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At least 19 recordsLinked to original sources

PubMed2026

Integrated Bulk and Single-Cell RNA-Seq Analysis Reveals Transcriptional Activation of PTGS2 by FOS in Progression From T2DM to T2DM-Associated NAFLD.

Type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD) frequently coexist, exacerbating disease burden. However, the molecular mechanisms underlying the progression from T2DM to T2DM-associated NAFLD remain unclear. This study investigated the regulatory function of FOS-mediated PTGS2 activation in this transition. We integrated bulk RNA-seq data from GEO, single-cell transcriptomic data and transcriptomes from patients with T2DM-associated NAFLD. Differentially expressed genes were identified using the limma package, and T2DM-related gene modules were defined by weighted gene co-expression network analysis. LASSO regression and random forest identified 14 candidate genes, with PTGS2 and FOS prioritised. Single-cell analysis showed increased FOS and PTGS2 expression in monocytes, CD8+ T cells and Kupffer cells. Transcription factor prediction and dual-luciferase assays confirmed that FOS directly binds the PTGS2 promoter and drives its transcription. In vitro, FOS silencing decreased PTGS2 expression, cytokine secretion and apoptosis under high-glucose and free fatty acid conditions, whereas PTGS2 overexpression exacerbated inflammation and apoptosis independently of FOS expression. These findings demonstrate that FOS transcriptionally activates PTGS2, contributing to hepatic inflammation and apoptosis during the progression from T2DM to NAFLD. PTGS2 may serve as a promising biomarker and therapeutic target for T2DM-associated NAFLD.

Single-Cell Gene Expression Analysis↗

PubMed2026

FOS Regulates Myogenic and Adipogenic Differentiation via Extracellular Matrix Signaling.

In the livestock industry, intramuscular fat deposition is a key factor influencing meat tenderness and flavor. Although FOS (Fos proto-oncogene, AP-1 transcription factor subunit) has been implicated in the regulation of cell proliferation and differentiation, its differential roles in myogenic and adipogenic regulation remain unclear. In this study, we revealed that FOS markedly enhanced myogenic differentiation while inhibiting adipogenic differentiation in muscle stem cells, indicating that it exerts distinct effects on muscle development and intramuscular fat deposition. Mechanistically, FOS modulated extracellular matrix signaling by regulating FAK and PXN phosphorylation, acting as a molecular regulator between the muscle and fat lineages. Furthermore, exon SNPs in FOS were associated with slaughter weight and backfat thickness, and the mutant genotypes weakened its antiadipogenic effect. Collectively, these findings suggest that FOS is an important regulator of myogenic and adipogenic differentiation and is a potential candidate gene for the genetic improvement of meat quality traits.

Animals↗

PubMed2026

Cranberry juice potentiates sensitivity of uropathogenic Escherichia coli (UPEC) strains to fosfomycin and decreases occurrence of spontaneous resistance.

Uropathogenic Escherichia coli (UPEC) is the leading cause of urinary tract infections (UTIs). The growing prevalence of antimicrobial resistance underscores the need for alternative or complementary strategies to enhance antibiotic activity. Fosfomycin (FOS) remains a recommended first-line treatment for uncomplicated UTIs due to its broad activity and low resistance rates; however, spontaneous resistance frequently arises through mutations in bacterial transport systems. Cranberry juice is known for its anti-adhesive and anti-infective properties; however, its potential to modulate antibiotic activity remains poorly understood. Here, we show that cranberry juice markedly potentiates the antibacterial activity of FOS and limits the emergence of resistance in UPEC clinical isolates. In 72% of the 32 tested isolates, cranberry juice significantly increased FOS inhibition activities and reduced spontaneous FOS-resistant mutant frequencies by up to five orders of magnitude. Whole-genome sequencing revealed distinct mutational patterns: FOS-resistant mutants selected without cranberry juice primarily carried glpT mutations, whereas those obtained with juice harbored mutations in uhpT or associated regulatory genes. Reporter assays indicated that cranberry juice represses glpT expression while maintaining UhpT-mediated FOS uptake, thereby sustaining antibiotic entry and activity. These results demonstrate that cranberry juice alters bacterial carbohydrate transport regulation to potentiate FOS activity and suppress resistance emergence. This study provides novel evidence that a natural product can enhance FOS activity, highlighting its potential as an antibiotic adjuvant for UTI management.IMPORTANCEAntimicrobial resistance is a growing threat to public health, and new strategies are needed to preserve the activity of existing antibiotics. This study reveals that cranberry juice, a widely consumed natural product, enhances the antibacterial activity of fosfomycin against uropathogenic Escherichia coli by modulating bacterial sugar transport systems. By shifting fosfomycin uptake from GlpT- to UhpT-mediated pathways, cranberry juice both potentiates antibiotic activity and suppresses the emergence of resistant mutants. These findings provide new insight into how dietary components can influence antibiotic response, offering a promising basis for developing natural adjuvants that extend the lifespan of current antimicrobial agents.

Fosfomycin↗

PubMed1976

Fosfomycin resistance: selection method for internal and extended deletions of the phosphoenolpyruvate:sugar phosphotransferase genes of Salmonella typhimurium.

Selection for resistance to the antibiotic fosfomycin (FOS; L-cis 1,2-epoxypropylphosphonic acid, a structural analogue of phosphoenolpyruvate) was used to isolate mutants carrying internal and extended deletions of varying lengths within the ptsHI operon of Salmonella typhimurium. Strains carrying "tight" ptsI point mutations and all mutants in which some or all of the ptsI gene was deleted were FOS resistant. In contrast, strains carrying ptsH point mutations were sensitive to FOS. Resistance to FOS appeared to result indirectly from catabolite repression of an FOS transport system, probably the sn-glycerol-3-phosphate transport system. Resistant ptsI mutants became sensitive to FOS when grown on D-glucose-6-phosphate, which induces an alternate transport system for FOS, or when grown in the presence of cyclic adenosine 3',5'-monophosphate. A detailed fine-structure map of the pts gene region is presented.

Anti-Bacterial Agents↗

PubMed2026

Inulin, Containing Frutco-Oligosaccharides, and Generalized Anxiety Disorder 7-Item Scale Scores in College Students.

This study was conducted to determine the effects of fructo-oligosaccharide (FOS) inulin on anxiety symptoms in college students. Forty million adults in the United States suffer from anxiety. Previous studies have viewed gut microbiota and its potential link to anxiety in both humans and mice. However, no previous studies focused on the effect of FOS inulin on college students. Fourteen subjects received 4.9 g per day of FOS inulin as the treatment (TX) or no supplement as the control (CON) for 28 days. Both the TX and CON groups were given the Generalized Anxiety Disorder 7-Item Scale (GAD-7) on days 1 and 28. Both groups were also given a 3-day food log at the beginning of the experiment and otherwise maintained their regular diet. Results showed a statistically significant decrease in median GAD-7 scores in both groups (P = .017, r = .637 and P = .042, r = .587 for the TX and CON groups, respectively). However, when comparing the GAD-7 scores between groups, no statistically significant results were found. FOS inulin supplementation did not alleviate anxiety symptoms in college students participating in this study.

Adolescent↗

PubMed2022

Enhancer and super-enhancer landscape in polycystic kidney disease.

Widespread aberrant gene expression is a pathological hallmark of polycystic kidney disease (PKD). Numerous pathogenic signaling cascades, including c-Myc, Fos, and Jun, are transactivated. However, the underlying epigenetic regulators are poorly defined. Here we show that H3K27ac, an acetylated modification of DNA packing protein histone H3 that marks active enhancers, is elevated in mouse and human samples of autosomal dominant PKD. Using comparative H3K27ac ChIP-Seq analysis, we mapped over 16000 active intronic and intergenic enhancer elements in Pkd1-mutant mouse kidneys. We found that the cystic kidney epigenetic landscape resembles that of a developing kidney, and over 90% of upregulated genes in Pkd1-mutant kidneys are co-housed with activated enhancers in the same topologically associated domains. Furthermore, we identified an evolutionarily conserved enhancer cluster downstream of the c-Myc gene and super-enhancers flanking both Jun and Fos loci in mouse and human models of autosomal dominant PKD. Deleting these regulatory elements reduced c-Myc, Jun, or Fos abundance and suppressed proliferation and 3D cyst growth of Pkd1-mutant cells. Finally, inhibiting glycolysis and glutaminolysis or activating Ppara in Pkd1-mutant cells lowerd global H3K27ac levels and its abundance on c-Myc enhancers. Thus, our work suggests that epigenetic rewiring mediates the transcriptomic dysregulation in PKD, and the regulatory elements can be targeted to slow cyst growth.

Animals↗

PubMed2010

Human dopamine β-hydroxylase promoter variant alters transcription in chromaffin cells, enzyme secretion, and blood pressure.

BACKGROUND: Dopamine β-hydroxylase (DBH) plays an indispensable role in catecholamine synthesis by converting dopamine into norepinephrine. Here, we characterized a DBH promoter polymorphism (C-2073T; rs1989787; minor allele frequency ~16%) that influences not only gene transcription but also enzyme secretion and blood pressure (BP) in vivo. METHODS: Plasma DBH activity was measured spectrophotometrically. DBH genetic effects on BP were tested in subjects with the most extreme BP values in a large primary care population. Functional effects of promoter variants were studied by site-directed mutagenesis in DBH promoter haplotype/luciferase reporter plasmids transfected into chromaffin cells. Sequence motifs were predicted from position weight matrices, and endogenous transcription factor binding was probed by Chromatin ImmunoPrecipitation (ChIP). RESULTS: The T-allele of common promoter variant C-2073T was contained in a promoter haplotype that associated with plasma DBH activity, a trait also predicted by that variant itself. Promoter haplotypes including C-2073T predicted BP in the population, and the effect was also referable to C-2073T itself. Computationally, C-2073 disrupted a predicted match for transcription factor c-FOS. Site-directed mutagenesis at C-2073T altered not only basal promoter activity, but also transactivation by c-FOS, as well as the chromaffin cell secretory stimuli nicotine or pituitary adenylate cyclase-activating polypeptide (PACAP). Endogenous c-FOS bound to the motif in chromatin. CONCLUSIONS: These results suggest that DBH promoter variant C-2073T is functional in vivo: this promoter variant seems to initiate a cascade of transcriptional and biochemical changes including augmented DBH secretion, eventuating in elevation of basal BP, and hence cardiovascular risk. The observations suggest new strategies for probing the pathophysiology, risk, and treatment of hypertension.

Animals↗

PubMed2026

[Mechanism of Tianshu Capsules in treating migraine rats based on gut microbiota].

This study aims to investigate the therapeutic effect of Tianshu Capsules(TS) on migraine rat model and explore its potential mechanism of action from the perspectives of the structure of the gut microbiota and functional pathway regulation. A migraine rat model was established via subcutaneous injection of nitroglycerin. The Sprague-Dawley rats were randomly divided into a control group, a model group, a low-dose TS group, a medium-dose TS group, a high-dose TS group, and an ibuprofen group. The efficacy of TS in improving migraine was evaluated by general condition observation and measurement of the craniofacial pain threshold. The expression of the gene c-fos in the trigeminal ganglion was determined by quantitative real-time polymerase chain reaction(PCR). The contents of endothelin-1(ET-1), calcitonin gene-related peptide(CGRP), and 5-hydroxytryptamine(5-HT) in serum were measured by enzyme-linked immunosorbent assay(ELISA). Fecal samples were subjected to metagenomic sequencing for systematic analysis of gut microbial diversity, taxonomic composition difference, and functional pathway changes of Kyoto Encyclopedia of Genes and Genomes(KEGG), and their correlations with behavioral and biochemical indices were further evaluated. The results show that TS significantly improves the increased body temperature and decreased craniofacial pain threshold in migraine rats. It also markedly suppresses the elevated expression levels of the gene c-fos in the trigeminal ganglion and reduces the levels of ET-1, CGRP, and 5-HT in serum. Metagenomic beta diversity analysis and differential taxonomic abundance analysis reveal that the migraine model induces significant gut microbiota dysbiosis, characterized by enrichment of harmful genera, including Streptococcus and Enterococcus, as well as a decline in the abundance of beneficial bacteria such as Allobaculum, Eubacterium, and Muribaculum. Functional pathway analysis results of KEGG further reveal that the relative abundances of pathways associated with biosynthesis of phenylalanine, tyrosine, and tryptophan, bacterial secretion system, citrate cycle, and biosynthesis of secondary metabolites are significantly decreased in the model group. TS intervention increased the abundance of the genus, such as Parabacteroides, Eubacterium, Allobaculum, and Muribaculum, while decreasing levels of microbiota, including Staphylococcus. TS also significantly upregulated pathways associated with barrier function(tight junction), amino acid biosynthesis pathways, and biosynthesis pathways of neurotransmitter precursors such as cysteine and methionine metabolism. In addition, it downregulated inflammatory pathways(Toll and IMD signaling) and pathways related to Staphylococcus aureus infection, thereby restoring the structure and function of the microbiota to a state close to those of the normal group. Spearman correlation analysis reveals that partial gut microbiota are significantly associated with migraine-related behavioral and biochemical indices(c-fos, ET-1, CGRP, and 5-HT). In conclusion, TS can regulate the disrupted gut microbiota structure and microbial functions related to neurotransmitter metabolism, intestinal barrier function, and inflammatory regulation in migraine model rats, which may be one of the potential key ways through which TS exert its anti-migraine effect.

Animals↗

PubMed1979

An investigation of coronary heart disease in families. The Framingham offspring study.

The Framingham Heart Study (FHS) was started in 1948 as a prospective investigation of cardiovascular disease in a cohort of adult men and women. Continuous surveillance of this sample of 5209 subjects has been maintained through biennial physical examinations. In 1971 examinations were begun on the children of the FHS cohort. This study, called the Framingham Offspring Study (FOS), was undertaken to expand upon knowledge of cardiovascular disease, particularly in the area of familial clustering of the disease and its risk factors. This report reviews the sampling design of the FHS and describes the nature of the FOS sample. The FOS families appear to be of typical size and age structure for families with parents born in the late 19th or early 20th century. In addition, there is little evidence that coronary heart disease (CHD) experience and CHD risk factors differ in parents of those who volunteered for this study and the parents of those who did not volunteer.

Adult↗

PubMed2025

KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in NUP98-Rearranged Acute Myeloid Leukemia.

UNLABELLED: NUP98 fusion oncoproteins (FO) are a hallmark of childhood acute myeloid leukemia. NUP98 FOs drive leukemogenesis through phase-separated condensate formation and maintenance of an active chromatin landscape at stem cell-associated genes in cooperation with epigenetic regulators. In this study, we show that MYST family histone acetyltransferase (HAT) complex proteins, including KAT6A/MOZ, KAT7/HBO1, and the common KAT6A/7 complex subunit BRPF1, associate with NUP98 FOs on chromatin and within condensates. MYST HATs are molecular dependencies in NUP98-rearranged (NUP98-r) leukemia, and genetic inactivation or pharmacologic inhibition of KAT6A and KAT7 impairs NUP98-r cell fitness. KAT6A/7 inhibition decreased global H3K23ac levels, displaced NUP98::HOXA9 from chromatin at the Meis1 locus, and led to myeloid cell differentiation. Additionally, KAT6A/7 inhibition decreased leukemic burden in multiple NUP98-r leukemia xenograft mouse models, synergized with menin inhibitor treatment, and was efficacious in menin inhibitor-resistant cells. In summary, we show that MYST family HATs are therapeutically actionable dependencies in NUP98-r acute myeloid leukemia. SIGNIFICANCE: KAT6A and KAT7 associate with NUP98 FOs to drive leukemogenesis. Inhibition of their HAT activity is an effective therapeutic strategy in NUP98-r leukemias, including those resistant to menin inhibition. Moreover, combined KAT6A/7 and menin inhibition is synergistic, supporting clinical translation to improve outcomes for NUP98 FO-driven leukemias.

Humans↗

PubMed2026

Fyn signaling in the medial prefrontal cortex regulates resistance to stress-induced object recognition impairments in male rats.

Genome-wide association studies on patients with depression have identified FYN and FYB, an FYN-binding protein, as being linked to depression. We have reported that experimental manipulations in gene expression in the medial prefrontal cortex (mPFC) alter stress-induced object recognition impairments in animals. Therefore, we examined the impact of alterations in FYN and FYB expression in the mPFC of adult male rats on resistance to stress-induced impairments in object recognition. Animals with virus-mediated knockdown or overexpression of Fyn in the mPFC were subjected to either a brief 20-min restraint with 20 intermittent tail shocks, which does not induce object recognition impairment, or a prolonged 60-min restraint with 60 intermittent tail shocks, which does. In an object recognition task, control rats maintained intact object recognition following a brief stress, whereas rats with Fyn knockdown or overexpression in the mPFC showed impaired object recognition. Prolonged stress impaired object recognition in both control rats and rats with Fyn knockdown or overexpression. Additionally, rats with Fyn knockdown in the mPFC exhibited fewer c-Fos-positive cells in the mPFC in response to brief stress, accompanied by a trend toward increased c-Fos in the amygdala compared with control rats. Fyn knockdown also reduced Fyb expression in the mPFC. Furthermore, Fyb knockdown in the mPFC impaired object recognition following brief stress, suggesting that the observed effects are consistent with involvement of a coupled Fyn-Fyb signaling axis rather than Fyn alone. These findings suggest that altered Fyn-related signaling in the mPFC may underlie the resistance to stress-induced object recognition impairments.

Animals↗

PubMed2025

A cell-state axis underlying colonization in carcinomas with implications for metastasis risk prediction and interception.

Metastasis to the liver drives mortality in pancreatic ductal adenocarcinoma (PDAC), yet mechanisms of colonization remain unclear. Using genomic barcoding, we developed a clonal competition model under immune surveillance, isolating murine PDAC subclones with high or low liver-colonization potential. Combined transcriptome and chromatin-accessibility analyses revealed a distinct "metastatic-potential axis," separate from the normal-to-PDAC and classical-basal axes. We established "MetScore" as a biomarker of this axis. MetScore distinguishes metastases from primary PDAC tumors in patients, predicts outcomes beyond classical-basal classifications, and generalizes across carcinoma subtypes, suggesting conserved colonization mechanisms. High-MetScore PDAC cells preferentially occupy immune cell-enriched niches, suggesting they remodel the metastatic microenvironment. Functional screening identified c-Fos as a positive mediator of colonization and a candidate anti-metastatic target. Collectively, we identify a cell-state axis underpinning PDAC liver colonization, introduce MetScore as a broadly applicable biomarker, and nominate actionable targets for peri-operative therapeutic intervention.

Animals↗

PubMed2026

Luteolin is associated with alleviation of cigarette smoke-induced cellular senescence and inflammation in mice involving the CREB/c-Fos/NQO1 pathway.

Cigarette smoke (CS) exposure is a major risk factor for chronic obstructive pulmonary disease (COPD) and is closely associated with cellular senescence. Previous studies have demonstrated the efficacy of luteolin in treating aging-related symptoms. This study aims to elucidate the therapeutic potential of luteolin against CS-induced cellular senescence. Using a CS-exposed mouse model and cigarette smoke extract (CSE) treated mouse lung epithelial cells (TC-1), we demonstrate that luteolin significantly attenuates CS-induced histopathological alterations and inflammatory cytokine release while alleviating cellular senescence. Transcriptome sequencing suggests that NQO1 and Fos may serve as a common molecular target for both CS-induced pathology and luteolin treatment. Subsequent Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis (GSEA) enrichment analysis and pathway validation experiments revealed that the cAMP agonist Forskolin inhibits senescence marker expression by activating the CREB pathway, exhibiting a mechanism similar to that of luteolin. Notably, luteolin activation of this pathway may not depend on PKA activation. Ultimately, the study found that luteolin mitigates inflammatory responses and prevents lung epithelial cell senescence via the CREB/c-Fos/NQO1 pathway. These findings not only suggest the pivotal role of NQO1 in regulating CS-induced cellular senescence but also underscore the potential of luteolin as a therapeutic drug.

Animals↗

PubMed2026

Biophysical mechanisms underlying the generation and maintenance of rule-learning engram.

Training rodents in a particularly difficult olfactory-discrimination task results with acquisition of high-skill to perform the task superbly, termed 'rule-learning'. We show that rule-learning occurs abruptly, in a "light-bulb moment". Using whole-cell patch-clamp recordings from the piriform cortex (PC) of Fos2A-iCreER/TRAP2 mice, we target activated-neurons, expressing immediate early genes (IEG). We notice, from the onset of training, IEG-positive neurons from trained animals display enhanced intrinsic excitability. Subsequently, synaptic excitation and inhibition are enhanced in these neurons, in a coordinated, cell-wide process. Additionally, in parallel, we detect the density of IEG-expressing neurons sharply declines. Double labeling with TRAP and c-Fos reveal that nearly two-thirds of the rule-memory cell ensemble neurons are activated from the beginning of training. Silencing TRAP-expressing neurons using inhibitory DREADD leads to a complete loss of rule memory. Hence, we propose that rule learning occurs at a discrete moment and is developed through a gradual process that stabilizes the memory of the rule.

Animals↗

PubMed2025

Distinct Behavioral Profiles and Neuronal Correlates of Heroin Vulnerability Versus Resiliency in a Multi-Symptomatic Model of Heroin Use Disorder in Rats.

OBJECTIVE: The behavioral and diagnostic heterogeneity within the opioid use disorder (OUD) diagnosis is not readily captured in current animal models, limiting the translational relevance of the mechanistic research that is conducted in experimental animals. The authors hypothesized that a nonlinear clustering of OUD-like behavioral traits would capture population heterogeneity and yield subpopulations of OUD vulnerable rats with distinct behavioral and neurocircuit profiles. METHODS: Over 900 male and female heterogeneous stock rats, a line capturing genetic and behavioral heterogeneity present in humans, were assessed for several measures of heroin use and rewarded and non-rewarded seeking behaviors. A nonlinear stochastic block model clustering analysis was used to assign rats to OUD vulnerable, intermediate, and resilient clusters. Additional behavioral tests and circuit analyses using c-fos protein activation were conducted on the vulnerable and resilient subpopulations. RESULTS: OUD vulnerable rats exhibited greater heroin taking and seeking behaviors relative to those in the intermediate and resilient clusters. Akin to human OUD diagnosis, further vulnerable rat subclustering revealed subpopulations with different combinations of behavioral traits, including sex differences. Lastly, heroin cue-induced neuronal patterns of circuit activation differed between resilient and vulnerable phenotypes. Behavioral sex differences were recapitulated in patterns of circuitry activation, including preferential engagement of extended amygdala stress circuitry in males and cortico-striatal drug cue-seeking circuitry in females. CONCLUSION: Using a nonlinear clustering approach in rats, the analysis captured behavioral diagnostic heterogeneity reflective of human OUD diagnosis. OUD vulnerability and resiliency were associated with distinct neuronal activation patterns, posing this approach as a translational tool in assessing neurobiological mechanisms underpinning OUD.

Animals↗

PubMed2026

Identification of cryosensitive niches and a targetable FOS/AP‑1 program in the human ovarian cortex by single‑cell and spatial transcriptomics.

BACKGROUND: The ovary is a vital and dynamic reproductive organ. Ovarian tissue cryopreservation (OTC) plays a vital role in preserving female fertility. However, the cellular subtypes most susceptible to cryoinjury and the molecular mechanisms underlying cryopreservation-associated damage remain poorly understood. This study aimed to identify cell populations vulnerable to freezing-thawing and to elucidate the key transcriptomic alterations and signaling pathways associated with ovarian cryoinjury at the single-cell and spatial levels. METHODS: Ovarian cortical tissues from patients undergoing three gender reassignment surgery (GRS) were divided into fresh and vitrification-rapid warming groups. Following collagenase IV digestion, 10x Genomics single-cell RNA-seq was used for dissociated ovarian cell suspensions (27,185 fresh and 25,480 frozen-thawed cells). Eight major cell clusters were identified. Additionally, 110 oocytes (66 fresh, 44 vitrification-rapid warming) were isolated and analyzed using the Smart-seq2 platform. Spatial transcriptomics was performed via BGI Stereo-seq. Molecular validation was performed via β-galactosidase staining, immunofluorescence, and qRT-PCR. RESULTS: Cryopreservation significantly altered the activity of pathways related to focal adhesion, oxidative stress, and apoptosis, particularly in stromal and perivascular cells. The number of FOS-positive perivascular cells was notably increased after vitrification-rapid warming, whereas the number of PTGDS-positive stromal cells decreased. Oocyte analysis revealed that cryopreservation primarily disrupted pathways involved in the cell cycle and meiosis, although the damage was not irreversible, supporting the relative safety of long-term cryostorage. Spatial transcriptomics and functional validation further confirmed the rapid and robust activation of the FOS/AP-1 pathway after vitrification-rapid warming, particularly in perivascular and granulosa cells. Treatment with T-5224 (a FOS/AP-1 inhibitor) significantly rescued the morphology and function of cultured frozen-thawed ovaries. CONCLUSIONS: Stromal and perivascular cells are the main cell types that are sensitive to ovarian cryopreservation. The FOS/AP-1 pathway is markedly activated after, suggesting the exacerbation of metabolic impairment. In oocytes within the ovarian cortex, the cell cycle and meiosis-related physiological processes were the primary processes affected.

Female↗

PubMed2026

Systematic Review and Transcriptomic Meta-analysis of Environmental Enrichment Reveal Core Molecular Programs of Brain Plasticity.

Environmental enrichment (EE) paradigms in rodents have long demonstrated that enhanced sensory, cognitive, social, and motor stimulation positively impacts brain function, improving learning, memory, and neuroplasticity. These effects have significant implications for understanding cognitive development and mitigating cognitive decline and brain aging. While numerous transcriptomic studies have explored EE-induced molecular changes, a unified view of the genes and pathways consistently modulated remains lacking. To address this gap, we performed a systematic review and meta-analysis. We conducted a comprehensive PubMed search for all studies published up to February 2025 that matched all the following inclusion criteria: (1) employed EE paradigms; (2) were conducted on rodents; (3) utilized genome-wide transcriptomic methods; (4) examined brain regions or neuronal populations. The 323 retrieved articles were manually screened for relevance to the study aims and data availability. Datasets from 20 eligible RNA-seq reports were reprocessed using a unified analysis pipeline and subjected to a meta-analysis with three complementary statistical methods. Despite considerable heterogeneity across studies, our integrative analysis identified consistent gene expression signatures linked to synaptic function, plasticity and their transcriptional regulation. In particular, our findings highlight the upregulation of the activity-dependent transcriptional program, including Fos and Jun family members. These molecular insights advance our understanding of how EE impacts on neuronal and behavioral outcomes, and may inform therapeutic strategies aimed at replicating or enhancing EE benefits. To promote open science and foster further research, we developed an accessible web application, mEEtaBrain, that enables the neuroscience community to navigate and interrogate our meta-analysis results. Substantial methodological heterogeneity across source studies increased variability in the meta-analysis outcomes. The use of stressors or disease models, particularly in rat studies, introduced a major confounding factor and limited reliable interspecies comparison. Overall, the studies exhibited a low to moderate risk of bias.

Neuronal Plasticity↗

PubMed2026

Uncovering molecular regulatory networks of low-temperature stress response in Trachinotus ovatus via integrated transcriptome and metabolome analyses.

Golden pompano (Trachinotus ovatus) is one of the most economically important marine fish species in China. It is susceptible to low-temperature stress, which significantly challenges its production and supply. Nevertheless, study on the regulatory mechanisms underlying low-temperature stress responses in golden pompano remains limited. Here, we firstly performed a time-series transcriptome analysis to reconstruct dynamic response patterns under low-temperature stress in golden pompano. Transcriptome profiling identified common differentially expressed genes (DEGs), including fos, hlf, and hmgb1, as well as condition-specific DEGs across distinct low-temperature stress groups. Based on cluster analysis, all DEGs were classified into five distinct expression patterns, reflecting diversified regulation of expression in golden pompano during low-temperature stress. Furthermore, condition-specific regulatory modules were explored via weighted gene co-expression network analysis (WGCNA), highlighting that the two module hub genes, serbf2 and lipc, might respond to low-temperature stress by regulating the lipid catabolic process. Subsequently, untargeted metabolomic analysis revealed that glycerophospholipid metabolism was a significantly enriched common pathway, highlighting its crucial role in mediating the response to low-temperature stress. Finally, by integrating transcriptomic and metabolomic analyses, a gene-metabolite interaction network associated with glycerophospholipid metabolism under low-temperature stress was established. These findings underscore the significance of multiple candidate genes and glycerophospholipid metabolism in golden pompano's response to low-temperature stress, thereby laying a solid molecular foundation for the development of low-temperature-tolerant fish strains.

Animals↗