The axial rotation of the Earth, together with the light of the sun, generates 24-hour cycles of day and night, and this light-dark cycle is the basis of 24-hour circadian rhythms. Living organisms have their own endogenous circadian rhythms, also with a duration of approximately 24 hours, driven by environmental factors, especially light and darkness [1]. And it is widely known that circadian rhythms of mammals are regulated by an internal biological clock located in the suprachiasmatic nuclei (SCN) situated directly above the optic chiasm [2]. Maintaining the biological clock is crucial for coordinated function throughout the human body because this near-24-hour oscillations are found in essentially every physiological process in the human brain and body [3,4]. The period, phase and amplitude of circadian rhythms can be affected by circadian gene variants, light exposure, social cues, meal times and work schedules [5-8]. Light is the most effective
Aging is a universal, irreversible process accompanied by physiological declines that culminate in death. Rapid progress in gerontology research has revealed that aging can be slowed through mild stress-induced hormesis. We previously reported that hyperbaric normoxia (HN, 2 atm absolute pressure with 10% O2) induces a cytoprotective response in vitro by regulating fibronectin. In the present study, we investigated the hormetic effects of prenatal HN exposure on Drosophila healthspan related to molecular defense mechanisms. HN exposure had no disruptive effect on developmental rate or adult body weight. However, lifespan was clearly enhanced, as was resistance to oxidative and heat stress. In addition, levels of reactive oxygen species were significantly decreased and motor performance was increased. HN stress has been shown to trigger molecular changes in the heat shock response and ROS scavenging system, including hsp70, catalase, glutathione synthase, and MnSOD. Furthermore, to determine the hormetic mechanism underlying these phenotypic and molecular changes, we performed a genome-wide profiling in HN-exposed and control flies. Genes encoding chitin metabolism were highly up-regulated, which could possibly serve to scavenge free radicals. These results identify prenatal HN exposure as a potential hormetic factor that may improve longevity and healthspan by enhancing defense mechanisms in Drosophila.
Human cells are continuously exposed to various stress factors in their
physiological environment. Evidence suggests that certain mechanical stress
can affect cell cycle progression and cell proliferation. However, the
signaling pathways involved in this process are not well understood. To
investigate this, we developed a pressure chamber capable of producing an
elevated barometric pressure (EBP) environment of 2?atmospheric absolute
pressure (ATA). We then studied the effect of EBP on cell proliferation and
its underlying mechanism. Our results show that EBP inhibited cell
proliferation by delaying the G2/M phase. Specifically, EBP reduced the
expression levels of cell adhesion-related genes and downregulated integrin
subunit genes, resulting in weaker interaction between cells and
extracellular matrix proteins. In addition, Ras-related C3 botulinum toxin
substrate 1 (Rac1) and cell division control protein 42 homolog (Cdc42)
activity was suppressed, and actin assembly was decreased. These findings
suggest that the EBP-mediated G2/M phase delay is due to attenuated cell
adhesion and actin cytoskeleton assembly, leading to the inhibition of cell
proliferation. Our results provide a crucial molecular mechanism for how
certain pressure (changes) can negatively regulate cell proliferation. These
findings could potentially be used in the future to develop a pressure
therapy to inhibit cell proliferation in cancer patients.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.