Lipid droplets (LDs) are intracellular organelles with neutral lipid cores surrounded by a phospholipid monolayer and coated with various proteins ( 1-3 ). LDs have been found in almost all eukaryotic organisms from yeast to mammals ( 4 ). They interact with other cellular organelles ( 5-8 ), and their dynamics is closely related to the progression of metabolic diseases, such as obesity, fatty liver, type 2 diabetes mellitus, and atherosclerosis ( 9 ). Recent studies have also shown that LDs are involved in the reproduction of infectious hepatitis C virus particles ( 10 ) and in protecting cells from damage ( 11 ). The identifi cation of perilipin, ADRP, and Tip47 (PAT) family proteins has provided useful marker proteins to facilitate the purifi cation of LDs. Recent proteomic studies suggesting that LDs are not simply inert cellular inclusions for the storage of neutral lipids, but rather functional cellular organelles, has established a new era in LD research ( 3,(12)(13)(14)(15)(16)(17)(18).Although LDs are highly dynamic organelles involved in many cellular activities, especially lipid metabolism, the molecular mechanisms that govern LD formation remain largely unknown. The current model of LD biogenesis speculates that LDs are derived from the endoplasmic reticulum (ER) by a process that begins with the accumulation of neutral lipids between the leafl ets of phospholipid bilayers ( 3,19 ). Many studies have attempted to unravel how LDs form and grow, but this hypothesis still lacks direct evidence and the molecular mechanism Abstract Storage of cellular triacylglycerols (TAGs) in lipid droplets (LDs) has been linked to the progression of many metabolic diseases in humans, and to the development of biofuels from plants and microorganisms. However, the biogenesis and dynamics of LDs are poorly understood. Compared with other organisms, bacteria seem to be a better model system for studying LD biology, because they are relatively simple and are highly effi cient in converting biomass to TAG. We obtained highly purifi ed LDs from Rhodococcus sp. RHA1, a bacterium that can produce TAG from many carbon sources, and then comprehensively characterized the LD proteome. Of the 228 LD-associated proteins identifi ed, two major proteins, ro02104 and PspA, constituted about 15% of the total LD protein. (Grant 2009CB919000, Grant 2010CB833703; Grant 2011CBA00900), and the National Natural Science Foundation of China (Grant 30871229, Grant 30971431, and Grant 31000365 Abbreviations: ER, endoplasmic reticulum; LD, lipid droplet; MLDS, microorganism lipid droplet small; MSM, mineral salt medium; NB, nutrient broth; PAT, perilipin, ADRP, and Tip47; PspA, phage shock protein A; TAG, triacylglycerol; TEM, transmission electron microscopy.

Pyroptosis participates in the formation and development of atherosclerosis (As) by promoting inflammatory factor release and is closely related to the stability of atherosclerotic plaque. MicroRNAs can regulate the expression of target genes at the posttranscriptional level. Previous studies have shown that miR-125a-5p increases in hyperlipidemic-hyperglycemic conditions and is involved in apoptosis, but its specific role in pyroptosis and As remains unclear. We propose that miR-125a-5p may be implicated in oxidized low-density lipoprotein (oxLDL)-induced vascular endothelial cells (VECs) pyroptosis and therefore conducted the current study. We observed that miR-125a-5p can inhibit tet methylcytosine dioxygenase 2 (TET2) expression at the posttranscription level, resulting in abnormal DNA methylation, mitochondrial dysfunction, and increased reactive oxygen species production, activated nuclear factor-κB that induces activation of inflammasome and maturation, release of proinflammatory cytokines interleukin (IL)-1β and IL-18, and pyroptosis. Given the role of VECs in vascular physiology, oxLDL-induced VEC pyroptosis may promote the development of As. Our current study reveals a novel pathway associated with pyroptosis program regulation, which comprises miR-125a-5p and TET2 in VECs.Modulation of their expression levels may serve as a potential target for therapeutic strategies of As. K E Y W O R D Satherosclerosis, miR-125a-5p, pyroptosis, ROS, TET2

Purpose – The purpose of this study is to explore the relationships among business strategy, market competition and earnings management. Design/methodology/approach – This paper uses 2,037 Chinese A-share listed firms from 2010 to 2012 to test the research questions using regression analyses. Findings – The firms that follow cost leadership strategy (cost leaders) are more likely to have a higher level of real earnings management. The firms that follow differentiation strategy (differentiators) are less likely to use real earnings management. For cost leaders, the market competition further increases the level of real earnings management, whereas the level of earnings management of differentiators is not significantly impacted by the market competition. Practical implications – Results of this study indicate the feasibility of differentiation strategy in China and suggest that management should be encouraged to use such a strategy or to use a hybrid strategy to achieve its operational and financial goals. Originality/value – The study contributes to the research of earning management by providing evidence on that business strategy has significant impacts on earnings management. It also shows an incremental influence of market competition on earnings management through its impacts on business strategy.

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Trimethylamine N-oxide (TMAO) is produced from the phosphatidylcholine metabolism of gut flora and acts as a risk factor of cardiovascular disease.However, the underlying mechanisms for its proatherogenic action remain unclear.This study aimed to observe the effect of TMAO on endothelial cell pyroptosis and explore the underlying mechanisms. Our results showed that TMAO promoted the progression of atherosclerotic lesions in apolipoprotein E-deficient (apoE −/− ) mice fed a high-fat diet. Pyroptosis and succinate dehydrogenase complex subunit B (SDHB) upregulation were detected in the vascular endothelial cells of apoE −/− mice and in cultured human umbilical vein endothelial cells (HUVECs) treated with TMAO. Overexpression of SDHB in HUVECs enhanced pyroptosis and impaired mitochondria and high reactive oxygen species (ROS) level. Pyroptosis in the SDHB overexpression of endothelial cells was inhibited by the ROS scavenger NAC. In summary, TMAO promotes vascular endothelial cell pyroptosis via ROS induced through SDHB upregulation, thereby contributing to the progression of atherosclerotic lesions.