Effects of sepsis on the metabolism of sphingomyelin and cholesterol in mice with liver dysfunction

Li, Jiaqi; Xia, Kun; Xiong, Mingdi; Wang, Xi; Yan, Nianlong

doi:10.3892/etm.2017.5226

Cited by 15 publications

(13 citation statements)

References 32 publications

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“…Lipid rafts, enriched with cholesterol and sphingolipids, are ordered microdomains within plasma membranes. Sphingomyelin (SM) is an essential component of sphingolipids (18). SM is additionally associated with the formation of other membrane microdomains, including clathrin-coated pits and caveolae, thus serving an important role in the regulation of trans-membrane signaling (19).…”

Section: Introductionmentioning

confidence: 99%

Sphingomyelin synthase 1 regulates the epithelial‑to‑mesenchymal transition mediated by the TGF‑β/Smad pathway in MDA‑MB‑231 cells

et al. 2018

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Breast cancer is the most common cancer in women and a leading cause of cancer-associated mortalities in the world. Epithelial-to-mesenchymal transition (EMT) serves an important role in the process of metastasis and invasive ability in cancer cells, and transforming growth factor β1 (TGF-β1) have been investigated for promoting EMT. However, in the present study, the role of the sphingomyelin synthase 1 (SMS1) in TGF-β1-induced EMT development was investigated. Firstly, bioinformatics analysis demonstrated that the overexpression of SMS1 negatively regulated the TGFβ receptor I (TβRI) level of expression. Subsequently, the expression of SMS1 was decreased, whereas, SMS2 had no significant difference when MDA-MB-231 cells were treated by TGF-β1 for 72 h. Furthermore, the present study constructed an overexpression cells model of SMS1 and these cells were treated by TGF-β1. These results demonstrated that overexpression of SMS1 inhibited TGF-β1-induced EMT and the migration and invasion of MDA-MB-231 cells, increasing the expression of E-cadherin while decreasing the expression of vimentin. Furthermore, the present study further confirmed that SMS1 overexpression could decrease TβRI expression levels and blocked smad family member 2 phosphorylation. Overall, the present results suggested that SMS1 could inhibit EMT and the migration and invasion of MDA-MB-231 cells via TGF-β/Smad signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Sphingomyelin synthase 1 regulates the epithelial‑to‑mesenchymal transition mediated by the TGF‑β/Smad pathway in MDA‑MB‑231 cells

et al. 2018

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“…The SMS activity of sperm was measured as previously described [ 37 , 41 ]. Briefly, sperm were homogenized in a buffer containing 50mM Tris-HCl, 1mM EDTA, and 5% sucrose.…”

Section: Methodsmentioning

confidence: 99%

“…Thereafter, the supernatant was collected and then dried by nitrogen gas after being centrifuged at 8000 rpm/min, at 4, for 10 min. Finally, the content of SM was measured as previously described [ 41 , 42 ].…”

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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“…All mice were maintained under a 12-h light/dark cycle and supplied with standard food and water. Sepsis was induced in mice as previously described (20,21). Briefly, the mice were divided into three groups (5 per group): control, LPS, and L+P (LPS + PDTC) groups.…”

Section: Animal Model Of Alimentioning

confidence: 99%

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

Li¹,

Hou²,

Liu³

et al. 2019

Turk J Med Sci

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Background/aim: Pulmonary microvascular endothelial cells (PMVECs) play a pivotal role in the process of acute lung injury (ALI), which can be induced by lipopolysaccharide (LPS). Numerous reports have indicated that both miR-33 and RIP140 are involved in the inflammatory response in macrophages. In this study, we sought to investigate whether miR-33 and RIP140 participate in ALI induced by LPS. Materials and methods: First, we isolated and identified PMVECs from BALB/c mice. Subsequently, both PMVECs and BALB/c mice were treated with PBS, LPS, or pyrrolidine dithiocarbamate (PDTC) plus LPS and divided into three groups: control (PBS), LPS (LPS), and L+P (LPS plus PDTC) groups. We assessed pathology by hematoxylin and eosin staining, and miR-33 and RIP140 expression levels were examined using quantitative PCR and Western blot analyses. Results: Our results demonstrated that LPS can induce PMVEC injury and ALI and that LPS treatment significantly decreased miR-33 expression compared with controls (P < 0.001, n = 5). On the contrary, RIP140 was markedly overexpressed by LPS treatment (P < 0.001, n = 5). However, this alteration can be inhibited by pretreatment with PDTC before LPS (P < 0.05, n = 5). Conclusion: This study is the first to confirm that both miR-33 and RIP140 participate in LPS-induced PMVEC injury and ALI, which may help uncover the mechanism of ALI.

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Effects of sepsis on the metabolism of sphingomyelin and cholesterol in mice with liver dysfunction

Cited by 15 publications

References 32 publications

Sphingomyelin synthase 1 regulates the epithelial‑to‑mesenchymal transition mediated by the TGF‑β/Smad pathway in MDA‑MB‑231 cells

Sphingomyelin synthase 1 regulates the epithelial‑to‑mesenchymal transition mediated by the TGF‑β/Smad pathway in MDA‑MB‑231 cells

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

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

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