Melatonin alleviates LPS-induced abnormal pregnancy through MTNR1B regulation of m6A
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ABSTRACT:
PROVIDER: PRJNA896545 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22129180_1.fastq.gz | Fastqsanger.gz | |||
| SRR22129180_2.fastq.gz | Fastqsanger.gz | |||
| SRR22129181_1.fastq.gz | Fastqsanger.gz | |||
| SRR22129181_2.fastq.gz | Fastqsanger.gz | |||
| SRR22129182_1.fastq.gz | Fastqsanger.gz |
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Project description:In this study, the protective effect of melatonin and m6A on mouse pregnancy was studied by constructing an LPS-induced abnormal early pregnancy model in mice. Pregnant ICR mice were selected and intraperitoneal injection of LPS on D3 and D4 of pregnancy, melatonin was found to alleviated LPS-induced reductions in the number of implantation sites. Besides, melatonin alleviated the activation of inflammation, autophagy and apoptosis pathways, thereby protecting the pregnancy process of mice. We monitored m6A methylation by liquid chromatography-tandem mass spectrometry (LC-MS/MS) and m6A-sequencing (m6A-seq), we found that melatonin regulated m6A methylation levels.
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Project description:Melatonin is a powerful anti-inflammatory agent and antioxidant. To explore specific anti-inflammatory mechanisms, LPS was used to intervene in RAW 264.7 cells to construct an inflammation model. Then, cells were pretreated with melatonin at concentrations of 10-3M to 10-7M, respectively. The above cells were subjected to DRUG-seq sequencing to explore the specific mechanism of melatonin anti-inflammation.
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Project description:We compared the gene expression patterns of macrophages upon LPS stimulation with or without melatonin pretreatment
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Project description:Pregnancy is a highly intricate and delicate process, where inflammation during early stages may lead to pregnancy loss or defective implantation. Melatonin, primarily produced by the pineal gland, exerts several pharmacological effects. N6-methyladenosine (m6A) is the most prevalent mRNA modification in eukaryotes. This study aimed to investigate the association between melatonin and m6A during pregnancy and elucidate the underlying protective mechanism of melatonin. Melatonin was found to alleviate lipopolysaccharide (LPS)-induced reductions in the number of implantation sites. Additionally, it mitigated the activation of inflammation, autophagy, and apoptosis pathways, thereby protecting the pregnancy process in mice. The study also revealed that melatonin regulates uterine m6A methylation levels and counteracts abnormal changes in m6A modification of various genes following LPS stimulation. Furthermore, melatonin was shown to regulate m6A methylation through melatonin receptor 1B (MTNR1B) and subsequently modulate inflammation, autophagy, and apoptosis through m6A. In conclusion, our study demonstrates that melatonin protects pregnancy by influencing inflammation, autophagy, and apoptosis pathways in an m6A-dependent manner via MTNR1B. These findings provide valuable insights into the mechanisms underlying melatonin's protective effects during pregnancy and may have implications for potential therapeutic strategies in managing pregnancy-related complications.
| S-EPMC10815701 | biostudies-literature
Project description:Effect of melatonin during LPS-induced inflammation on RAW 264.7 cells
| PRJNA1121248 | ENA
Project description:Melatonin is a well-known agent that plays multiple roles in animals. Its possible function in plants is less clear. In the present study, we tested the effect of melatonin (N-acetyl-5-methoxytryptamine) on soybean growth and development. Both spraying of leaves and seed-coating with melatonin significantly promoted soybean growth as judged from leaf size and plant height. This enhancement was also observed in soybean production and their fatty acid content. Melatonin increased pod number, seed number and seed weight. However, the 100-seed weight was not influenced by melatonin application. Melatonin also improved soybean tolerance to salt and drought stresses. Transcriptome analysis revealed that melatonin up-regulated the expression of many genes and alleviated the inhibitory effects of salt stress on gene expressions. Further detailed analysis of the affected pathways documents that melatonin likely achieved its promotional roles in soybean through enhancement of genes involved in cell division, photosynthesis, carbohydrate metabolism, fatty acid biosynthesis and ascorbate metabolism. Our results demonstrate that melatonin has significant potential for improving of soybean growth and seed production. Further study should uncover more about the molecular mechanisms of melatoninM-bM-^@M-^Ys function in soybeans and other crops. Four different treatments were chosen, water, salt, 100M-BM-5M melatonin and salt plus 100M-BM-5M melatonin. The comparison of salt/melatonin-treated sample versus water-treated sample reveals salt or melatonin induced transcriptome changes. The comparison of melatonin plus salt treated sample versus salt-treated sample reveals melatonin induced changes when salt exists.
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Project description:Hypertrophic scar (HS) is a fibrotic skin condition and characterized by abnormal proliferation of myofibroblasts and accumulation of extracellular matrix. Melatonin, an endogenous hormone, can alleviate fibrosis in multiple models of diseases. This study examined the effect of melatonin on fibrosis in primary fibroblasts from human HS (HSFs) and a rabbit ear model and potential mechanisms. Melatonin treatment significantly decreased the migration and contraction capacity, collagen and α-smooth muscle actin (α-SMA) production in HSFs. RNA-sequencing and bioinformatic analyses indicated that melatonin modulated the expression of genes involved in autophagy and oxidative stress. Mechanistically, melatonin treatment attenuated the AKT/mTOR activation through affecting the binding of MT2 receptor with PI3K to enhance autophagy, decreasing fibrogenic factor production in HSFs. Moreover, melatonin treatment inhibited HS formation in rabbit ears by enhancing autophagy. The anti-fibrotic effects of melatonin were abrogated by treatment with an autophagy inhibitor (3-methyladenine, 3-MA), an Akt activator (SC79), or an MT2 selective antagonist (4-phenyl-2propionamidotetralin, 4-P-PDOT). Therefore, melatonin may be a potential drug for prevention and treatment of HS.
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Project description:This study performed single-cell RNA sequencing (scRNA-seq) analyses on peripheral blood neutrophils from cystic fibrosis (CF) patients and healthy controls (HC) in their native state and LPS-activated state. Differences in global gene transcription were interrogated and compared. Results demonstrate that CFTR loss of function in CF neutrophils led to abnormal immune programming, exemplified by precocious priming at their native state, and abnormal immune response to LPS.
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Project description:Objective: Melatonin and auxin are both tryptophan-derived indole molecules. Much attention has been given to proposed auxin-like activities of melatonin (regulating growth concentration-dependently). However, it still largely remains unclear whether melatonin and auxin regulate signalling pathways in a similar fashion. The purpose of this study is to directly compare the transcriptome response of Arabidopsis with melatonin or auxin. Method: mRNA profiles of 12-day old rosettes treated for a further of 3 days with +/- melatonin (5µM, 1005µM) or NAA(4.5µM) were generated by RNA-sequencing in triplicates (three independent biological experiments), using Illumina NextSeq 550 technology. Results: Comparative global transcriptome analysis conducted on Arabidopsis rosette treated with melatonin or NAA under exact same set of experimental conditions revealed differential number of genes and type of pathways. While auxin (4.5µM) regulated a large number of genes and elicited a diverse response, melatonin (100µM) showed a modest effect on transcriptome with only few genes significantly regulated whereas none regulated at approximately equimolar concentration with NAA (5µM) as compared to untreated solvent control (0.1% EtOH). Interestingly, the most prominent category of genes regulated by melatonin trended towards biotic stress defense pathways. Conclusions: These findings indicate that melatonin and auxin act quite differently toward signaling pathways in Arabidopsis. Melatonin has its own set of mechanisms to exert its functions, with strong inclination toward biotic defense pathways.
2019-12-02 | GSE134079 | GEO
Project description:Melatonin is a known modulator of follicle development, it acts through several molecular cascades via binding to its two high-affinity, G-protein coupled receptors MT1 and MT2. Even though it is believed that melatonin can modulate granulosa cell (GC) functions, there is still limited knowledge of how it can act in human GC through MT1 and MT2 and which one is the major receptor implicated in the effects of melatonin on the metabolic processes in the dominant follicle. To better characterize the roles of the MT1 and MT2 receptors on the effects of melatonin on follicular atresia and the regulation of proliferation and differentiation of granulosa cells during the antral stage, human granulosa-like tumor cells (KGN) were treated with specific melatonin receptor agonists and antagonists, and gene expression was analyzed with RNA-seq technology. Following appropriate normalization and the application of a fold change cut-off of 1.5 (FC 1.5, p ≤ 0.05) for each treatment, lists of the principal differentially expressed genes (DEGs) are generated. Analysis of major upstream regulators suggested that the MT1 receptor may be involved in the melatonin antiproliferative effect by reprogramming the metabolism of human GC by activating the PKB signaling pathway. Our data suggest that melatonin may act complementary through both MT1 and MT2 receptors to modulate human GC steroidogenesis, proliferation, and differentiation. However, MT2 receptors may be the ones implicated in transducing the effects of melatonin on the prevention of GC luteinization and follicle atresia at the antral follicular stage through stimulating the PKA pathway.
2022-10-26 | GSE201943 | GEO