Journal of Pineal Research最新文献

EXPRESSION OF CONCERN: J. Wang, X. Xiao, Y. Zhang, D. Shi, W. Chen, L. Fu, L. Liu, F. Xie, T. Kang, W. Huang, and W. Deng, “Simultaneous Modulation of COX-2, p300, Akt, and Apaf-1 Signaling by Melatonin to Inhibit Proliferation and Induce Apoptosis in Breast Cancer Cells,” Journal of Pineal Research 53, no. 1 (2012): 77–90, https://doi.org/10.1111/j.1600-079X.2012.00973.x.

This Expression of Concern is for the above article, published online on 03 January 2012 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Gianluca Tosini; and John Wiley & Sons Ltd. A third party raised concerns that a FACS plot had been duplicated between Figures 1B and 6C, while both are intended to represent different treatments and quantification. An investigation by the publisher confirmed this duplication and also found evidence of image duplication between Figures 3D and 4A involving western blot data, as well as a panel mismatch in Figure 6D involving fluorescence data.

The authors responded to an inquiry by the publisher with an explanation and some additional data, but they could not supply all of the original raw data for the article. The Expression of Concern has been agreed to because the concerns of image and data duplication in the article cannot be resolved. The authors were informed of the Expression of Concern.

EXPRESSION OF CONCERN: M. Erşahin, Z. Özdemir, D. Özsavcı, et al., “Melatonin Treatment Protects Against Spinal Cord Injury Induced Functional and Biochemical Changes in Rat Urinary Bladder,” Journal of Pineal Research 59, no. 2 (2012): 340–348, https://doi.org/10.1111/j.1600-079X.2011.00948.x.

This Expression of Concern is for the above article, published online on 05 December 2011 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Gianluca Tosini; and John Wiley & Sons Ltd. A third party raised concerns of an overlap between Figures 8A and 8C. An investigation by the publisher confirmed these concerns. The authors responded to an inquiry by the publisher and stated the original data were no longer available. As such, the data related to this concern cannot be validated. This Expression of Concern has been published in order to inform and alert readers about the concerns in Figure 3. The authors were informed of this Expression of Concern.

EXPRESSION OF CONCERN: D. Mukherjee, A. K. Ghosh, A. Bandyopadhyay, et al., “Melatonin Protects Against Isoproterenol-Induced Alterations in Cardiac Mitochondrial Energy-Metabolizing Enzymes, Apoptotic Proteins, and Assists in Complete Recovery From Myocardial Injury in Rats,” Journal of Pineal Research 53, no. 2 (2012): 166–179, https://doi.org/10.1111/j.1600-079X.2012.00984.x.

This Expression of Concern is for the above article, published online on 20 February 2012 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Gianluca Tosini; and John Wiley & Sons Ltd. A third party raised concerns that the beta-actin control bands in Figures 3A, 4A, 4B, 5A, 5B, 6A, 6B, 7A, and 7B were duplicates and had also been used in an earlier article by most of the same authors [Mukherjee et al. 2010 (https://doi.org/10.1111/j.1600-079X.2010.00749.x)].

The authors responded to an inquiry by the publisher and stated that the studies reported in both articles were part of a single experimental project conducted between 2008 and 2009, which used identical sample sets processed under uniform conditions. Most of the original data were no longer available. As such, the publisher is not able to validate the data related to these concerns. Additionally, this article did not adequately indicate that both articles derived from the same experimental procedure and did not declare the re-use of beta-actin control bands. This Expression of Concern has been published in order to inform and alert readers about these concerns. The authors were informed of this Expression of Concern.

Reaching term gestation requires a complex interplay between the uterus and hormonal signals regulating its contractile profile. Most pregnancy-associated hormones vary in their overall level of release throughout pregnancy, but also have a circadian release pattern, including progesterone, oxytocin, and melatonin. It remains poorly understood how the circadian release of hormones impacts uterine function. To determine how time-of-day, mouse strain, and melatonin proficiency were associated with the uterotonic efficacy of oxytocin, the primary hormone promoting uterine contractions, we used melatonin-deficient C57BL/6 and melatonin-proficient CBA/C57BL/6 (CBA/B6) female mice on gestation day 18. Through RNAscope, we found that oxytocin receptor (Oxtr) mRNA exhibited a time-of-day variation that differed between the uterine endometrium and myometrium. This uterine layer-specific, time-of-day difference in Oxtr was associated with a shift in phase of the molecular clock reporter PER2::Luciferase. A strain-specific effect of PER2::Luciferase rhythms were observed in the uterus, where CBA/B6 had a shorter PER2::Luciferase period than C57BL/6. In addition, CBA/B6 uteri had lower spontaneous uterine contraction force compared to C57BL/6. Despite the difference in spontaneous contractions and circadian period, the capacity of oxytocin to induce contractions varied by time-of-day, independent of mouse strain. Together, these findings reveal that uterine responsiveness to oxytocin is gated by circadian time, with Oxtr expression and uterine contractions showing diurnal variation. At the same time, mouse strain was associated with PER2::Luciferase period and baseline uterine contractility. These results underscore the relevance of circadian timing in uterine physiology and that strain differences impact basal uterine function.

Circadian rhythm alignment depends on environmental light detection via opsins. Pinopsin, originally identified in the pineal organ of birds and later in amphibian pineal complex and eyes, may play a role in this process, though its function has not been genetically tested. Evolutionary analysis suggests pinopsin was independently lost in several vertebrate lineages, including mammals (Synapsida), some reptiles (e.g. snakes and crocodiles), and teleost fish, but retained in birds, turtles, lizards, and non-teleost Actinopterygii. We conducted a detailed genomic search of the pinopsin gene across 95 amphibian species and assessed its function in Xenopus laevis tadpoles using CRISPR/Cas9-mediated knockout. Our survey indicates that pinopsin is highly conserved in salamanders and most anurans, but absent in many caecilians (Gymnophiona), which have a fossorial lifestyle with limited light exposure. To investigate its biological role, we generated X. laevis F0 pinopsin knockout tadpoles and evaluated two light-sensitive responses: (1) day/night melatonin fluctuations inferred from skin pigmentation changes, and (2) locomotor activity over a 24-h photoperiod. We show these responses depend only on pineal light sensitivity and are independent of eye sensitivity at developmental stage 46/47. Our findings reveal: (1) Pinopsin is co-expressed with Aanat, a key enzyme in melatonin synthesis; (2) knockout tadpoles show paler skin during the light phase, suggesting pinopsin suppresses melatonin production in daylight; and (3) reduced daytime locomotor activity in F0 mutants, consistent with melatonin-induced lethargy. Overall, pinopsin emerges as a critical opsin for light-regulated circadian-associated behavior in Xenopus, with likely conserved roles across amphibians (anurans and salamanders in general) and other non-mammalian vertebrates, including birds, turtles, and lizards.

Exogenous melatonin has emerged as a pivotal multifunctional signaling molecule, recognized for its critical role in enhancing stress tolerance and improving crop productivity. N6-methyladenosine (m6A) is the most prevalent internal modification found in eukaryotic mRNA and plays a crucial role in regulating plant growth, development, and stress responses. Despite its importance, the regulatory mechanisms of the m6A pathway in rice exposed to exogenous melatonin remain inadequately investigated. This study investigates systematic analysis of m6A-regulatory gene families in rice. We identified a total of 124 genes, which include 7 writers, 22 readers, and 95 erasers. The distribution of these genes is uneven across the 11 chromosomes of the rice genome. Analysis of conserved domains revealed structural signatures that are specific to each gene family. Phylogenetic relationships with dicot and monocot species offered insights into evolutionary trajectories. Notably, gene structure and motif analyses revealed functional divergence within and between gene families. Cis-element analysis identified abundance motifs associated with stress adaptation, hormonal signaling, and TFs, including ABRE, DRE, and MYB. Furthermore, synteny analysis unveiled both conserved regions and lineage-specific expansions, particularly within the YTH and ALKBH families. The protein interaction network revealed robust connections among subgroups and identified 10 hub genes. GO and KEGG analyses indicated significant enrichment in stress-related pathways, including secondary metabolite biosynthesis, flavonoid biosynthesis, and cysteine and methionine metabolism. RT-qPCR validates that melatonin Osm6As significantly influences the expression of targeted genes, with melatonin upregulations exhibiting a time-dependent pattern. Furthermore, GFP tagging of OsECT2 revealed that protoplasts are evenly distributed, suggesting robust nuclear enrichment of fluorescence. This study offers new insights into the epitranscriptomic regulatory responses of the m6A-modifier.