| INTRODUC TI ONPolymyositis (PM) is the common disease of idiopathic inflammatory myopathy that affects skeletal muscle, lung, heart, joints, etc. 1 Interstitial lung diseases (ILDs) is the most common complication which seriously affects the prognosis of PM patients. 2 A retrospective study showed the morbidity rate was 48.9% in patients with PM/dermatomyositis (DM)-related ILD in Chinese Han population. 3 Another study reported the mortality rate was 47.1% in myositis patients with ILD. 4 Based on the high morbidity and mortality rates, finding effective preventive and therapeutic methods is important for improving prognosis of patients with PM-related ILD. Interstitial lung diseases AbstractExcessive neutrophil extracellular trap (NET) formation may contribute to polymyositis (PM)-associated interstitial lung diseases (ILD), but the underlying mechanism is not fully revealed. In this study, we found that NET accelerated the progression of ILD and promoted pulmonary fibrosis (PF) in vivo. miR-7 expression was downregulated in lung tissue of PM group than control group, and NETs further decreased miR-7 expression. TLR9 and Smad2 were up-regulated in lung tissue of PM group than control group, and NETs further increased TLR9 and Smad2 expressions. In vitro experiments showed that PMA-treated NETs accelerated the proliferation of LF and their differentiation into myofibroblast (MF), whereas DNase I decreased the promotion effect of NETs. Neutrophil extracellular trap components myeloperoxidase (MPO) and histone 3 also promoted the proliferation and differentiation of LF. In addition, we demonstrated that TLR9 involved in the regulation of NETs on LF proliferation and differentiation, and confirmed the interaction between miR-7 and Smad2 in LF. Finally, miR-7-Smad2 pathway was confirmed to be involved in the regulation of TLR9 on LF proliferation and differentiation. Therefore, NETs promote PM-related ILD, and TLR9-miR-7-Smad2 signalling pathway is involved in the proliferation of LFs and their differentiation into MFs. K E Y W O R D Sdifferentiation, interstitial lung diseases, lung fibroblast, myofibroblast, neutrophil extracellular traps, polymyositis

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The association between inflammatory factor expression and blood pressure with urinary protein in the placenta of pregnant women with pregnancy-induced hypertension (PIH) was investigated to provide a new vision for the clinical prevention and treatment of PIH. Rats were used as animal models and were randomly divided into three groups (control, hypertension and treatment groups) on day 15 of pregnancy with 20 rats in each group. The 10% hypoxia-induced PIH group was induced with administration of an anti-hypertensive drug, and the treatment group was giventreprostinil for one week after the 10% hypoxia-induced PIH. On the 21st day, the experiment was terminated and the placenta was taken to measure the mRNA and protein expression levels of IL-6 and TNF-α, respectively. Pearson's correlation analysis demonstrated the correlation between IL-6 and TNF-α with blood pressure and urinary protein. The blood pressure and urinary protein concentrations in the hypertension group were significantly higher than that in the control group, and the expression levels of IL-6 and TNF-α in the hypertension group were significantly higher (P<0.05). The treatment group significantly reduced inflammatory cytokines and blood pressure and urinary protein levels (P<0.05). Pearson's correlation analysis showed that IL-6 and TNF-α were positively correlated with blood pressure and urinary protein concentration. The blood pressure and urinary protein concentration in PIH rats and the expression levels of IL-6 and TNF-α were significantly higher, and IL-6 and TNF-α were positively correlated with blood pressure and urine protein concentration.

BackgroundParacrine signaling of the hepatocyte growth factor (HGF) cytokine plays an important role in survival and invasion ability of placental trophoblasts. However, the intracellular factors and biological pathways underlying these responses remain unclear.MethodsThis study investigated whether HGF affected the expression of homeobox gene HLX1, which is principally expressed in reproductive tissues and in some immune cells, and evaluated the implications of such in the HGF-induced human trophoblast cell line HTR-8/SVneo.ResultsHGF was found to up-regulate both HLX1 mRNA and protein levels. Transient transfection of small interfering RNA (siRNA) targeting HLX1 abrogated its induction by HGF. Functionally, HLX1 siRNA not only reduced the growth and invasion capacities of HTR-8/SVneo cells at the basal level, but also inhibited these responses induced by HGF treatment.ConclusionsHLX1 is an essential downstream signaling component of HGF that leads to growth and invasiveness of trophoblast cells.