Animal Cells and Systems最新文献

Understanding the population genetic structure of marine decapods is essential for their effective conservation and management, particularly for species like the Chinese mitten crab (Eriocheir sinensis), which exhibits a complex life cycle and high invasive potential. In this study, we applied a population genomics approach using SLAF-seq to generate genome-wide SNP data from 120 unrelated individuals collected across six locations in China and Korea. We found a fine-scale but discernible level of genetic differentiation by regional populations correlated with geography. Individuals from Seocheon (Korea) and Wenzhou (southeastern China) exclusively share a distinct genetic ancestry component that makes them divergent from the rest, which we speculate may have been introduced by hybridization with congeneric species. We detected genetic outliers (9 out of 120 individuals) that show ongoing long-distance dispersal along the coastline of the Yellow Sea, likely happening during the planktonic larval phase. Collectively, our findings provide a genomic basis for delineating management strategies, supporting informed stock enhancement, and guiding region-specific conservation efforts for E. sinensis across East Asia.

Animal-vehicle collisions (AVCs) substantially contribute to wildlife population decline and adversely impact threatened species with already limited numbers. In this study, we aimed to investigate the factors contributing to AVCs involving two threatened species in the Republic of Korea: the leopard cat (Prionailurus bengalensis) and Eurasian otter (Lutra lutra). These two species are the most frequently affected by AVCs among threatened mammals in Korea. To achieve this, we used data from the Korea Roadkill Observation System (KROS), a government-sponsored web-based AVC monitoring system. Our analysis focused on 17 variables, categorized into bioclimatic, landscape, and traffic factors, using machine-learning-based predictive modeling. From 2019 to 2021, 589 AVC incidents of P. bengalensis and 228 AVC incidents of L. lutra were recorded in KROS. Our findings indicate that AVC frequencies peaked during the most active seasons of the year, corresponding to the mating or dispersal periods, with P. bengalensis showing the highest AVC frequency in fall and L. lutra peaking in summer. For P. bengalensis, habitat suitability consistently exerted a strong influence on AVC risk across all seasons, whereas for L. lutra, the key factors affecting AVC risk highly varied seasonally. These results underscore the importance of seasonal and species-specific approaches for AVC mitigation. Targeted strategies, including wildlife corridors, underpasses, and speed reduction zones in high-risk areas, are recommended to mitigate AVC risks. By identifying the key factors and their seasonal dynamics, this study provides critical insights for conserving threatened wildlife and effectively reducing AVC incidents.

Mitochondrial genomes (mitogenomes) are powerful molecular tools for exploring phylogenetic relationships, deciphering adaptation and divergence, as well as disease transmission potential among insects. In this study, we performed a comparative mitogenomic and phylogenetic analysis of two major mosquito vectors - Aedes albopictus and Culex pipiens molestus - collected from South Korea, together with mitogenome data from 18 additional mosquito species representing three Culicidae genera (Aedes, Anopheles, and Culex) retrieved from GenBank. The assembled mitogenomes, each comprising 13 protein-coding genes, 22 tRNAs, and two rRNAs, revealed conserved gene order and structural features typical of Diptera. Comparative analyses with multiple species representing the three genera uncovered lineage-specific patterns in codon usage, base composition, and control region variability. Phylogenetic relationships inferred using maximum likelihood and Bayesian methods based on concatenated mitochondrial protein-coding genes robustly resolved genus-level relationships and supported the monophyly of the two major Culicidae clades, Aedes (tribe Aedini) and Culex (tribe Culicini), with Anopheles sinensis and Anopheles gambiae serving as outgroups. Time-calibrated Bayesian analyses indicated a deep divergence between Anopheles and the Aedes-Culex clade during the Paleogene (∼51.8 Mya), followed by the separation of Aedes and Culex around ∼39.7 Mya. Notably, Ae. albopictus diverged from its congeners ∼11.7 Mya, while Cx. p. molestus exhibited a much more recent divergence (∼2.35 Mya), suggesting distinct evolutionary pressures and histories. This study demonstrates the utility of mitogenomic data for reconstructing mosquito evolutionary history and provides insights relevant to vector biology, ecology, and public health.

Depression induce by chronic neuroinflammation disrupts daily life and work, underscoring the importance of its treatment. It this study, depressive- and anxiety-like behaviors were induced in mice by injecting bacillus Calmette-Guérin (BCG), resulting from chronic neuroinflammation. Daily stimulation with specific acupuncture points (Baihui and Yintang, GV20 and GV29) with electroacupuncture (EA) for 14 days significantly alleviated depressive- and anxiety-like behaviors. Additionally, it also markedly reduced the levels of pro-inflammatory cytokines, including interleukin (IL)-6, IL-1β, and tumor necrosis factor-α, as well as inflammatory markers such as cyclooxygenase-2, in both the plasma and hippocampus. EA Stimulation significantly increased brain-derived neurotrophic factor (BDNF) mRNA expression in the hippocampus. Our results demonstrated that EA stimulation improved depression- and anxiety-like behaviors induced by chronic inflammation, an effect associated with the decreased expression of BDNF via regulation of NF-κB pathway.

Anomura is a morphologically and ecologically diverse infraorder of decapod crustaceans, yet its evolutionary and phylogenetic patterns remain underexplored using mitochondrial genome-based approaches, particularly regarding adaptive evolution across diverse environments. Here, we present a comprehensive phylogenomic analysis of 42 anomuran mitochondrial genomes, including three newly sequenced species: two intertidal Hapalogastrinae (Hapalogaster dentata and Oedignathus inermis) and one deep-sea pagurid (Pagurus rathbuni). The arrangement of protein-coding genes was identical to that reported in previously studied Lithodidae and Paguridae species; however, several tRNA genes exhibited translocations. Moreover, more than half of the 22 tRNA genes were predicted to adopt atypical cloverleaf form, and all protein-coding genes were under purifying selection. In addition, analysis of the mitochondrial control region revealed a conserved repeat structure (∼47 bp motif repeated ∼3.6 times), from which depth-associated Gibbs free energy patterns were broadly inferred. These patterns suggest potential links between control-region stability, depth-dependent adaptation, and the evolutionary process of carcinization. Time-calibrated analyses suggest that H. dentata and O. inermis diverged from other lithodids approximately 37-50 million years ago, while P. rathbuni diverged around 32 million years ago. These divergence events coincide with the Eocene-Oligocene transition, a period characterized by global cooling, sea-level decline, and shifts in ocean circulation. This temporal correspondence suggests that such environmental changes may have been associated with the diversification and adaptive evolution of Anomura. Overall, this study advances our understanding of anomuran phylogeny and highlights the complex interplay among adaptation to the environment, carcinization, and mitochondrial genome evolution.

Non-coding RNAs (ncRNAs) are RNA molecules that are not translated into proteins. Recent advances in RNA biology have uncovered roles of ncRNAs in physiological processes, including aging. Here, we review how various classes of ncRNAs regulate aging and longevity, by focusing on recent research using the nematode Caenorhabditis elegans, an excellent model for aging research. We also discuss the potential of ncRNAs as diagnostic biomarkers and therapeutic targets for aging and age-related diseases. Because many aging-regulating genes and pathways in C. elegans are evolutionarily conserved, our review will provide important information regarding the functions of ncRNAs in aging and longevity in other species, including mammals.

Oral lichen planus (OLP) is a chronic inflammatory condition characterized by CD8+ T cell-mediated apoptosis of oral epithelial cells. While psychological stress has been implicated in OLP pathogenesis, the underlying mechanisms remain unclear. This study explores the role of epinephrine, a primary stress-related catecholamine, in OLP progression. We found that high concentrations of epinephrine induce cytotoxicity in oral keratinocytes, marked by reduced cell viability and increased DNA damage. High-dose epinephrine also elevates oxidative stress by downregulating antioxidant proteins SOD2 and SESN2. Additionally, it activates the STAT3 signaling pathway through both alpha- and beta-adrenergic receptors. Furthermore, epinephrine increases levels of HMGB1 and extracellular ATP, key damage-associated molecular patterns (DAMPs) that could perpetuate chronic inflammation in OLP. These findings suggest that stress-induced epinephrine may exacerbate OLP by promoting oxidative stress, epithelial damage, and immune activation. Given the increased vascularization in OLP lesions, epinephrine's effects may be amplified in affected tissues. Understanding the link between stress and OLP pathogenesis could provide new therapeutic targets for managing this condition.

Colorectal cancer (CRC) is a challenging disease. Recent studies have gradually emphasized the development of novel immunotherapies rather than traditional treatments. Toll-like receptor (TLR) agonists are critical in innate immune responses to orchestrate anti-tumor efficacies, which are attributed to their aptitude to stimulate antigen-presenting cells (APCs) and thus activate tumor-specific T cells. Although several TLR agonists have been proposed for treating tumors, their therapeutic efficacy remains controversial. Therefore, the current study aimed to develop a novel TLR2 agonist, Amuc_1100 C-terminal (Amuc_C), a purified membrane protein from Akkermansia muciniphila (A. muciniphila), and evaluate its anti-tumor properties. Herein, a murine CRC model, CT26, was employed. Tumor-bearing mice received intertumoral treatment with Amuc_C. The anti-tumor effects were determined by flow cytometry, cytokine enzyme-linked immunosorbent assay (ELISA), and immunofluorescence assays. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was then employed to uncover the potent mechanisms. Amuc_C significantly increased the amounts of tumor-infiltrating lymphocytes and systemic immune cells, especially cytotoxic T cells, M1 macrophages, and type 1 dendritic cells. Furthermore, Amuc_C triggered IL-1β, TNF-α, and IFN-γ productions, significantly decreasing tumor growth, and prolonged overall survival. The immunotherapeutic mechanisms revealed by proteomics data were related to the activation of immune responses, the induction of cell cycle arrest, and the inhibition of cell proliferative signaling pathways. In summary, the current study has demonstrated that administration of Amuc_C improves the APCs and escalates adaptive anti-tumor immunity. With the demand for effective anti-tumor treatments, our results provide a compelling proof-of-concept of a TLR2 agonist for cancer immunotherapy.

Parkinson's disease (PD) is a progressive neurological disorder characterized by the degeneration of midbrain dopaminergic neurons and disabling motor impairments. Heat shock protein family A member 9 (HSPA9) play a crucial role in neuronal homeostasis by regulating the import of various mitochondrial proteins. HSPA9 is down-regulated in neurodegenerative diseases such as Alzheimer's disease and PD, and its loss leads to excessive mitochondrial fragmentation with oxidative stress, which subsequently causes damage to dopaminergic neurons. Moreover, HSPA9 interacts with multiple PD-associated proteins, including Pink1, DJ-1, and α-synuclein, however precise roles of HSPA9 in PD pathophysiology remain unclear. To further explore the contributions of HSPA9 in PD pathogenesis, we developed an HSPA9 knockout mouse. Haploinsufficiency of Hspa9 (Hspa9 ^+/-) was associated with the loss of tyrosine hydroxylase-positive neurons in the striatum and substantia nigra. Furthermore, Hspa9 haploinsufficiency induced excessive mitochondrial fission, enhanced apoptotic signaling, and resulted in diminished motor performance during the rotarod test. Administration of the mitochondrial neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in Hspa9 ^+/- mice further exacerbated the loss of dopaminergic neurons, aggravated motor impairments, and enhanced activation of apoptosis effector caspase-3. These results suggest that down-regulation of HSPA9 may contribute to the development and progression of PD, potentially offering a new therapeutic strategy for PD treatment.

Bisphenol A (BPA) is a widely used xenoestrogen that can disrupt neuroendocrine and immune regulation through multiple hormone receptors. This study investigated BPA-induced long non-coding RNA (lncRNA)-mRNA interactions in the cerebral cortex and hypothalamic-pituitary-thyroid (HPT) axis of adult male mice. Transcriptome sequencing and comprehensive lncRNA annotation identified 14,858 novel lncRNA transcripts. Integrated network analysis using weighted gene co-expression network analysis (WGCNA) revealed four distinct tissue-specific modules: neuronal signaling alterations (Tac1, Htr1b, Npy), RNA splicing modifications (Srsf5), PI3K/Akt-mediated cellular dysfunction (Creb5, Cdkn1a), and immune receptor signaling disruptions (Trbv15, Fcrla). These findings suggest that BPA reprograms transcriptional networks in a tissue-specific manner, potentially disrupting hormone-related neurotransmission, metabolic regulation, and immune signaling via lncRNA-mediated mechanisms. Such systems-level reprogramming of the immune-neuroendocrine network (INEN) provides novel mechanistic insights and biomarker candidates for assessing and mitigating the health impacts of environmental endocrine disruptors.