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Background and Objective: Neutrophils‐derived exosomes have been shown to cause tissue inflammation in many diseases, but their role in periodontitis, a neutrophil‐mediated disease, is unknown. Here, we investigated the effect of neutrophil‐like cells derived exosomes on osteogenic dysfunction of periodontal ligament stem cells (PDLSCs) in periodontitis. Methods: Neutrophil‐like cells were derived from HL‐60 cells by dimethylsulfoxide stimulation. Exosomes were isolated by ultracentrifugation and characterized using transmission electron microscopy, nanoflow cytometry and western blot. MicroRNA‐223 (miR‐223) expression were analyzed by real‐time PCR. Western blot, alkaline phosphatase (ALP), and alizarin red staining were conducted to assess whether exosomes could affect the osteogenic differentiation of PDLSCs. The expression of miR‐223 was inhibited in PDLSCs by transfecting with miR‐223 inhibitor. Cyclic guanosine monophosphate (cGMP) expression was determined by enzyme‐linked immunosorbent assay. Results: We found that miR‐223 was significantly increased in neutrophils and neutrophil‐like cells derived exosomes. Treatment with exosomes derived from neutrophil‐like cells upregulated miR‐223 expression and inhibited the osteogenic differentiation of PDLSCs, while transfection with miR‐223 inhibitor significantly promoted PDLSCs osteogenic differentiation. In addition, co‐treatment with KT5823, a cGMP–PKG pathway inhibitor, markedly abrogated the rescue effects of miR‐223 inhibitor on the osteogenic differentiation of PDLSCs. Conclusions: Our findings suggest that neutrophil‐like cells derived exosomes might inhibit osteogenic differentiation of PDLSCs by transporting miR‐223 and regulating the cGMP–PKG signaling pathway. [ABSTRACT FROM AUTHOR]

Objectives Worldwide, lung cancer accounts for the majority of cancer-related deaths. Aberrant expression of mi RNAs has increasingly been reported to be associated with tumour progression. This study aimed to explore the role of miR-301b in regulating apoptosis in lung cancer. Materials and methods Expression of miR-301b was assessed by real-time PCR in cell lines, human patient tissues and cells treated under hypoxia and DMOG. Scramble si RNA, miR-301b inhibitor and miR-301b mimics were transfected into lung cancer cells to determine their effects on apoptosis. Additionally, a mouse xenograft model was used to explore functions of miR-301b on apoptosis, in vivo. Finally, relationships between Bim and miR-301b levels were explored by luciferase reporter assay and Western blotting. Results We found that miR-301b was highly expressed in lung cancer tissues and cell lines. Expression of miR-301b was induced by hypoxia, and miR-301b suppressed expression of Bim by targeting its 3′UTR. Functionally, ectopic expression of miR-301b enhanced cell population growth, reduced apoptosis and reduced sensitivity of cells to chemotherapy. In the xenograft model, overexpression of miR-301b promoted tumour growth. Additionally, miR-301b and Bim expression were inversely correlated in clinical lung cancer samples. Conclusions This study provides new insights into the function of mi RNA-301b in lung cancer and suggests that mi RNA-301b could be a potential molecular target for chemotherapy. [ABSTRACT FROM AUTHOR]