Journal of Pineal Research最新文献

Intestinal barrier dysfunction with high serum endotoxin is common in patients with liver fibrosis, but the mechanisms underlying liver fibrosis remain unclear. Melatonin is a well-recognized antioxidant and an anti-inflammatory agent that benefits multiple organs. However, the beneficial effects of melatonin on gut leakiness–associated liver fibrosis have not been systemically studied. Here, we investigated the protective mechanisms of melatonin against thioacetamide (TAA)–induced gut barrier dysfunction and hepatic fibrosis by focusing on posttranslational protein modifications through the gut–liver axis. Our results showed that gut leakiness markers, including decreased gut tight/adherens junction proteins (TJ/AJs) with increased intestinal deformation, apoptosis, and serum endotoxin, were observed early at 1 week after TAA exposure. Liver injury, apoptosis, and fibrosis were prominent at 2 and 4 weeks. Mechanistically, we found that gut TJ/AJs were hyper-acetylated, followed by ubiquitin-dependent proteolysis, leading to their degradation and gut leakiness. Gut dysbiosis, hepatic protein hyper-acetylation, and SIRT1 downregulation were also observed. Consistently, intestinal Sirt1 deficiency greatly enhanced protein hyper-acetylation, gut leakiness, endotoxemia, and liver fibrosis. Pretreatment with melatonin prevented or improved all these changes in both the gut and liver. Furthermore, melatonin blunted protein acetylation and injury in TAA–exposed T84 human intestinal and AML12 mouse liver cells. Overall, this study demonstrated novel mechanisms by which melatonin prevents gut leakiness and liver fibrosis through the gut–liver axis by attenuating the acetylation of intestinal and hepatic proteins. Thus, melatonin consumption can become a potentially safe supplement for liver fibrosis patients by preventing protein hyper-acetylation and gut leakiness.

Y. Bai, Y. Wei, H. Yin, et al., “PP2C1 Fine-Tunes Melatonin Biosynthesis and Phytomelatonin Receptor PMTR1 Binding to Melatonin in Cassava,” Journal of Pineal Research 73, no. 1 (2022): e12804. https://doi.org/10.1111/jpi.12804

After publication of the article, the authors identified inaccuracies in images in Figure 3A, namely SD-Trp-Leu-Ade-His for MePP2C1 and MeWRKY20 interaction. The authors have found the original data and corrected this error, which was due to the oversight during combing and dragging different figures in Photoshop software. It is important to emphasize that this correction does not compromise the scientific integrity of the study's conclusions. The authors sincerely apologize for any inconvenience caused by this oversight. The accurate images, obtained during the original experimental procedures, are provided below.

In addition, the authors also found inaccuracies in images in Figure 6B, namely Vector+Vector, MePMTR1+Vector, Vector+MePP2C1. The authors have found the original data and corrected these errors, which was due to the oversight that the adjacent figures were only labeled by number and stored in the same files during combing and dragging different figures in Photoshop software. It is important to emphasize that this correction does not compromise the scientific integrity of the study's conclusions. The authors sincerely apologize for any inconvenience caused by this oversight. The accurate images, obtained during the original experimental procedures, are provided below.

Li M-Q, Hasan MK, Li C-X, et al. Melatonin mediates selenium-induced tolerance to cadmium stress in tomato plants. J Pineal Res. 2016;61(3):291-302. https://doi.org/10.1111/jpi.12346

After the publication of the article, the authors identified inaccuracies in chlorophyll fluorescence images in Figure 4C, namely Water treatment of TRV (1st row, panel 1 from the left), Water treatment of TRV-TDC (1st row, panel 4 from the left), and Se treatment of TRV-TDC (1st row, panel 5 from the left). The accurate images, obtained during the original experimental procedures, are provided below. These corrections do not compromise the scientific integrity of the study's conclusions.

We apologize for this error.

Internal circadian phase assessment is increasingly acknowledged as a critical clinical tool for the diagnosis, monitoring, and treatment of circadian rhythm sleep−wake disorders and for investigating circadian timing in other medical disorders. The widespread use of in-laboratory circadian phase assessments in routine practice has been limited, most likely because circadian phase assessment is not required by formal diagnostic nosologies, and is not generally covered by insurance. At-home assessment of salivary dim light melatonin onset (DLMO, a validated circadian phase marker) is an increasingly accepted approach to assess circadian phase. This approach may help meet the increased demand for assessments and has the advantages of lower cost and greater patient convenience. We reviewed the literature describing at-home salivary DLMO assessment methods and identified factors deemed to be important to successful implementation. Here, we provide specific protocol recommendations for conducting at-home salivary DLMO assessments to facilitate a standardized approach for clinical and research purposes. Key factors include control of lighting, sampling rate, and timing, and measures of patient compliance. We include findings from implementation of an optimization algorithm to determine the most efficient number and timing of samples in patients with Delayed Sleep−Wake Phase Disorder. We also provide recommendations for assay methods and interpretation. Providing definitive criteria for each factor, along with detailed instructions for protocol implementation, will enable more widespread adoption of at-home circadian phase assessments as a standardized clinical diagnostic, monitoring, and treatment tool.

In mammals, seasonal opportunities and challenges are anticipated through programmed changes in physiology and behavior. Appropriate anticipatory timing depends on synchronization to the external solar year, achieved through the use of day length (photoperiod) as a synchronizing signal. In mammals, nocturnal production of melatonin by the pineal gland is the key hormonal mediator of photoperiodic change, exerting its effects via the hypothalamopituitary axis. In this review/perspective, we consider the key developments during the history of research into the seasonal synchronizer effect of melatonin, highlighting the role that the pars tuberalis–tanycyte module plays in this process. We go on to consider downstream pathways, which include discrete hypothalamic neuronal populations. Neurons that express the neuropeptides kisspeptin and (Arg)(Phe)–related peptide-3 (RFRP-3) govern seasonal reproductive function while neurons that express somatostatin may be involved in seasonal metabolic adaptations. Finally, we identify several outstanding questions, which need to be addressed to provide a much thorough understanding of the deep impact of melatonin upon seasonal synchronization.