Autophagy is a self protecting cellular catabolic pathway th

Autophagy is a self-protecting cellular catabolic pathway that degrades and recycles cytoplasmic contents for the maintenance of cellular homeostasis (Shao et al., 2016b). Macrophage autophagy plays an essential role in atherosclerosis by safeguarding Quinacrine hydrochloride hydrate against oxidative stress, reducing apoptosis, and enhancing lesional stability (Liao et al., 2012; Razani et al., 2012). Autophagosome-lysosomal fusion is an essential step in this process (Decuypere et al., 2013). LC3-II is a relatively sensitive biochemical marker of autophagy. LC3 is distributed in the cytoplasm under normal conditions (LC3-I), but when autophagy is induced, LC3-I is modified to become LC3-II, which is integrated into the membrane of the autophagosome (Wang et al., 2016). Our results showed that LC3 level was decreased when the expression of legumain was downregulated, while LC3 level was increased when the expression of legumain was upregulated. Thus, legumain-based suppression of oxLDL induced macrophage apoptosis through the upregulation of autophagy. However, the molecular mechanisms of legumain regulation of autophagy require further investigation. The potential mechanisms of legumain regulating cellular apoptosis or autophagy may associated with Integrin activations as well as activation of other proteases involved in autophagy (Dall and Brandstetter, 2013)
The conflict of interest disclosure
Acknowledgements This research was funded by the National Natural Science Foundation of China (No. 81402042), Shanghai Science and Technology (14140903400, 14YF1402600), and the Training Plan for Scientific Research of Renji Hospital (RJZZ13-021). The funders had no influence over the study design; data collection and analysis; decision to publish; or preparation of the manuscript.
Introduction Iodine is a micronutrient that is essential for the production of thyroid hormone, which is vitally important for the growth and development of the organism. Moderate amounts of iodine are necessary, but high iodine intake may induce damage. Several studies have shown that high levels of iodine may induce iodine-excess goiter, autoimmune thyroid diseases, hyperthyroidism and hypothyroidism (Bürgi, 2010), but the role of high iodine levels in damage to intelligence has been controversial. Nevertheless, Gao’s research suggests that excessive intake of iodine can damage the mouse nervous system, leading to retardation of brain development and impairment of its function (Gao et al., 2013). Moreover, another experiment examining excess iodine has shown that iodine can be transferred to the embryo via the placenta, which may lead to observable decreases in cognitive behavior in both the parental generation and their offspring (Zhang et al., 2012). Therefore, we speculate that high concentrations of iodine may exert a toxic effect and thus impair the development of intelligence. Nonetheless, the detailed molecular mechanisms underlying this process remain largely unknown. Previous studies have shown that high iodine can induce apoptosis in thyrocytes and mammary cells (Burikhanov and Matsuzaki, 2000, Gao et al., 2013, Vitale et al., 2000). Moreover, fluoride, which belongs to the halogen element group along with iodine, can induce autophagy in ameloblasts (Suzuki and Bartlett, 2014). Following these studies, we hypothesized that high levels of iodine may induce mental damage via two types of cell death, apoptosis and autophagy. Autophagy and apoptosis are two pathways to cell death. Apoptosis has been intensively studied in the past two decades and is widely appreciated as a major mechanism of regulated cell death employed not only upon cell damage or stress but also during normal development and morphogenesis (Nikoletopoulou et al., 2013). Caspase-3 is a pivotal element during the process of apoptosis (Cryns and Yuan, 1998, Fan et al., 2005), and poly ADP-ribose polymerase (PARP) is its substrate (Boulares et al., 1999). The release of cytochrome c from mitochondria to the cytoplasm may activate caspase-3, and then lead to apoptosis (Goldstein et al., 2000). The antigen P53 is a pro-apoptotic factor (Wu et al., 2015). Autophagy is a self-digesting mechanism that is morphologically characterized by the formation of double-membrane autophagosomes, which sequester impaired organelles of unwanted cellular components and deliver them to lysosomes for degradation and recycling (Eskelinen and Saftig, 2009, Noda and Inagaki, 2015). When stress intensity is too great, excessive autophagy may be induced, eventually leading to cell death. In this study, we measured the expression levels of autophagy-related proteins including p62, Beclin1 and LC3 (microtubule-associated protein 1 light chain 3) to probe the variation in autophagy induced by high concentrations of iodine.