MiR-181a has been presumed to target the 3′-untranslated regions (3′-UTR) of IL1a based on software predictions. miR-181a and IL1a have opposite expression levels in monocytes and macrophages in the inflammatory state. This led us to suspect that mir-181a has an important function in regulating inflammatory response by targeting IL1a. Fluorescence reporter assays showed that miR-181a effectively binds to the 3′-UTR of IL1a. The anti-inflammatory functions of miR-181a were investigated in lipopolysaccharides (LPS)-induced Raw264.7 and phorbol 12-myristate 13-acetate (PMA)/LPS-induced THP-1 cells. We found that miR-181a mimics significantly lowered IL1a expression levels in these cells and, interestingly, miR-181a inhibitors reversed this decrease. In addition, miR-181a mimics significantly inhibited increase in the levels of inflammatory factors (IL1b, IL6, and TNFa) in these cells. Furthermore, miR-181a mimics and inhibitors decreased and increased, respectively, production of reactive oxygen species in PMA/LPS-induced THP-1 cells. These results indicate that miR-181a regulates inflammatory responses by directly targeting the 3′-UTR of IL1a and down-regulating IL1a levels. Interestingly, we found that miR-181a inhibited production of inflammatory factors even in IL1a-induced THP-1 cells, suggesting that the anti-inflammatory effects of miR-181a possibly involves other targets in addition to IL1a. Thus, we provide the first evidence for anti-inflammatory effects of miR-181a mediated at least in part by down-regulating IL1a.

Certain individuals ingesting a low-fat diet are still prone to visceral obesity, and the reasons remain undetermined. This study aimed to investigate differentially expressed proteins of visceral adipose tissues between low-fat diet-fed obesity-resistant and obesity-prone C57BL/6 mice through a proteomics approach and to ascertain potential mechanisms associated with these obesity-prone animals. First, animals were fed low-fat or normal-chow diets for 6 weeks. Dietary intake and body weight were monitored during this period. After 6 weeks of the low-fat diet, obesity-prone and obesity-resistant mice (NOP and NOR groups) were defined as those within the upper and lower quarters for weight gain, respectively. Proteomic analysis showed that ubiquinol-cytochrome c reductase core protein 1 (Uqcrc1) and Enolase 3, β muscle were decreased by 8.1- and 8.8-fold in the visceral adipose tissues of the NOP mice compared to the NOR controls, respectively, while monoglyceride lipase (MGLL) and glucose-6-phosphate dehydrogenase (G6PDH) X-linked were increased by 5.3- and 4.7-fold, respectively. These results indicate that obesity-prone animals fed low-fat diets exhibited differentially expressed proteins, e.g., Uqcrc1, Enolase 3, MGLL and G6PDH involved in energy metabolism, glycolysis and fat synthesis in visceral adipose tissues, which are useful for defining molecular markers and understanding the mechanisms of the development of obesity.

The aim of this study was to investigate the association between expressions of five periodontal pathogens (Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Tannerella forsythensis (Tf), Treponema denticola (Td) and Prevotella intermedia (Pi) and the periodontal pocket depth (PD) in people suffering from periodontitis. A study of 1164 plaque samples from individuals with periodontitis were conducted by multiplex real-time quantitative fluorescence-polymerase chain reaction to evaluate the PD and loads of five periodontal pathogens. The total bacterial number did not differ significantly between people with different subtypes of periodontitis. However, expression of specific pathogens (Pg, Td, Tf, Pi) showed a significant increase with the development of periodontitis. Expression of Pg, Td and Tf showed close correlation between them as well as with PD. Analyses of receiver operating characteristic curves showed that expression of Pg, Td, Tf and Pi had good potential for grading periodontitis severity. We found a close correlation between the relative expression of Pg, Td and Tf and PD. Measuring expression of target bacteria in the oral cavity could facilitate the understanding of the role of bacteria in periodontitis. Taking the appropriate steps to eliminate these pathogens might aid the prevention of periodontitis development.