Dataset Information

The rCC16 Protein Protects Against LPS-Induced Cell Apoptosis and Inflammatory Responses in Human Lung Pneumocytes.

ABSTRACT: Objective:Our previous clinical study showed that low lung levels of CC16 strongly influence the occurrence and development of ARDS. The aim of the present study was to evaluate the therapeutic effect of rCC16 on LPS-induced inflammation in A549 cells and to determine its mechanism. Methods:Cell apoptosis and inflammation was induced by LPS stimulation. The cytotoxic effect of rCC16 was evaluated using the MTT assay. Cytokine levels were determined using enzyme-linked immunosorbent assays. The molecular mechanism of rCC16 was investigated by analyzing relevant signaling pathways. Results:The LPS treatment of A549 cells significantly decreased cell viability, increased the levels of the apoptotic proteins Bax, Bak and Cleaved Caspase-3, the secretion of inflammatory cytokines, and the expression levels of TLR4, p-NF/?B, MAPK proteins. While the levels of Bcl-2, p-AKT, p-mTOR, p-ERK1/2, NF/?B, p-AMPK, and p-p38 were significantly decreased in LPS-treated A549 cells. Our experimental results also confirmed that rCC16 inhibited LPS-induced apoptosis, promoted A549 cell proliferation by activating the PI3K/AKT/mTOR/ERK1/2 pathway, and inhibited the release of certain inflammatory factors, especially HMGB1, through dephosphorylation and inactivation of the TLR4/NF-?B/AMPK signaling pathways. Conclusion:These results highlight the potential utility of CC16 as an important cytokine for the prevention or treatment of inflammation and show that CC16 may play an important role in the future clinical treatment of ARDS.

SUBMITTER: Lin J

PROVIDER: S-EPMC7371929 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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The rCC16 Protein Protects Against LPS-Induced Cell Apoptosis and Inflammatory Responses in Human Lung Pneumocytes.

Lin Jinle J Li Jiemei J Shu Min M Wu Weigang W Zhang Wenwu W Dou Qingli Q Wu Jian J Zeng Xiaobin X

Frontiers in pharmacology 20200714

<h4>Objective</h4>Our previous clinical study showed that low lung levels of CC16 strongly influence the occurrence and development of ARDS. The aim of the present study was to evaluate the therapeutic effect of rCC16 on LPS-induced inflammation in A549 cells and to determine its mechanism.<h4>Methods</h4>Cell apoptosis and inflammation was induced by LPS stimulation. The cytotoxic effect of rCC16 was evaluated using the MTT assay. Cytokine levels were determined using enzyme-linked immunosorben ...[more]

PMID: 32760279

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Project description:BackgroundIt has been reported that hsa_circRNA_100833 (identified as circFADS2) and miR-133a play opposite roles in LPS-induced cell apoptosis, which contributes to the development of sepsis. This study was carried out to explore the interaction between circFADS2 and miR-133a in sepsis.MethodsExpression of circFADS2 and miR-133a in plasma from both sepsis patients (n=62) and healthy controls (n=62) was studied by RT-qPCR. Pearson's correlation coefficient analysis was utilized to analyze the correlation between circFADS2 and miR-133a levels across plasma samples from sepsis patients. Cell viability and apoptosis, levels of proteins associated with apoptosis (cleaved caspase-3 and cleaved caspase-9), and expression of pro-inflammatory cytokines in LPS-treated HBEpCs were detected by MTT assay, cell apoptosis assay, western blot, and ELISA, respectively. In addition, a dual-luciferase reporter assay was performed to verify the interaction between circFADS2 and miR-133a.ResultsCircFADS2 was under-expressed (0.56-fold vs. control) in sepsis, and miR-133a was highly expressed (2.05-fold vs. control) in sepsis. An inverse correlation between circFADS2 and miR-133a was observed across sepsis samples. LPS decreased cell viability, increased cell apoptosis, and elevated productions of tumor necrosis factor (TNF)-α, interleukins (IL)-1β, IL-6, and IL-8 in HBEpCs in a dose-dependent manner. In addition, circFADS2 was identified as a target gene of miR-133a. The further experiment revealed that circFADS2 overexpression and miR-133a inhibition prominently promoted cell viability (1.71-fold vs. pcDNA3.1; 1.65-fold vs. NC miRNA) and decreased apoptosis of LPS-treated HBEpCs (0.44-fold vs. pcDNA3.1; 0.47-fold vs. NC miRNA). Moreover, circFADS2 knockdown and miR-133a overexpression inhibited viability (0.36-fold vs. pcDNA3.1; 0.37-fold vs. NC miRNA) and increased apoptosis (1.54-fold vs. pcDNA3.1; 1.51-fold vs. NC miRNA) of LPS-treated HBEpCs. Notably, circFADS2 overexpression reduced the effects of miR-133a on LPS-treated HBEpCs.ConclusionsCircFADS2 is under-expressed in sepsis and may protect lung cells from LPS-induced apoptosis by downregulating miR-133a.

Dataset Information

The rCC16 Protein Protects Against LPS-Induced Cell Apoptosis and Inflammatory Responses in Human Lung Pneumocytes.

Publications

The rCC16 Protein Protects Against LPS-Induced Cell Apoptosis and Inflammatory Responses in Human Lung Pneumocytes.

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