EXPERIMENTAL CELL RESEARCH实验细胞研究
EXPERIMENTAL CELL RESEARCH(英文缩写 EXP CELL RES),ISSN 0014-4827,eISSN 1090-2422,中文译名:实验细胞研究 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 4.145 | Q3 |
| 2022 | 3.700 | Q2 |
| 2023 | 3.300 | Q2 |
| 2024 | 3.500 | Q2 |
| 2025 | 3.500 | Q2 |
EXPERIMENTAL CELL RESEARCH 最新收录文献
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1. Elevated asymmetric dimethylarginine drives hematopoietic stem cell metabolic reprogramming and dysfunction in chronic kidney disease.
1. 升高的不对称二甲基精氨酸驱动慢性肾脏病中造血干细胞代谢重编程及功能障碍PMID:日期:2026-10-02Chronic kidney disease (CKD) is commonly linked to hematopoietic abnormalities beyond the well-recognized anemia, with underlying mechanisms poorly understood. Here, we show that asymmetric dimethylarginine (ADMA), which accumulates in the CKD microenvironment, perturbs hematopoietic stem cell (HSC) homeostasis. Clinical data analysis reveals that serum ADMA levels rise with CKD progression and inversely correlate with the myeloid-to-lymphoid ratio. Notably, ADMA compromises HSC quiescence and long-term repopulating capacity, as observed in CKD mouse models established by 5/6 nephrectomy. Further investigations demonstrate that ADMA hyperactivates mammalian target of rapamycin (mTOR) signaling, promoting the transition from glycolysis to oxidative phosphorylation and inducing reactive oxygen species (ROS) overproduction in HSCs. Mechanistically, ADMA binds with high affinity to protein phosphatase 2 regulatory subunit Bβ (PPP2R2B), relieving its inhibition of mTOR signaling. Inhibition of mTOR signaling by rapamycin or clearance of ROS by NAC reverses ADMA-induced HSC functional defects. Collectively, our findings identify ADMA as a key mediator of CKD-associated hematopoietic dysfunction via the PPP2R2B-mTOR-mitochondria axis, providing a potential therapeutic target.
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2. Hydrostatic Compressive Stress Promotes MC3T3-E1 Cell Proliferation Through ROCK-Dependent Regulation of Cyclin D1 and CDK4.
PMID:日期:2026-10-01Mechanical stimulation plays a pivotal role in bone remodeling by increasing interstitial hydrostatic pressure and generating compressive stress within the bone microenvironment. However, the effects of different loading conditions on osteoblast responses and the underlying mechanotransduction mechanisms remain incompletely understood. In the present study, we utilized the MechanoCulture TR hydrostatic stimulation system to evaluate the effects of different hydrostatic compressive stress magnitudes and loading durations on MC3T3-E1 cells and elucidate the role of the ROCK signaling pathway in stress-induced proliferation. Among the conditions tested at a fixed frequency of 0.05 Hz, hydrostatic compressive stress at 5 kPa for 45 min elicited the strongest proliferative response and was accompanied by F-actin reorganization. Furthermore, compressive loading significantly upregulated the expression of ROCK, Cyclin D1, and CDK4. Conversely, inhibition of ROCK with Y-27632 reduced ROCK activity, altered F-actin organization, suppressed cell proliferation, and attenuated compression-induced upregulation of Cyclin D1 and CDK4. In conclusion, hydrostatic compressive stress promotes MC3T3-E1 cell proliferation through ROCK-dependent regulation of Cyclin D1 and CDK4. These findings support an important role for ROCK in the proliferative response of osteoblasts to hydrostatic compressive stress.
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3. mRNA-engineered stem cells produce nerve growth factor and induce neurite outgrowth in recipient cells.
PMID:日期:2026-09-28Innervation is essential for tissue healing, yet strategies to enhance nerve growth during repair remain limited. Here, we show that chemically modified messenger RNA (cmRNA) encoding nerve growth factor (NGF) can stimulate neurogenic responses in vitro. NGF cmRNA was delivered to human bone marrow-derived mesenchymal stem cells using lipid carriers, leading to efficient NGF production. In co-culture, NGF-secreting stem cells induced differentiation of neural crest-derived PC-12 cells, as evidenced by increased neurite outgrowth and branching. Proteomic analyses revealed activation of neurogenesis-related pathways in both cell types. Notably, NGF cmRNA-transfected stem cells produced lower NGF levels than recombinant protein yet achieved comparable neurite-outgrowth response, demonstrating the efficiency of the transcript-based approach. These findings demonstrate that NGF cmRNA can induce NGF production by hMSCs and promote neurite outgrowth in NGF-responsive PC12 cells in vitro. This approach may provide the neurotrophic component of future regenerative strategies combining NGF cmRNA with osteogenic signals; however, its effects on functional tissue innervation and bone healing remain to be established in vivo.
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4. Phosphorylation destabilizes Per3 to promote gallbladder carcinoma.
PMID:日期:2026-09-23Irregular circadian rhythm drives tumor malignant progression by governing a range of cellular processes, but its roles in gallbladder carcinoma (GBC) remain unclear. As a potential tumor suppressor gene, Per3 was down-regulated in GBC with a poor prognosis. Overexpression of Per3 inhibited GBC growth and metastasis in vitro and in vivo. Mechanistically, Per3 combined with P4HA1 to promote degradation of HIF-1α protein, consequently, HIF-1α-targeted genes were transcriptionally down-regulated to inhibit glycolytic capacity. Meanwhile, the key inducers of epithelial-mesenchymal transition (EMT), TGFB1 and TGFBI were transcriptionally repressed by Per3 combining at the promoters, subsequently reducing the mRNA levels of EMT-related genes and blocking EMT progression. The decrease of Per3 was determined at protein post-translational modification (PTM), not at transcription. Mass spectrometry identified that CKII, not CKI or other kinases, phosphorylated Per3 at S1048, which promoted ubiquitination-dependent degradation of Per3, leading to loss of its tumor-suppressive function. Collectively, these results reveal the mechanisms of Per3 S1048 phosphorylation-driven degradation and the roles of Per3 in regulating HIF-1α/glycolysis and TGF-β/EMT in gallbladder carcinoma.
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5. The role of Broad in regulating border cell migration during Drosophila oogenesis.
PMID:日期:2026-09-23Drosophila development is a highly regulated process governed by the precise timing and spatial cues of hormones and signaling pathways. The follicular epithelium of the Drosophila egg chamber has been a well-studied model system for identifying key molecular regulators of morphological changes and cell migration. Broad (Br), a zinc finger transcription factor, is a well-known early response gene of the steroid hormone ecdysone, which is essential for the initiation of metamorphosis. Our previous findings have shown that Br is a target of Notch signaling, and its suppression is required for proper epithelial cell cuboidal-to-squamous transition during Drosophila oogenesis. Here, we report that proper border cell (BC) migration requires the suppression of Br expression during Drosophila oogenesis. Br expression can be induced by Notch signaling as early as stage 4, but its expression decreases in BCs during cell migration at stage 9. Further findings revealed that JAK/STAT and ecdysone signaling are highly active during the onset of BC migration and contribute to Br suppression. We demonstrated that JAK/STAT suppresses Br expression to facilitate proper BC migration. In addition, we analyzed single-cell RNA sequencing data to highlight the shift in gene expression while Br was suppressed and BCs became mobile. The analysis confirmed the high expression of known BC markers, including slbo and sn, and identified br as specifically repressed in BCs, supporting the quality of the dataset and our experimental findings. Gene Ontology enrichment analysis revealed significant overrepresentation of biological processes related to cell migration, morphogenesis, and cell junction assembly, all of which are important for BC morphological transition and migration.
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6. H3K18 histone lactylation mediates hypoxia-induced FBXW11 upregulation and supports proliferative and self-renewal-associated properties of hair follicle stem cells.
PMID:日期:2026-09-23Hair follicle stem cells (HFSCs) reside in a relatively hypoxic niche and preferentially use glycolytic metabolism, but how metabolic adaptation is coupled to epigenetic regulation of HFSC function remains incompletely understood. Since oxidative phosphorylation produces more reactive oxygen species (ROS) than glycolysis, and excessive ROS production eliminates various stem cell properties including quiescence and self-renewal. Stem cells prefer glycolysis as their main energy source. Here, cultured human HFSCs were exposed to 2%O. Hypoxia increased HIF-1α expression, glycolysis-related gene expression, intracellular H3K18 histone lactylation (H3K18la), EdU incorporation, colony-forming efficiency, and HFSC-associated markers CK15, CK19, and CD34 expression. Separate treatment with the glycolysis inhibitors 2-deoxy-D-glucose (2-DG) or oxamate reduced lactate accumulation, H3K18la, and HFSC-associated marker expression. Integrated H3K18la CUT&Tag and RNA sequencing identified 822 genes with concordantly increased H3K18la peaks and mRNA levels, with ubiquitin-mediated proteolysis among the enriched pathways. FBXW11 was prioritized as a candidate E3 ubiquitin ligase target. IGV visualization and H3K18la ChIP-qPCR showed increased H3K18la enrichment at the FBXW11 locus under hypoxia, whereas 2-DG or the p300 inhibitor C646 attenuated H3K18la enrichment and FBXW11 expression. FBXW11 overexpression increased EdU incorporation, colony formation, and HFSC-associated marker expression, while FBXW11 knockdown attenuated hypoxia-induced clonogenic growth and proliferation. In an ex vivo whole-hair-follicle culture model, hypoxia enhanced hair shaft elongation, and this effect was reduced by FBXW11 knockdown. Together, these findings support a hypoxia-glycolysis/lactate-H3K18la-FBXW11 pathway that contributes to proliferative and self-renewal-associated phenotypes of cultured HFSCs and to hypoxia-responsive hair shaft growth ex vivo. Further in vivo studies are required to establish its role in physiological hair cycle.
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7. Matrine induces aggressive prostate cancer cell death via inhibition of PPARα activity: insights from transcriptomics, molecular docking, and functional studies.
PMID:日期:2026-09-22Prostate cancer remains a significant global health burden with limited treatment options for advanced stages. Matrine, a natural alkaloid from Sophora flavescens, has demonstrated anti-cancer potential. This study aimed to investigate its efficacy against aggressive prostate cancer cell death and elucidate the underlying molecular mechanism. The anti-proliferative effects of matrine were assessed in multiple prostate cancer cell lines (LNCaP, C4-2, PC3, Du145) using CCK-8, EdU, and colony formation assays. A subcutaneous xenograft model using PC3 cells in nude mice evaluated in vivo efficacy. Transcriptomic sequencing of matrine-treated PC3 cells identified altered pathways. Molecular docking analyzed the interaction between matrine and peroxisome proliferator-activated receptor α (PPARα). PPAR activity was measured via luciferase reporter assays, and subcellular localization was examined by immunofluorescence. Data were analyzed using Student's t-test or Mann-Whitney U test. Matrine dose-dependently inhibited cell viability, proliferation, and colony formation, with enhanced effects on aggressive, androgen-independent PC3 and Du145 cells. In vivo, matrine (100 mg/kg) suppressed tumor growth without significant toxicity. Transcriptomics revealed significant downregulation of lipid metabolism pathways, particularly the PPAR signaling pathway. Functional studies showed matrine suppressed general PPAR activity. Subsequent experiments identified PPARα as the primary target: matrine exhibited high binding affinity to PPARα in silico, inhibited its nuclear translocation and transcriptional activity, and its anti-proliferative effects were effectively reversed by a PPARα-specific agonist. This study demonstrates that matrine effectively suppresses aggressive prostate cancer cell death both in vitro and in vivo. The mechanism involves the inhibition of PPARα activity, leading to the disruption of associated lipid metabolism pathways. These findings highlight matrine as a natural PPARα inhibitor and provide a novel therapeutic rationale for targeting PPARα in prostate cancer treatment.
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8. Pyroptosis-Related Pathways and Their Impact on Immune Microenvironment Remodeling in Pediatric Ovarian and Adnexal Tumors.
PMID:日期:2026-09-21Pyroptosis is a gasdermin-mediated form of inflammatory cell death that may alter tumour-immune interactions. Its canonical, non-canonical and granzyme-associated pathways, together with NINJ1-dependent terminal membrane rupture, are reviewed here. Whether these mechanisms promote antitumour immunity or sustained inflammation depends on biological context. Pediatric ovarian and adnexal neoplasms include germ-cell tumours (GCTs), sex cord-stromal tumours (SCSTs), and less-common epithelial or other lesions. Histology, age, pubertal status, hormonal secretion, stage, and treatment exposure vary substantially across patients. Direct studies of pyroptosis and immune remodelling in these paediatric histologies remain scarce; evidence from adult epithelial ovarian cancer, non-ovarian tumours, cell lines, and mice cannot be treated as proof of a paediatric mechanism. This review retains a histology-specific framework to examine molecular pathways, the paediatric ovarian tumour immune microenvironment (TIME), candidate therapeutic approaches, and biomarkers. Established molecular or clinical observations are separated from cross-tumour extrapolations and untested hypotheses. Particular attention is paid to developmental immunity, endocrine context, on-target and off-target inflammation, and evidence required before clinical translation.
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9. A nucleus-associated miR-661-C/EBPα-PPARγ regulatory axis skews BMSC lineage commitment in SONFH.
9. 核相关miR-661-C/EBPα-PPARγ调控轴在股骨头坏死中改变骨髓间充质干细胞谱系定向分化PMID:日期:2026-09-18Steroid-induced osteonecrosis of the femoral head (SONFH) is characterized by marrow adiposity, trabecular deterioration, and impaired bone repair, but the progenitor-level regulatory mechanisms underlying this process remain incompletely defined. Here, we investigated whether dysregulated bone marrow stromal cell (BMSC) lineage commitment contributes to SONFH progression and identified a nucleus-associated miRNA mechanism that promotes adipogenic skew. Human femoral heads from patients with femoral neck fracture or SONFH showed increased empty osteocytic lacunae, trabecular rarefaction, and Perilipin-1-positive marrow adiposity. Patient-derived SONFH BMSCs displayed enhanced adipogenic potential and impaired osteogenic differentiation, accompanied by increased C/EBPα/PPARγ and reduced RUNX2/OCN expression. Cross-source miRNA prioritization and validation identified miR-661 as an upregulated candidate associated with this lineage imbalance. miR-661 overexpression promoted lipid accumulation, suppressed mineral deposition, and activated a pro-adipogenic transcriptional program. Mechanistically, miR-661 showed nuclear enrichment and did not induce a detectable change in β-catenin expression or nuclear localization, directing our focus to the C/EBPα-PPARγ axis. ChIP-qPCR, promoter DNA pull-down, dual-luciferase reporter assays, and C/EBPα RIP-qPCR showed that miR-661 was associated with increased C/EBPα occupancy at the PPARG promoter. Importantly, C/EBPα knockdown attenuated miR-661-induced PPARG, FABP4, and adipogenic activation, whereas C/EBPα rescue restored these effects. Nuclear AGO2-RIP-qPCR further demonstrated enrichment of miR-661 in nuclear AGO2-containing complexes, and AGO2 ChIP-qPCR showed miR-661-dependent AGO2 occupancy at the PPARG promoter, which was reduced by miR-661 inhibition and lost with a seed-mutant miR-661 mimic. In vivo, local antagomiR-661 delivery alleviated steroid-induced osteonecrosis-like bone loss and marrow adiposity. These findings identify miR-661 as a nuclear, AGO2-associated regulator of the C/EBPα-PPARγ axis that drives BMSC adipogenic lineage bias in SONFH.
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10. miR-582-5p promotes hepatic steatosis and inflammation via FAIM/PPARα axis in MASH.
PMID:日期:2026-09-16该文献暂无摘要。