Sleep disturbances can disrupt the overall circadian rhythm. However, the impact of sleep deprivation on the circadian rhythm of the liver and its underlying mechanisms still requires further exploration. In this study, we subjected male mice to 5 days of sleep deprivation and performed liver transcriptome sequencing analysis at various time points within a 24-h period. Subsequently, we monitored the autonomic activity and food intake in these male mice for six days post-sleep deprivation. We observed alterations in sleep-wake and feeding rhythms in the first two days following sleep deprivation. Additionally, we also observed a decrease in 24-h serum-glucose levels. Liver transcriptome sequencing has shown that sleep deprivation induces the rhythmic transcription of a large number of genes, or alters the rhythmic properties of genes, which were then significantly enriched in the carbohydrate, lipid, and protein metabolism pathways. Our findings suggest that under conditions of prolonged sleep deprivation, the expression of metabolic-related genes in the liver was reset, leading to changes in the organism’s metabolic state to ensure energy supply to sustain prolonged wakefulness.
Multiple sclerosis (MS) is an autoimmune disease characterized by T cell infiltration and demyelination of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) is a classical preclinical animal model of MS.In this study, we found that rotating magnetic field (RMF) treatment exerts potential preventive effects on the discovery of EAE, including reducing the severity of the disease and delaying the onset of the disease.The results indicated that RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4 + cells in the spleen and lymph nodes by downregulating the expression of CCL-2, CCL-3 and CCL-5, but has no significant effect on myelin oligodendrocyte glycoprotein (MOG) specific T cell responses.Simultaneously, RMF treatment adjusted the imbalance between regulatory T (Treg) cell and T helper 1 (Th1) cells or T helper 17 (Th17) cells by increasing the proportion of Treg cells and inhibiting the ratio of Th1 and Th17 cell subsets.These findings suggest that exposure to RMF may improve EAE disease by promoting CD4+ cell accumulation into peripheral lymphoid tissue, improving the imbalance between Treg and Th1/Th17 cells.Therefore, as a mild physical therapy approach, RMF, is likely to be a potential way to alter the development of EAE.
Abstract Primary open‐angle glaucoma (POAG) is the second leading cause of irreversible blindness worldwide. Increased endothelin‐1 (ET‐1) has been observed in aqueous humour (AH) of POAG patients, resulting in an increase in the out‐flow resistance of the AH. However, the underlining mechanisms remain elusive. Using established in vivo and in vitro POAG models, we demonstrated that water channel Aquaporin 1 (AQP1) is down‐regulated in trabecular meshwork (TM) cells upon ET‐1 exposure, which causes a series of glaucomatous changes, including actin fibre reorganization, collagen production, extracellular matrix deposition and contractility alteration of TM cells. Ectopic expression of AQP1 can reverse ET‐1‐induced TM tissue remodelling, which requires the presence of β‐catenin. More importantly, we found that ET‐1‐induced AQP1 suppression is mediated by ATF4, a transcription factor of the unfolded protein response, which binds to the promoter of AQP1 and negatively regulates AQP1 transcription. Thus, we discovered a novel function of ATF4 in controlling the process of TM remodelling in ET‐1‐induced POAG through transcription suppression of AQP1. Our findings also detail a novel pathological mechanism and a potential therapeutic target for POAG.
Abstract Regional gender differences in autosomal chromosome disorders have been observed repeatedly. However, the corresponding diversity changes remain unconfirmed. By analyzing previously published thalassemia data from the Dai people in Dehong and Xishuangbanna (two regions in Yunnan Province, China), we found that several sequence types, including HBA CNV and HBB mutations, significantly depend on gender in Xishuangbanna but not in Dehong. With the supportive evidence from previous researches, we accept that some certain mutations depend on gender regionally. This association seems peculiar. It is among one common people on a small geographical scale, while other recorded thalassemia gender difference varies by ethnics and continent.
Abstract Polycomb repressive complexes (PRCs) are pivotal epigenetic regulators preserving cell identity by restricting the transcription responsiveness to sub-threshold levels of extracellular signals. Their roles in osteoblast function and bone formation remain largely unexplored. Here in aging osteoblasts, we observed a selective activation of PRC1.1 complex, with KDM2B acting as a chromatin-binding factor and BCOR and PCGF1 serving as essential catalytic partners for histone H2A monoubiquitylation (H2AK119ub1). Using genetic models, we found that osteoblast-specific KDM2B inactivation significantly enhances bone remodeling under steady-state conditions and in scenarios of bone loss. This enhancement is attributed to H2AK119ub1 downregulation which leads to the derepression of Wnt signaling. Furthermore, we developed a small molecule termed iBP, that specifically inhibits the interaction between BCOR and PCGF1, thereby suppressing PRC1.1 activity. Notably, iBP promotes bone formation in mouse models of bone loss. Therefore, our findings suggest that targeting PRC1.1 augments cellular responses to Wnt signaling and may offer a promising strategy to counteract bone deterioration.
Corrigendum: Resetting the circadian clock of Alzheimer's mice via GLP-1 injection combined with time-restricted feedingName of all authors as they appear in the published original article:Yanqiong Dong 1 2, Le Cheng 1 3, Yingying Zhao 2Affiliations of all authors as they appear in the published original version of the article:1 Department of Basic Medicine Sciences, School of Basic Medical Sciences, Dali University, Dali, Yunnan, China 2 Department of Physiology, School of Basic Medical Sciences, Shenzhen University Health Sciences Center, Shenzhen, Guangdong, China 3 BGI-Yunnan, BGI-Shenzhen, Kunming, Yunnan, China* Correspondence: zhaoyingying@szu.edu.cn Keywords: amyloid-β , circadian rhythm, glucagon-like peptide-1, time-restricted feeding, Alzheimer's diseaseCorrigendum on: Yanqiong Dong, Le Cheng, Yingying Zhao. (2022). Resetting the circadian clock of Alzheimer's mice GLP-1 injection combined with time-restricted feeding. Front Physiol. 13, 911437. doi:10.3389/fphys.2022.911437. Error in Figure/TableIn the published article, there was an error in Figure1B as published. Figure 1B is not fully displayed. The corrected Figure1B and its caption Alzheimer's disease mice exhibit circadian rhythm disturbances appear below. The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.FIGURE 1 Alzheimer's disease mice exhibit circadian rhythm disturbances.
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