Surfactant Protein (SP) induces preterm birth by promoting oxidative stress via upregulating Storkhead-Box Protein 1.

Preterm birth is the leading cause of infant mortality. The mechanisms that instigate preterm birth remain elusive and this makes it difficult to predict or prevent preterm birth. In this study, the authors found that SP-A induced pathological damage to the placenta and promoted preterm birth. Through mechanism, SP-A promoted the expression of STOX1 which further promoted the oxidative stress in the placenta by inhibiting the activities of a series of antioxidant enzymes including SOD, CAT and GSH-Px. SP-A also induced dysregulation of arginine metabolism by inhibiting NOS2 and ARG2. Overexpression of STOX1 aggravated SP-A induced oxidative stress, pathological damage, and preterm birth, whereas knockdown of STOX1 alleviated SP-A induced oxidative stress, pathological damage and preterm birth. The present study uncovers that SP-A induces preterm birth by promoting oxidative stress via upregulating STOX1, which provides new targets for the prediction and prevention of preterm birth.

PAD4 silencing inhibits inflammation whilst promoting trophoblast cell invasion and migration by inactivating the NEMO/NF-κB pathway.

Preeclampsia (PE), presenting with onset hypertension and proteinuria, is a pregnancy-specific disorder that can result in maternal and fetal morbidity and mortality. Insufficient trophoblast invasion and migration has been considered to be an important cause of this disease. The present study aimed to investigate the role of peptidyl arginine deiminase 4 (PAD4), whose knockdown has been previously indicated to reduce inflammation and susceptibility to pregnancy loss in mice, in the development of PE in vitro. Lipopolysaccharide (LPS) was used to treat a human trophoblast cell line (HTR8/SVneo). After PAD4 silencing via transfection with short hairpin RNA against PAD4, the concentrations of inflammatory factors IL-6, IL-12 and monocyte chemoattractant protein (MCP)-1 were measured using ELISA. Cell viability was also measured using Cell Counting Kit-8 assay. HTR8/SVneo cell invasion and migration were detected using Transwell and wound healing assays, respectively. Western blotting was used to measure the expression of citrullinated NF-κB essential modulator (NEMO) and nuclear NF-κB p65 protein levels. TNF-α was applied for evaluating the potential regulatory effects of PAD4 on NF-κB in LPS-stimulated HTR8/SVneo cells. LPS increased the levels of IL-6, IL-12 and MCP-1 and reduced the migration and invasion of HTR8/SVneo cells. PAD4-knockdown was found to markedly reduce the levels of IL-6, IL-12 and MCP-1 secretion. HTR8/SVneo cell invasion and migration was also significantly elevated after PAD4 silencing following LPS exposure. In addition, LPS stimulation notably upregulated the protein levels of citrullinated NEMO and nuclear NF-κB p65, which was restored by PAD4 knockdown. Furthermore, TNF-α treatment partially counteracted the effects of PAD4 knockdown on the secretion of IL-6, MCP-1 and IL-12, which are markers of inflammation, and invasion and migration in LPS-induced HTR8/SVneo cells. To conclude, these results suggest that PAD4 silencing can suppress inflammation whilst promoting invasion and migration by trophoblast cells through inhibiting the NEMO/NF-κB pathway. These findings furthered the understanding in the complex molecular mechanism that can trigger PE and provide a promising target for the treatment of this disease.

Surfactant Protein (SP) induces preterm birth by promoting oxidative stress via upregulating Storkhead-Box Protein 1

Abstract Preterm birth is the leading cause of infant mortality. The mechanisms that instigate preterm birth remain elusive and this makes it difficult to predict or prevent preterm birth. In this study, the authors found that SP-A induced pathological damage to the placenta and promoted preterm birth. Through mechanism, SP-A promoted the expression of STOX1 which further promoted the oxidative stress in the placenta by inhibiting the activities of a series of antioxidant enzymes including SOD, CAT and GSH-Px. SP-A also induced dysregulation of arginine metabolism by inhibiting NOS2 and ARG2. Overexpression of STOX1 aggravated SP-A induced oxidative stress, pathological damage, and preterm birth, whereas knockdown of STOX1 alleviated SP-A induced oxidative stress, pathological damage and preterm birth. The present study uncovers that SP-A induces preterm birth by promoting oxidative stress via upregulating STOX1, which provides new targets for the prediction and prevention of preterm birth.

Effects and correlation of gross motor intervention on movement and social skills of autistic children / 中国学校卫生

Objective@#To explore the effects and correlation of gross motor intervention on social skills of autistic children. To provide new ideas for rehabilitation intervention of autistic children s social ability.@*Methods@#Recruiting 23 autistic children through WeChat in Nanchang, randomly divided into experimental groups (n=13) and control group (n=10). The experimental group underwent 6 weeks of large muscle exercise intervention, in the control group, Test of Gross Motor Development 3 (TGMD3), Social Responsiveness Scale(SRS) and the Autism Social Skills Scale (ASSS) examined changes in social skills, and analyze the relationship between sports and social ability.@*Results@#TGMD-3 score in the intervention group before intervention was (34.31±9.79) and increased significantly after intervention (59.77±13.92)(t=-15.28, P<0.01). There was no statistical significance before and after experiment in the control group (P>0.05). The scores of SRS and ASSS in the experimental group were (96.77±15.79, 97.31±29.22) before the intervention, and (82.92±15.86, 117.62±24.93) after the intervention, and the differences were statistically significant(t=4.55, -5.61, P<0.01). The difference between the SRS and ASSS scores of the control group before and after experiment was not statistically significant(P>0.05). Both the TGMD-3 score and the object manipulation score were related to the SRS total score (r=-0.49, -0.45) and ASSS total score(r=0.54, 0.51)(P<0.05).@*Conclusion@#Gross motor intervention can improve the motor and social skills of children with autism, and there is a positive correlation between motor ability and social skills in children with autism.

Silencing of Synuclein-γ inhibits human cervical cancer through the AKT signaling pathway.

BACKGROUND: Synuclein-γ has been demonstrated to be highly expressed in various human cancers including cervical cancer, and has been shown to play a critical role in tumor aggressiveness. We aimed to investigate the role of Synuclein-γ in human cervical cancer in vitro and in vivo. METHOD: Reverse transcription-quantitative polymerase chain reaction assay and Western blot assay were used to detect the mRNA and protein expression, respectively. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and colony formation assay were performed to measure the viabilities of cancer cells. Flow cytometry assay was used to detect the cell cycle and apoptosis. Moreover, an animal experiment was performed to evaluate the biological behavior of Synuclein-γ in vivo. RESULTS: In the current study, we found that Synuclein-γ was obviously over-expressed in cervical cancer tissues compared to the adjacent non-cancer tissues. Cervical cancer cells transfected with Synuclein-γ siRNA demonstrated significant inhibition of cancer proliferation (P < 0.01), cell cycle arrest at G0/G1 phase, and cell apoptosis (P < 0.05). Moreover, down-regulation of Synuclein-γ significantly inhibited cervical cancer growth in vivo. In addition, protein levels of AKT, c-Myc and Cyclin D1 were much lower in the Synuclein-γ siRNA-treated groups than that in the control group. CONCLUSIONS: Synuclein-γ inhibition reduced cervical cancer tumor growth through the AKT pathway. This effect represented a therapeutic opportunity and provided a novel target for cervical cancer treatment.