The incidence and mortality of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) are still very high, but stem cells show some promise for its treatment. Here we found that intratracheal administration of human umbilical cord-mesenchymal stem cells (UC-MSCs) significantly improved survival and attenuated the lung inflammation in lipopolysaccharide (LPS)-induced ALI mice. We also used the proteins-chip and bioinformatics to analyze interactions between UC-MSCs treatment and immune-response alternations of ALI mice. Then we demonstrated that UC-MSCs could inhibit the inflammatory response of mouse macrophage in ALI mice, as well as enhance its IL-10 expression. We provide data to support the concept that the therapeutic capacity of UC-MSCs for ALI was primarily through paracrine secretion, particularly of prostaglandin-E2 (PGE2). Furthermore, we showed that UC-MSCs might secrete a panel of factors including GM-CSF, IL-6 and IL-13 to ameliorate ALI. Our study suggested that UC-MSCs could protect LPS-induced ALI model by immune regulation and paracrine factors, indicating that UC-MSCs should be a promising strategy for ALI/ARDS.

Hepatocellular carcinoma (HCC) is one of the most common malignancies. Long non-coding RNAs (lncRNAs) are involved in HCC. This study aimed to explore the effects of lncRNA MALAT1 on HCC development. MALAT1, ZEB1, and miR-143-3p in HCC tissues was detected by qRT-PCR. Effect of MALAT1 on the proliferation and metastasis of HCC cells was estimated by cell-counting, wound-healing, and transwell assays. Luciferase reporter assays were used to explore miR-143-3p's target, ZEB1. QRT-PCR and Western blot were employed to determine the effects of MALAT1 or/and miR-143-3p on ZEB1 expression. MALAT1 was upregulated in HCC tissues. ZEB1 was a target of miR-143-3p. miR-143-3p binds with MALAT1, and was regulated by MALAT1. The regulation of MALAT1 on ZEB1 was mediated by miR-143-3p. Transfection with siR-MALAT1 significantly inhibited cell proliferation and invasion, while knockdown of miR-181a partially reversed these effects. Our findings suggest that MALAT1 may regulate ZEB1 expression by sponging miR-143-3p and promotes hepatocellular carcinoma progression. J. Cell. Biochem. 118: 4836-4843, 2017. © 2017 Wiley Periodicals, Inc.

Hepatic fibrosis occurs during chronic hepatic injury and is involved in hepatic stellate cells (HSCs) activated by several types of immune cells. Among the immune cells, hepatic macrophages and their crosstalk with HSCs play a vital role in all stages of hepatic fibrosis. Exosomes, which are 30‐150 nm lipid bilayer vehicles, can transfer specific lipid, nucleic acids, proteins, and other bioactive molecules. Exosomes can act as good communication between macrophages and HSCs. Herein, we investigated the role of exosomes between THP‐1 macrophage and HSCs in the progression of liver fibrosis. Exosomes originating from lipopolysaccharide (LPS)‐treated THP‐1 macrophages promoted HSCs proliferation and induced the increased expression of fibrotic genes. LPS could alter the miRNA profile in exosomes secreted from THP‐1 macrophages. The changed miR‐103‐3p in exosomes could promote HSCs proliferation and activation by targeting Krüppel‐like factor 4 (KLF4) and it plays important roles in the crosstalk between THP‐1 macrophages and HSCs during the progression of liver fibrosis. Moreover, miR‐103‐3p in serum exosomes from liver fibrosis patients could be a biomarker for liver fibrosis. Therefore, exosomes may have important roles in the crosstalk between macrophage and HSCs in the progression of chronic liver diseases.

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A predominant Th17 population is a marker of allergic rhinitis (AR). The aryl hydrocarbon receptor (AhR) exhibits strong immunomodulation potential via regulation of the differentiation of T lymphocytes and dendritic cells (DCs) after activation by its ligand, such as 2-(1 0 H-indole-3 0 -carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE). The aim of this study was to analyze the effect of AhR on Th17 differentiation by investigating the action of ITE on DCs and CD4 þ T cells from patients with AR. In all, 26 AR patients and 12 healthy controls were included in this study. The expression of interleukin (IL)-1b, IL-6, IL-10, and IL-17 in the culture supernatant and the presence of Th17 cells in CD4þ T cells and DC-CD4 þ T-cell co-culture system were measured before and after treatment with ITE. We show that ITE significantly induced cell secretion of IL-10 and inhibited IL-1b and IL-6 production in DCs, and promoted IL-10 production and suppressed IL-17 expression in CD4 þ T cells in vitro. It also suppressed the expansion of Th17 cells in vitro. Our work demonstrates that ITE acts on DCs and CD4 þ T cells to inhibit the Th17 response that suppresses AR; the AhR-DC-Th17 axis may be an important pathway in the treatment of AR. ITE, a nontoxic AhR ligand, attenuated the Th17 response; thus, it appears to be a promising therapeutic candidate for suppressing the inflammatory responses associated with AR.