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Skin provides a physical and immune barrier to protect the body from foreign substances, microbial invasion, and desiccation. Aging reduces the barrier function of skin and its rate of repair. Aged skin exhibits decreased mitochondrial function and prolonged low-level inflammation that can be seen in other organs with aging. Peroxisome proliferator-activated receptor (PPAR)-γ coactivator-1α (PGC-1α), an important transcriptional coactivator, plays a central role in modulating mitochondrial function and antioxidant production. Mitochondrial function and inflammation have been linked to epidermal function, but the mechanisms are unclear. The aim of this review is to discuss the mechanisms by which PGC-1α might exert a positive effect on aged skin barrier function. Initially, we provide an overview of the function of skin under physiological and aging conditions, focusing on the epidermis. We then discuss mitochondrial function, oxidative stress, cellular senescence, and inflamm-aging, the chronic low-level inflammation observed in aging individuals. Finally, we discuss the effects of PGC-1α on mitochondrial function, as well as the regulation and role of PGC-1α in the aging epidermis. [ABSTRACT FROM AUTHOR]

Simple Summary: Animal-mediated seed dispersal plays a crucial role in the regeneration of plant populations and the stability of forest ecosystems. In this study, we used the tagging method to measure the effects of seeds of different sizes at different frequencies on seed fate and dispersal distance. We found that rodents consumed more small seeds in situ, dispersed and scatter-hoarded more large seeds, and dispersed large seeds over longer distances. Rodents showed a negative frequency dependence for small seeds and a positive frequency dependence for large seeds on being eaten in situ. Moreover, rodents showed a negative frequency dependence for large seeds and a positive frequency dependence for small seeds on being eaten after removal and scatter-hoarding. These findings provide insights into the frequency dependence of animal predation on seed size, animal-mediated seed dispersal, and the regeneration of plant populations. Frequency-dependent predation is common in predator–prey interactions. Size is an important characteristic of seeds and is crucial in the regeneration stage of plant seeds. However, the frequency dependence of animal predation on seed size has not been reported. In this study, we conducted a field experiment and used different sizes of Liaodong oak (Quercus wutaishanica) seeds to test the frequency dependence of intraspecific seed size selection in rodents. We used the number ratio of large to small seeds as the frequency. The results show that the rate of small seeds being eaten in situ was significantly higher than that of large seeds (p < 0.05). The rates of different-sized seeds being eaten after removal decreased with increasing frequencies, and there was no significant difference between frequencies except for 1:9 and 9:1. The rates of large seeds being scatter-hoarded were significantly higher than those of small seeds at different frequencies (p < 0.05). The eating distances after removal of large seeds were significantly longer than those of small seeds at the same frequencies (p < 0.05). Furthermore, the scatter-hoarding distances of large seeds were significantly longer than those of small seeds at three frequencies (1:9, 3:7, and 9:1) (p < 0.05). That is, rodents consumed more small seeds in situ, dispersed and scatter-hoarded more large seeds, and dispersed large seeds over longer distances. Rodents exhibited a negative frequency dependence for small seeds and a positive frequency dependence for large seeds on being eaten in situ. Moreover, rodents exhibited a negative frequency dependence for large seeds and a positive frequency dependence for small seeds on being eaten after removal and scatter-hoarding. These results reveal the frequency dependence of rodent selection on seed size and provide new insights into animal-mediated seed dispersal and the regeneration of plant populations. [ABSTRACT FROM AUTHOR]

Epithelial ovarian cancer (EOC) ranks third in the incidence of gynecological malignancies. m6A methylation as RNA modification plays a crucial role in the evolution, migration, and invasion of various tumors. However, the role of m6A methylation in ovarian cancer (OC) only recently has begun to be appreciated. Therefore, we used various bioinformatic methods to screen the public GEO datasets of epithelial ovarian cancer (EOC) for m6A methylation-related regulators. We identified methyltransferase 16 (METTL16) that was dramatically downregulated in EOC as such a regulator. We also identified metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a known target lncRNA of METTL16, in these five GEO datasets. RT-qPCR and immunohistochemical staining confirmed that compared with the normal ovarian tissues and cells, METTL16 was significantly downregulated, while lncRNA MALAT1 was significantly upregulated, in 30 EOC tissues of our own validation cohorts and EOC cell lines, revealing a negative correlation between METTL16 and lncRNA MALAT1. Moreover, our analysis unveiled a correlation between downregulated METTL16 and the known adverse prognostic factors of EOC patients in our own cohorts. The CCK-8, EdU, scratch wound healing, and transwell invasion assays revealed that METTL16 significantly suppressed the proliferating, migrating, and invading abilities of OC cells. The inhibitory effects of METTL16 on the in vivo tumor growth of EOC cells were measured by subcutaneous tumor formation assay in mice. Furthermore, the RIP, RNA stability assay, western blotting, and cytoimmunofluorescence staining showed that METTL16 hindered the growth of EOC cells through promoting the degradation of MALAT1 by binding that, in turn, upregulates β-catenin protein and promotes nuclear transport of β-catenin protein in EOC cells. This study suggests that METTL16 acts as a tumor suppressor gene of EOC by achieving its inhibitory function on the malignant progression of EOC through the METTL16/MALAT1/β-catenin axis that are new targets for EOC diagnosis and therapy. [ABSTRACT FROM AUTHOR]