

Luo

et al. 2020

Molecules

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Sphingomylin participates in sperm function in animals, and also regulates the Akt and ERK signaling pathways, both of which are associated with the asthenospermia. Sphingomyelin synthase 2 (SMS2) is involved in the biosynthesis of sphingomylin. To determine the relationship between SMS2 and human sperm function, we analyzed the distribution of SMS2 in human sperm and testes, and SMS2 expression in patients with asthenospermia and normozoospermia; human sperm were treated with anti-SMS2, and the sperm motility, penetration ability into methylcellulose, capacitation and acrosome reaction, and sperm [Ca2+]i imaging were evaluated, while the Akt and ERK pathway and cleaved caspase 3 were also analyzed. Results showed that SMS2 was localized in the testis and human sperm, and the protein levels of normozoospermia were higher than asthenospermia. Inhibition of SMS2 activity significantly decreased sperm motility and penetration ability into methylcellulose, but had no influence on capacitation and acrosome reaction, or on intracellular [Ca2+]i compared to IgG-treated control groups. Moreover, the phosphorylation level of Akt was decreased, whereas the phosphorylation of ERK and cleaved-caspase 3 levels were significantly increased. Taken together, SMS2 can affect sperm motility and penetration ability into methylcellulose, and participate in apoptosis associated with the Akt and ERK signaling pathways.

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miR-33 and RIP140 participate in LPS-induced acute lung injury

Cited by 9 publications

References 27 publications

[Retracted] Ginkgolide A Participates in LPS‐Induced PMVEC Injury by Regulating miR‐224 and Inhibiting p21 in a Targeted Manner

[Retracted] Ginkgolide A Participates in LPS‐Induced PMVEC Injury by Regulating miR‐224 and Inhibiting p21 in a Targeted Manner

MiR-199a-3p-regulated alveolar macrophage-derived secretory autophagosomes exacerbate lipopolysaccharide-induced acute respiratory distress syndrome

Sphingomyelin Synthase 2 Participate in the Regulation of Sperm Motility and Apoptosis

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