Background: Rheumatoid arthritis (RA), a kind of autoimmune disorder, is featured by many physical symptoms and proliferation of fibroblast-like synoviocytes (FLSs). The relevance of long non-coding RNAs (lncRNAs) in the progression of RA has been probed. Hence, the goal of this report was to investigate the action of plasmacytoma variant translocation 1 (PVT1), a lncRNA, in FLSs and the basic mechanism. Methods: Initially, RA rats were developed to evaluate the expression of PVT1, microRNA-543 (miR-543), and signal peptide-CUB-EGF-like containing protein 2 (SCUBE2) in synovial tissues. Enhancement or loss of PVT1 or miR-543 was achieved to explore their effects on proliferation, cell cycle, and apoptosis of FLSs. The interaction between PVT1 and miR-543 and between miR-543 and its putative target SCUBE2 was examined to elucidate the correlations. Finally, the protein expression of proliferation-and apoptosis-associated genes were assessed by western blot assays. Results: PVT1 was overexpressed in synovial tissues from RA patients through microarray expression profiles. The PVT1 and SCUBE2 expression was boosted, and miR-543 was reduced in synovial tissues of rats with RA. PVT1 specifically bound to miR-543, and miR-543 negatively regulated SCUBE2 expression. Overexpression of PVT1 or silencing of miR-543 enhanced SCUBE2 expression, thereby promoting proliferation and interleukin-1β (IL-1β) secretion, while inhibiting apoptosis rate of FLSs. Conversely, si-SCUBE2 reversed the role of miR-543 inhibitor. Conclusion:The key findings support that PVT1 knockdown has the potency to hinder RA progression by inhibiting SCUBE2 expression to sponge miR-543.

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A Ni based mesoporous γ-Al2O3 (MA) catalyst was prepared via partial hydrolysis without organic surfactants and employed in the carbon dioxide methanation reaction.

Introduction: Cavernosal nerve (CN) injury is commonly caused by radical prostatectomy surgery, and it might directly lead to erectile dysfunction (ED). Currently, the role of mitogen-activated protein kinase (MAPK) family proteins in phenotypic transformation of corpus cavernosum smooth muscle cell (CCSMC) after CNs injury is poorly understood. Aim: To investigate the role of p38 MAPK in hypoxia-induced phenotypic transformation of CCSMCs after CN injury. Methods: In total, 20 SpragueeDawley rats (male and 8 weeks of age) were randomly divided into 2 groups, including a sham group and CNCI group. In the sham group, rats were sham-operated by identifying 2 CNs without causing direct damage to the CNs. In the CNCI group, rats were subjected to bilateral CN crush injury. CCSMCs were isolated from the normal corpus cavernosum tissues of the SpragueeDawley rat and then cultured in 21% or 1% O 2 concentration context for 48 hours. Main Outcome Measures: Intracavernous pressure/mean arterial pressure were analyzed to measure erectile response. The impact of hypoxia on penile pathology, as well as the expression of extracellular signal-regulated kinases, the c-Jun NH2-terminal kinase, and p38 MAPK, were analyzed. Results: Compared with the sham group, the intracavernous pressure/mean arterial pressure rate and a-smooth muscle actin expression of CNCI group were decreased significantly (P ¼ .0001; P ¼ .016, respectively), but vimentin expression was significantly increased (P ¼ .023). Phosphorylated p38 level in CNCI group was decreased significantly (P ¼ .017; sham: 0.17 ± 0.005; CNCI: 0.14 ± 0.02). The CCSMCs in the normoxia group were long fusiform, whereas the morphology of CCSMCs in the hypoxia group became hypertrophic. After hypoxia for 48 hours, the expression of a-smooth muscle actin and phosphorylated p38 MAPK was decreased significantly (P ¼ .01; P ¼ .024, normoxia: 0.66 ± 0.18, hypoxia: 0.26 ± 0.08, respectively), and the expression of hypoxia-inducible factor-1a and collagen I was increased significantly in hypoxia group (P ¼ .04; P ¼ .012, respectively). Conclusions: Hypoxia induced the phenotypic transformation of CCSMCs after CNCI might be associated with the downregulation of phosphorylated p38 MAPK. Chen S, Huang X, Kong X, et al. Hypoxia-Induced

miR‐141‐3p is proven to play a prominent role in various inflammation‐related diseases. Nonetheless, little is known concerning the function of miR‐141‐3p in vascular smooth muscle cells (VSMCs) dysfunction and the underlying mechanism. ApoE knockdown (ApoE−/−) C57BL/6 mice and human VSMCs were employed to establish atherosclerosis (AS) animal model and cell model, respectively. The expressions of miR‐141‐3p and Keap1 mRNA were detected by quantitative real‐time polymerase chain reaction (qRT‐PCR). Enzyme‐linked immunosorbent assay (ELISA) was conducted to determine inflammatory cytokines IL‐6, IL‐β and TNF‐α. Cell proliferation, migration and apoptosis were analyzed by BrdU assay, Transwell assay and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, respectively. Luciferase reporter assay was carried out to determine the regulatory relationship between miR‐141‐3p and Keap1. Additionally, Western blot was used to detect the function of miR‐141‐3p on the expression levels of Keap1, Nrf2 and HO‐1 in VSMCs. miR‐141‐3p was remarkably down‐regulated in both AS animal model and cell model while the expression of Keap1 was elevated. Proliferation and migration of VSMCs were suppressed after miR‐141‐3p mimics transfection and cell apoptosis was promoted. miR‐141‐3p also inhibited the expressions of IL‐6, IL‐β, TNF‐α and Keap1 but promoted the expressions of Nrf2 and HO‐1. Moreover, the binding site between miR‐141‐3p and the 3′UTR of Keap1 was confirmed. miR‐141‐3p is down‐regulated during AS, and it can alleviate VSMCs' dysfunction by targeting the Keap1/Nrf2/HO‐1 axis.

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Microbial degradation is a useful tool for inhibiting or preventing polycyclic aromatic hydrocarbons (PAHs) widely distributed in marine environment after oil spill accidents. This study aimed to evaluate the potential and diversity of bacteria Bacillus sp. PAH-2 on Benzo (a) anthracene (BaA), Pyrene (Pyr), and Benzo (a) pyrene (BaP), their composite system, aromatic components system, and crude oil. The seven-day degradation rates against BaA, Pyr, and BaP were 20.6%, 12.83%, and 17.49%, respectively. Further degradation study of aromatic components demonstrated PAH-2 had a high degradation rate of substances with poor stability of molecular structure. In addition, the degradation of PAHs in crude oil suggested PAH-2 not only made good use of PAHs in such a more complex structure of pollutants but the saturated hydrocarbons in the crude oil also showed a good application potential.