Search Results (3,154)

Salinity is a critical environmental stressor that inhibits seed germination and seedling growth globally. This study aimed to determine the optimal priming conditions for hot pepper (Capsicum annuum L.) seeds to alleviate salt stress-induced germination and growth reductions. Priming treatments included hydro-priming, chemical-priming (24-epibrassinolide (EBL), sodium nitroprusside (SNP), and polyamines), halo-priming (KNO₃), and modified drum-priming. Following treatment, germination characteristics, total polyphenol content (TPC), ABTS⁺ radical scavenging activity, and seedling growth traits were evaluated under 100 mM NaCl stress. Optimal conditions were identified as hydro-priming (50 h), chemical-priming (10⁻⁶ M EBL, 10⁻⁴ M SNP, 50 mM putrescine), halo-priming (300 mM KNO₃), and drum-priming (20 h hydration and 60 h incubation). Although NaCl treatment significantly reduced all germination traits, priming effectively mitigated these declines. A modified drum-priming method resulted in the shortest mean germination time (MGT) of 4.0 days, the highest germination rate (GR) of 25.2%·day⁻¹, and a 94% healthy seedling percentage (HSP), whereas the results for the untreated control were recorded as 6.6 days, 15.2%·day⁻¹, and 66%, respectively, under stress conditions. EBL and drum-priming showed the highest TPC and ABTS⁺ radical scavenging activity. Furthermore, priming prevented salt-induced reductions in seedling growth. EBL and drum-priming treatments resulted in the highest vitality index (VI). These results indicate that drum-priming and EBL priming are highly effective strategies for enhancing salt tolerance and ensuring uniform stand establishment in pepper seeds. Full article

Pulmonary arterial hypertension (PAH) is a severe and progressive cardiopulmonary disorder with limited treatment options. Camellia petelotii (Merr.) Sealy (CP) contains multiple flavonoids and other phytochemicals, but its active compounds and molecular mechanisms in PAH remain unclear. Active compounds of CP were screened by comprehensive literature mining and absorption, distribution, metabolism, and excretion (ADME) evaluation. PAH-related hub targets were identified from transcriptomic data using weighted gene co-expression network analysis (WGCNA), machine learning, and external validation. Functional enrichment, immune infiltration, and single-cell RNA-sequencing analyses were performed to characterize their biological roles and cellular localization. Molecular docking and molecular dynamics simulations assessed compound–target interactions. The effects of CP were further evaluated in hypoxia-induced rat pulmonary artery smooth muscle cells (RPASMCs). Five core bioactive compounds were identified, among which luteolin and quercetin were prioritized for further analysis. HSP90AA1 and ROCK2 were screened as hub targets. Bioinformatic analyses suggested that these targets were mainly associated with the “Lipid and atherosclerosis” pathway, metabolic reprogramming, and modulation of the immune microenvironment. Single-cell analysis showed broad expression of HSP90AA1 and enrichment of ROCK2 in fibroblasts and endothelial cells. Molecular docking and molecular dynamics simulations supported stable binding of luteolin to HSP90AA1. In vitro, CP extract inhibited hypoxia-induced hyperproliferation of RPASMCs and reduced HSP90AA1 protein expression. HSP90AA1 may represent a candidate molecular mediator of CP in PAH, and CP inhibited hypoxia-induced RPASMC proliferation in association with downregulation of HSP90AA1. Full article

Proteostasis, defined as the coordinated regulation of protein synthesis, folding, trafficking, and degradation, is essential for maintaining cellular integrity and supporting normal development. During reproduction and early life stages, efficient proteostasis is crucial for gamete quality, successful fertilization, embryonic development, and neurodevelopmental outcomes. Increasing evidence suggests that impaired proteostasis contributes to infertility and may be intertwined with biological vulnerabilities associated with assisted reproductive technologies [ARTs]. This review provides an integrative perspective on the role of disrupted proteostasis in infertility, ART procedures, and neurodevelopmental differences [NDD]. We review epidemiological and molecular findings indicating proteostasis failure in both male and female infertility, with particular emphasis on molecular chaperones. Among these, heat shock protein 60 [Hsp60] is discussed as a central mediator linking mitochondrial function, protein quality control, and reproductive competence. We further highlight that ART procedures coincide with sensitive periods of epigenetic reprogramming and proteostasis regulation during early embryogenesis, indicating that disturbances in proteostasis may affect epigenetic stability and subsequent neurodevelopmental outcomes. In addition, this review emphasizes the importance of proteoforms and proteome complexity as critical determinants of reproductive success and neurodevelopmental robustness in the context of ART. Finally, we discuss the potential of proteomic and chaperone-based biomarkers as emerging tools to optimize ART strategies, improve gamete and embryo selection, and enhance risk assessment and clinical outcomes. The current review underscores proteostasis as a fundamental yet underrecognized mechanism linking reproductive biology, ART outcomes, and long-term neurodevelopment while highlighting future directions for translational investigations. Full article

This study explored the physiological responses and gene expression profiles of the Manila clam (Ruditapes philippinarum) and the hard clam (Mercenaria mercenaria) under heat and hyposaline stress. Experimental conditions involved increasing the temperature from 25 °C to 35 °C and decreasing salinity from 25 ppt to 15 ppt over a 6 h acclimation period, followed by 72 h exposure. Key physiological and immune indicators, including filtration rate, oxygen consumption rate, ammonia excretion rate, and the expression of related genes, were measured. Under heat stress, R. philippinarum exhibited higher filtration, oxygen consumption, and ammonia excretion rates than M. mercenaria at most sampling time points. The expression of fatty acid desaturase (Δ6FAD) and heat shock protein (HSP70) genes increased and then decreased for both species, whereas superoxide dismutase (Cu/Zn SOD) gene expression gradually decreased over time. Furthermore, the expression levels of all three genes were generally significantly higher in M. mercenaria compared to R. philippinarum. Under hyposaline stress, R. philippinarum exhibited significantly higher filtration, oxygen consumption, and ammonia excretion rates than M. mercenaria between 24 h and 72 h. Expression levels of the Na⁺-K⁺-ATPase (NKAα), HSP70, and Cu/Zn SOD genes remained higher in M. mercenaria compared to R. philippinarum. Overall, the present study indicates that M. mercenaria maintains relative stability and R. philippinarum exhibits greater physiological fluctuation under both heat and hyposaline stress. This study highlights bivalve species-specific responses to environmental stressors and provides valuable insights for aquaculture planning and ecological management in different environmental regions, particularly in the context of global climate change. Full article

Background: Information on the autopolyploid of Gossypium herbaceum remains limited until now. Previously, the autotetraploid of G. herbaceum was successfully generated via colchicine-induced chromosome doubling from the diploid cultivar ‘Hongxing’ in our lab. Methods: To investigate the drought stress response mechanism of this tetraploid, the autotetraploid S4 was used as the experimental material. The plants were subjected to drought stress during the flowering stage, followed by measurements of physiological and biochemical indicators and transcriptomic sequencing analysis. Results: Under drought stress, MDA content increased, and cell membranes sustained oxidative damage. Photosynthetic parameters, such as net photosynthetic rate (Pn), were significantly suppressed, while the activity of osmotic regulators and key antioxidant enzymes increased significantly. After rehydration, all of the above physiological indicators showed varying degrees of recovery. Transcriptome analysis revealed that, when comparing the treatment group with the control group, a total of 5530 differentially expressed genes (DEGs) were identified, with 2714 up-regulated and 2816 down-regulated. Furthermore, this study investigated the drought resistance mechanism involving the interaction between the MAPK signaling pathway and other metabolic pathways in the autotetraploid. Nine drought-resistant genes, including MAPK3, bHLH47, GaRbohD, RIBA1, PIP1-3, RCA1, RbohD, CYP707A and HSP70, were selected and analyzed using real-time quantitative PCR; the results were generally consistent with the transcriptomic data. Conclusions: These findings substantially enhance our understanding of the molecular mechanisms underlying drought responses in autotetraploids. This novel autotetraploid genotype expands the available cotton germplasm resources and is expected to hold significant value for research on polyploidy evolution. Full article

This study aimed to investigate the protective effects of fenofibrate against sepsis-induced acute lung injury using a feces-induced peritonitis (FIP) rat model, with particular emphasis on the modulation of HSP70 and Nrf2 as key cellular defense mechanisms. The FIP model was employed to mimic colon-origin abdominal sepsis, frequently encountered in general surgery, including conditions such as colonic perforation and anastomotic leakage. Thirty male Wistar albino rats were randomly assigned to control, FIP, and FIP + fenofibrate groups. Sepsis was induced by intraperitoneal injection of a fecal-saline suspension. Fenofibrate (100 mg/kg) was administered intraperitoneally after the FIP procedure. After 24 h, lung tissues and blood samples were collected. Assessments included histopathology (H&E staining), thoracic CT imaging, arterial blood gas analysis, ELISA-based quantification of plasma cytokines (IL-6, IL-1β, TNF-α), MDA for oxidative stress, and lung tissue levels of HSP70 and Nrf2. Feces-induced peritonitis caused severe acute lung injury, evidenced by increased histopathological damage (p < 0.001), impaired gas exchange (PaO₂ and PaCO₂, p < 0.01), elevated inflammatory cytokines (IL-6, IL-1β, TNF-α; p < 0.001), increased oxidative stress (MDA, p < 0.001), and suppressed lung Nrf2 and HSP70 expression (p < 0.001). Fenofibrate significantly attenuated lung injury, improved gas exchange (p < 0.05), reduced inflammation (p < 0.01–p < 0.001), decreased MDA (p < 0.001), and increased Nrf2 (p < 0.001) and HSP70 (p < 0.01). Fenofibrate attenuates sepsis-induced acute lung injury by reducing inflammation and oxidative stress while preserving HSP-70 and Nrf2-mediated cytoprotective pathways. These findings are clinically relevant to general surgery, as septic lung injury commonly arises from colon-origin abdominal sepsis, including colonic perforation and anastomotic leakage. Full article

Quercetagetin (QG), a principal flavonol from marigold (Tagetes erecta L.), is recognized for its potent antioxidant properties. However, its efficacy in mitigating intestinal injury under heat stress (HS) conditions remains unclear. We investigated the protective effects of QG using a mouse model of HS (41 °C, 70% humidity). Mice received oral QG (100 mg/kg/day) or saline for seven consecutive days before and during HS exposure. We assessed jejunal histopathology, oxidative stress markers, inflammatory cytokines, gene expression, and gut microbiota composition via 16S rRNA sequencing. QG supplementation significantly ameliorated HS-induced jejunal damage. It enhanced the activities of superoxide dismutase (SOD) and catalase (CAT) while reducing malondialdehyde (MDA) and pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). QG downregulated the mRNA expression of heat shock proteins (Hsp70, Hsp90) and upregulated antioxidant-related genes (SOD1, GPX4, CAT, NQO1, Nrf2). Furthermore, QG preserved intestinal barrier integrity by upregulating tight junction proteins (Occludin, Zo-1, Claudin). 16S rRNA analysis revealed that QG significantly reshaped the gut microbiota, marked by an increased relative abundance of Lactobacillus and a decrease in potentially harmful taxa such as Allobaculum, Oscillibacter, and Colidextribacter. QG effectively alleviates HS-induced intestinal injury by enhancing antioxidant capacity, suppressing inflammation, and modulating the gut microbiota. These findings provide a scientific basis for the potential application of QG as a functional feed additive to improve animal health under heat stress conditions. Full article

Parkinson’s disease (PD) is a common neurodegenerative disorder marked by progressive loss of dopaminergic neurons in the substantia nigra pars compacta and the accumulation of Lewy bodies, intracellular inclusions enriched in α-synuclein. Synphilin-1 interacts with α-synuclein, localizes to Lewy bodies, and has been implicated in inclusion formation and neuroprotection in cellular and animal models; however, its physiological function in vivo remains poorly defined. Here, we generated and characterized a synphilin-1 knockout (Sph-1 KO) mouse by targeted genetic deletion of the Sph-1 locus and performed a comprehensive phenotyping battery including behavioral testing as well as biochemical, histological, structural, and ultrastructural analyses. Sph-1 KO mice survived to nearly two years of age and showed normal body weight, lifespan, motor performance, learning and memory, anxiety-like behavior, attention, and gross brain morphology. Western blot analyses indicated that levels of α-synuclein and synaptic proteins were largely unchanged. While outer mitochondrial membrane proteins were unaffected, the mitochondrial matrix protein HSP60 was reduced, consistent with altered mitochondrial proteostasis in the absence of synphilin-1. Strikingly, histochemical analyses, magnetic resonance imaging, and electron microscopy revealed early-onset hydrocephalus in Sph-1 KO mice associated with severe loss and disorganization of motile ependymal cilia in the ventricular lining, a cell type that normally expresses high levels of synphilin-1. Ultrastructural and immunohistochemical analyses revealed disrupted ependymal architecture, mislocalization of acetylated α-tubulin to the cytoplasm, cellular swelling, and enlarged, aberrant mitochondria, whereas cortical neurons appeared largely structurally unaffected. Together, these findings identify synphilin-1 as a key regulator of microtubule organization and cytoskeletal/organelle homeostasis in ependymal cells, required to maintain motile ciliogenesis, cerebrospinal fluid flow, and ventricular integrity. This unexpected role for synphilin-1 in ciliated brain epithelia, along with a reduction in the critical mitochondrial chaperone HSP60, broadens our understanding of synphilin-1 biology and provides a new framework for its potential relevance to PD-associated pathology. Full article

Bactrocera dorsalis (Hendel) is a major fruit-feeding pest that poses a severe and persistent threat to the horticulture industry in tropical and subtropical regions. Methyl eugenol (ME) is a powerful male-specific attractant phytochemical and pheromone precursor that has been widely exploited in lure-and-kill pest management programs. Upon ingestion, ME is metabolized (E)-coniferyl alcohol (E-CF) and 2-allyl-4,5-dimethoxyphenol (DMP), which are stored in the male rectal glands and released during courtship to attract females. Despite its ecological significance, the fundamental molecular mechanism underlying ME perception remains poorly understood. Here, we performed a comparative transcriptomic analysis of ME-responsive and ME-non-responsive male B. dorsalis across four tissues (head, gut, midleg, and wing). A total of 15,727 genes were annotated, of which 970 were associated with odorant-binding proteins (OBPs), odorant receptors (ORs), gustatory receptors (GRs), ionotropic receptors (IRs), and chemosensory proteins (CSPs), as well as detoxification families comprising cytochrome P450s (CYPs), carboxylesterases (CaEs), glutathione S-transferases (GSTs), and uridine diphosphate (UDP)-glycosyltransferases (UGTs), and the stress-related heat shock proteins (HSPs) genes. Differential expression analysis identified 7222, 7763, and 6105 differentially expressed genes (DEGs) in the head, gut, and wings/midlegs, respectively, between ME-responsive and ME-non-responsive males. Notably, CYPs, UGTs, and HSPs involved in detoxification and stress response were significantly downregulated. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed that CYPs were significantly enriched in metabolic detoxification pathways. These findings reveal a complex molecular interplay between olfaction and detoxification and suggest that ME induces coordinated genetic pathways supporting survival, reproduction, and environmental adaptability. This knowledge provides a foundation for the development of eco-friendly pest management strategies targeting these molecular mechanisms. Full article

Photoaging is an extrinsic skin aging process caused by chronic ultraviolet (UV) radiation. A core pathological feature of photoaging is excessive oxidative stress, which can further induce ferroptosis. The HSP70 family plays a critical role in this stress response by protecting the key antioxidant enzyme GPX4. In this study, we established UV-induced photoaging models in cultured cells and 3D skin organoids. UPLC-MS/MS analysis of Chenpi transdermal permeate (prepared by in vitro transdermal penetration of Chenpi extract through mouse skin) identified hesperidin as the primary bioactive compound of Chenpi (dried peel of the plant Citrus reticulata Blanco after the aging process). The efficacy of hesperidin was validated in human keratinocytes (HaCaTs), fibroblasts (HSFs), and skin organoids. Mechanistically, transcriptomic and metabolomics analysis indicated that ferroptosis is a key pathway through which hesperidin ameliorates photoaging. Limited proteolysis mass spectrometry (LiP-MS), transcriptomics, and molecular dynamics simulation results demonstrated that hesperidin directly binds to the molecular chaperone HSPA1L. By upregulating HSPA1L expression, hesperidin enhanced the stability of GPX4 and suppressed UV-triggered ferroptosis. Our findings identify the HSPA1L/GPX4 axis as a critical redox regulatory pathway targeted by hesperidin, providing a mechanistic foundation for anti-photoaging therapies. Full article

Background: Chronic kidney disease (CKD) associated vascular calcification (VC) is a leading cause of cardiovascular mortality, partially driven by osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs). Chaperone-mediated autophagy (CMA) is a selective lysosomal degradation cellular process. However, the precise role and mechanism of CMA in CKD-associated vascular calcification remain unknown. Methods: We studied calcified arteries from CKD patients and rats fed on a high-phosphate diet using histological and ultrastructural methods. VSMCs' calcification was induced by a calcification medium containing high phosphate and calcium. CMA activity was measured by a KFERQ reporter and lysosomal staining. The expression of LAMP2a and HSP90AA1 was knocked down by siRNA, overexpressed by plasmid, and activated by QX77.1. Bioinformatic analysis, protein interaction studies, immunofluorescence and co-immunoprecipitation were performed to investigate the potential mechanism of CMA in VC. Results: The expression of LAMP2a was increased in human calcified radial artery tissues (n = 3, p < 0.05) and rats' calcified aortic tissues (n = 3, p < 0.01), accompanied by lysosomal abnormalities. The activity of CMA was increased during the osteogenic transdifferentiation of VSMCs, as indicated by increased expression of RUNX2 and reduced expression of SM22α (p < 0.05). LAMP2a knockdown attenuated VSMCs’ calcification (p < 0.05), whereas pharmacological activation of CMA aggravated calcification in VSMCs (p < 0.01). Bioinformatic screening identified HSP90AA1 as a candidate involved in CMA in vascular calcification. Elevated HSP90AA1 expression was observed in human calcified radial artery tissues (n = 3, p < 0.01) and rat calcified aortic tissues (n = 3, p < 0.01), which promoted osteogenic transdifferentiation of VSMCs (p < 0.05). HSP90AA1 interacted with LAMP2a and positively regulated its expression (p < 0.01). Conclusions: These findings support an association between CMA activation and CKD vascular calcification. It suggests that HSP90AA1 facilitates vascular calcification in chronic kidney disease involving chaperone-mediated autophagy. Full article

The expansion of fifth-generation (5G) wireless networks has increased environmental exposure to mid-band and millimeter-wave radiofrequency electromagnetic fields (RF-EMF), but their molecular effects on male reproductive tissues remain insufficiently understood. This study evaluated whether repeated exposure to 3.5 GHz and 24 GHz RF-EMF alters testicular stress-associated molecular responses by integrating electromagnetic dosimetry with an in vivo rat model. Whole-body specific absorption rate (SAR) and 10 g peak SAR were estimated using a rat voxel model and scaled to the 20 cm antenna-to-cage geometry used during exposure. Thirty-six adult male Sprague Dawley rats were allocated to sham, 3.5 GHz, or 24 GHz groups and exposed for 1 h/day or 7 h/day over 60 days. Testes were examined histologically and assessed for HSP27, HSP70, and HSP90 protein expression. SAR values were low overall, although absorption was higher at 3.5 GHz than at 24 GHz. Histological evaluation showed preserved seminiferous tubule architecture without consistent structural injury. In contrast, molecular analysis demonstrated frequency- and duration-dependent modulation of heat shock proteins, including early HSP70 downregulation at both frequencies, followed by HSP90 upregulation at 3.5 GHz and HSP27 upregulation at 24 GHz. These findings indicate that low-level 5G-relevant RF-EMF exposure can modify molecular stress responses in testicular tissue even in the absence of overt histological damage. Full article

Larix olgensis, a keystone timber species in Northeast China, is increasingly threatened by Neofusicoccum laricinum-induced shoot blight, a devastating disease that compromises forest health and necessitates sustainable management strategies. Here, we demonstrate that the endophytic bacterium Bacillus amyloliquefaciens JL54 elicits multifaceted defense responses in L. olgensis, enhancing resistance to pathogen infection. Greenhouse assays revealed that JL54 pretreatment reduced disease incidence by 12.5% and achieved 43.75% control efficacy while maintaining host vigor. Histochemical analyses identified JL54-induced rapid hydrogen peroxide (H₂O₂) accumulation, extensive lignin deposition, and localized programmed cell death (PCD), indicative of a primed immune response. Transcriptomic analyses uncovered distinct temporal defense patterns: early-stage responses (0 h post-inoculation) were characterized by upregulation of cutin, suberin, and wax biosynthesis pathways, reinforcing physical barriers, whereas late-stage responses (12 h post-inoculation) were dominated by ribosome- and proteostasis-related pathways (e.g., heat shock proteins [HSPs], glutathione S-transferases [GSTs]) to mitigate cellular damage. Biochemical assays corroborated these findings, with JL54 colonization reducing membrane lipid peroxidation (27.2% decrease in malondialdehyde content) and significantly elevating the activity of key defense enzymes, including peroxidase (POD), phenylalanine ammonia-lyase (PAL), and GST. Phytohormone profiling implicated jasmonic acid (JA) as the central mediator of induced systemic resistance (ISR), with JL54-potentiated JA signaling preceding pathogen containment. Collectively, these results demonstrate that JL54 contributes to a coordinated defense strategy in L. olgensis, integrating structural reinforcement (cuticle/lignin), oxidative stress management, and JA-mediated immune priming. These insights advance the understanding of endophyte-conferred resistance in conifers and highlight JL54’s potential as a biocontrol agent for sustainable forestry. Full article

Heat shock proteins 70 (HSP 70) are molecular chaperonins ubiquitously expressed in both prokaryotes and eukaryotes and are involved in the modulation and exacerbation of the immune response. The present study aimed to assess the immunohistochemical expression of HSP70 and apoptosis markers, such as TUNEL and Caspase-3, in 17 cases of cutaneous lupus erythematosus (CLE) in dogs to determine whether HSP70 expression correlates with cell apoptosis and to highlight possible involvement of HSP70 in the pathogenesis of CLE. The results revealed positive HSP70 expression in epidermal and inflammatory cells across all cases, with a significant correlation between HSP70 expression score and TUNEL-positive cells but not with Caspase-3-positive cells. This correlation could indicate a possible role for HSP70 in cell death via a caspase-independent apoptotic mechanism or other programmed cell death mechanisms, such as pyroptosis or necroptosis. The precise mechanisms by which HSP70 acts in this specific pathological context remain incompletely understood, but the results of this study provide important information for future investigations into autoimmune skin disease in dogs. Full article

An algorithm called Dicke state quantum search for the hitting set problem (DSQS-HSP), generates quantum circuits to solve the k-hitting set problem (k-HSP), by initializing the working qubits in an n-qubit Dicke state $\left|D_k^n\right.⟩$ of exactly k qubits in $\left|1\right.⟩$. The quantum circuit reduces the search space size from $2^n$ to D = $\left(\begin{array}{c}n\\ k\end{array}\right)$, the number of symmetric superposition states in $\left|D_k^n\right.⟩$. A quantum-flag oracle checks the hitting condition, and a mirror-readout mechanism projects valid solutions to the output register. The circuit yields two outcome types: the all-zero string with probability (D−M)/D and solution strings, each with probability 1/D, where M is the number of solutions. The resource growth of qubits, gates, circuit depth, and circuit execution repetitions is O($n^k$), which remains polynomial in the best case for min(k, n − k) ≪ n/2. Experimental results using IBM Qiskit Aer Simulator confirm that the DSQS-HSP can produce quantum circuits to successfully solve the k-HSP. Full article