IF 5.2 2区生物学

Cells Pub Date : 2026-04-19 DOI: 10.3390/cells15080724

Sybil C L Hrstka, Maya Jahnke, Kylie Meng-Lin, Sarah Lindorfer, Henry Noma, Ronald F Hrstka, Nathan P Staff

{"title":"Human iPSC-Derived Dorsal Root Ganglion Organoid Modeling of Chemotherapy-Induced Peripheral Neuropathy.","authors":"Sybil C L Hrstka, Maya Jahnke, Kylie Meng-Lin, Sarah Lindorfer, Henry Noma, Ronald F Hrstka, Nathan P Staff","doi":"10.3390/cells15080724","DOIUrl":"https://doi.org/10.3390/cells15080724","url":null,"abstract":"Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting toxicity affecting 30-40% of patients treated with neurotoxic chemotherapy. Sensory symptoms arise from injury to dorsal root ganglion (DRG) neurons and their axons; yet, the underlying mechanisms remain incompletely understood. While human induced pluripotent stem cell (iPSC)-derived sensory neuron (iSN) monolayers have provided mechanistic insight, they lack the three-dimensional architecture and cellular heterogeneity of native DRG tissue. Here, we generated human iPSC-derived DRG organoids (iDRGOs) containing mixed neuronal and peripheral glial populations and established a quantitative neurite outgrowth assay to model chemotherapy-induced neurotoxicity in a 3D context. iDRGOs from three healthy donors were exposed to bortezomib, vincristine, or paclitaxel. All three drugs caused dose-dependent neurite outgrowth impairment without significant short-term changes in organoid size, consistent with early axonal injury. Vincristine reduced MAP2 levels when normalized to total protein, whereas bortezomib and paclitaxel showed divergent microtubule-associated responses compared to monolayer cultures. The developmental stage significantly influenced the baseline neurite outgrowth, highlighting the need for age standardization. These results establish iDRGOs as a physiologically relevant human platform that complements monolayer models for mechanistic studies and therapeutic screening in CIPN.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 8","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Microphthalmia/Transcription Factor E (MiT/TFE) Pathways in Pulmonary Diseases: Current Evidence and Emerging Mechanisms. 肺疾病中的小眼/转录因子E （MiT/TFE）通路：目前的证据和新出现的机制

IF 5.2 2区生物学

Cells Pub Date : 2026-04-18 DOI: 10.3390/cells15080719

Priyanka Singh, Evans Kwabena Abor, Wei Shi

{"title":"Microphthalmia/Transcription Factor E (MiT/TFE) Pathways in Pulmonary Diseases: Current Evidence and Emerging Mechanisms.","authors":"Priyanka Singh, Evans Kwabena Abor, Wei Shi","doi":"10.3390/cells15080719","DOIUrl":"https://doi.org/10.3390/cells15080719","url":null,"abstract":"The MiT/TFE family transcription factors play a critical role in lysosomal biogenesis, autophagy, mitochondrial turnover and lipid catabolism by regulating the Coordinated Lysosomal Expression and Regulation (CLEAR)gene network. The dysregulation of MiT/TFE activity has been implicated in the onset and progression of cancer and neurodegeneration, but its functions in association with pulmonary diseases remain poorly understood. In this review, we systematically summarize the findings from human pulmonary diseases and associated genetic disorders, such as asthma, cancer, Birt-Hogg-Dube (BHD) syndrome, and lung injury models that implicate MiT/TFE dysregulation in pathogenic progression. We also discussed MiT/TFE regulation and signaling through pathways involving mTORC1, AMPK, and lysosomal stress in different cellular contexts. Finally, we discussed significant mechanistic gaps, such as the absence of in vivo models targeting the combined activity of TFEB and TFE3 in disease progression and prevention. In conclusion, these insights seek to offer a comprehensive framework for understanding MiT/TFE signaling in human lung diseases and could present a promising opportunity for directing future mechanistic and translational research.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 8","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115231/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epigenetics as Biomarkers of Cumulative Physical Performance in Community-Dwelling Adults: A Cross-Sectional Feasibility Study. 表观遗传学作为社区居住成人累积体能表现的生物标志物：一项横断面可行性研究。

IF 5.2 2区生物学

Cells Pub Date : 2026-04-18 DOI: 10.3390/cells15080718

Maayan Insler, Maxim Shapiro, Vered Hermush, Naama M Kopelman, Gil Atzmon, Shmuel Springer

{"title":"Epigenetics as Biomarkers of Cumulative Physical Performance in Community-Dwelling Adults: A Cross-Sectional Feasibility Study.","authors":"Maayan Insler, Maxim Shapiro, Vered Hermush, Naama M Kopelman, Gil Atzmon, Shmuel Springer","doi":"10.3390/cells15080718","DOIUrl":"https://doi.org/10.3390/cells15080718","url":null,"abstract":"With global life expectancy steadily rising, promoting healthy aging is becoming a critical objective of public health. Physical function tends to decline gradually, often beginning in midlife, when subtle changes start to occur and accumulate undetected until later years. This study examines the feasibility of using DNA methylation-based epigenetic clocks as biomarkers for cumulative physical performance in 24 community-dwelling adults aged 39 years and older. Our findings reveal that several epigenetic age estimators, particularly DNAmAgeHannum, are significantly associated with a novel composite score criterion derived from standardized motor function assessments (DNAmAge: ρ = -0.48, p < 0.026; DNAmPhenoAge: ρ = -0.48, p < 0.026) with DNAmAgeHannum (ρ = -0.59, p < 0.005). These findings support the potential of using epigenetic aging markers to detect early physiological decline, even in relatively healthy, midlife populations, offering a promising tool for the early identification of age-related functional deterioration.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 8","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13114901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exosomal microRNAs from Alveolar Macrophages Reveal a Protective Role of the Lung Microbiome Against Oncogenic Signaling During PAH Exposure. 肺泡巨噬细胞外泌体microrna揭示肺微生物组在多环芳烃暴露期间对致癌信号的保护作用

IF 5.2 2区生物学

Cells Pub Date : 2026-04-18 DOI: 10.3390/cells15080715

Harish Chandra, Brijesh Yadav, Damaris Kuhnell, Scott Langevin, Jacek Biesiada, Mario Medvedovic, Jagjit S Yadav

{"title":"Exosomal microRNAs from Alveolar Macrophages Reveal a Protective Role of the Lung Microbiome Against Oncogenic Signaling During PAH Exposure.","authors":"Harish Chandra, Brijesh Yadav, Damaris Kuhnell, Scott Langevin, Jacek Biesiada, Mario Medvedovic, Jagjit S Yadav","doi":"10.3390/cells15080715","DOIUrl":"https://doi.org/10.3390/cells15080715","url":null,"abstract":"Polycyclic aromatic hydrocarbons (PAHs), such as benzo[a]pyrene (B[a]P), are major risk factors for lung cancer and other diseases, acting through the aryl hydrocarbon receptor (AHR). Alveolar macrophages (AMs) help regulate the lung microenvironment by responding to inhaled toxicants and resident microbiota. Although small extracellular vesicles (sEVs, aka exosomes) released by AMs mediate intercellular communication and immune responses, the influence of lung microbiota on sEV biogenesis and the mechanisms underlying sEV dysregulation during PAH exposure remain unknown. Here, we investigated the interplay between AMs, B[a]P, and lung microbiota, focusing on sEV-associated miRNAs (exo-miRNAs). Murine AMs (MH-S) were exposed to varying B[a]P concentrations in the presence or absence of murine lung microbiota with or without an AHR antagonist. sEVs from each condition were characterized and profiled for miRNA. Distinct miRNA signatures emerged: high-dose B[a]P enriched miRNAs linked to cancer progression, whereas lung microbiota alone or with low-dose B[a]P induced tumor-suppressor miRNAs that limit proliferation and metastasis and promote apoptosis, an effect enhanced by AHR antagonism. Lung microbiota appeared to counteract high-dose B[a]P by modulating tumor-suppressive exo-miRNAs. This study demonstrates that lung microbiota-induced exo-miRNAs critically shape AM-derived sEV-miRNA signaling during PAH exposure. The identified exosomal miRNAs could serve as important exposure biomarkers and therapeutic targets for mitigating B[a]P-induced toxicity and cancer development.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 8","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13114357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Extracellular Vesicles Derived from VEGF mRNA-Engineered Mesenchymal Stem Cells Promote Endothelial Cell Survival. 来自VEGF mrna工程的间充质干细胞的细胞外囊泡促进内皮细胞存活。

IF 5.2 2区生物学

Cells Pub Date : 2026-04-18 DOI: 10.3390/cells15080717

Cuiping Zhang, Peng Huang, Matthew Pak, Jennifer A Korchak, Abba C Zubair

{"title":"Extracellular Vesicles Derived from VEGF mRNA-Engineered Mesenchymal Stem Cells Promote Endothelial Cell Survival.","authors":"Cuiping Zhang, Peng Huang, Matthew Pak, Jennifer A Korchak, Abba C Zubair","doi":"10.3390/cells15080717","DOIUrl":"https://doi.org/10.3390/cells15080717","url":null,"abstract":"Extracellular vesicles derived from mesenchymal stem cells (MSC-EVs) exhibit great therapeutic potential in ischemia-associated conditions and diseases such as myocardial infarction, ischemic stroke, and wound healing. Enhancing the therapeutic efficacy of MSC-EVs could advance their clinical application. Diverse cargos (proteins, mRNA, microRNA, etc.) in MSC-EVs contribute to the therapeutic effects in various diseases. Vascular endothelial growth factor (VEGF) is one of the primary driving molecules in promoting angiogenesis and protecting endothelial cells lining blood vessels from apoptosis. In this study, we explored the feasibility of engineering parent MSCs with VEGF mRNA to potentiate therapeutic effects of their derived EVs. We first detected elevated levels of VEGF mRNA and protein in transfected MSCs and demonstrated the bioactivity of secreted VEGF by an angiogenesis assay. Furthermore, EVs derived from VEGF mRNA-engineered MSCs (VEGF-MSC-EVs) contained high levels of VEGF mRNA and protein and showed superior ability to protect human umbilical vein endothelial cells (HUVECs) from apoptosis compared to EVs derived from control MSCs (control MSC-EVs). To our knowledge, this is the first report demonstrating that VEGF-MSC-EVs boost therapeutic efficacy by promoting endothelial cell survival. Our findings offer a novel approach for cell-free therapy in ischemia-associated conditions and diseases.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 8","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of Vitrification on Lipidomics in Porcine Cumulus-Oocyte Complexes After In Vitro Maturation. 玻璃化处理对猪卵丘细胞体外成熟后脂质组学的影响。

IF 5.2 2区生物学

Cells Pub Date : 2026-04-18 DOI: 10.3390/cells15080716

Xinyu Huang, Zhen He, Decai Xiang, Jing Fu, Xuemei Li, Junyu Jiang, Guobo Quan, Guoquan Wu, Baoyu Jia

{"title":"Effect of Vitrification on Lipidomics in Porcine Cumulus-Oocyte Complexes After In Vitro Maturation.","authors":"Xinyu Huang, Zhen He, Decai Xiang, Jing Fu, Xuemei Li, Junyu Jiang, Guobo Quan, Guoquan Wu, Baoyu Jia","doi":"10.3390/cells15080716","DOIUrl":"https://doi.org/10.3390/cells15080716","url":null,"abstract":"Due to its high efficiency and safety, oocyte vitrification finds broad application in many fields of life sciences, such as clinical assisted reproduction and conservation of animal genetic resources. However, vitrification may cause cellular damage and reduce the quality of oocytes and their cumulus cells (CCs), which could be closely related to disorders in lipid metabolism. At present, the impact of vitrification upon the lipid profile of oocytes and CCs has not been systematically elucidated. In this study, we used porcine germinal vesicle cumulus-oocyte complexes (COCs) as a model to analyze their lipid characteristics after vitrification and in vitro maturation (IVM), utilizing untargeted lipid metabolomics. Our results showed that an overall count of 37 down-regulated and 8 up-regulated differential lipids was identified in the vitrified oocytes. Pathway analysis confirmed the enrichment in glycerophospholipid metabolism and fat digestion and absorption, etc. Combined with transcriptomic analysis, three enriched pathways were revealed, including the AMPK signaling pathway, metabolic pathways, and fatty acid elongation. On the other hand, a total of four down-regulated and eight up-regulated differential lipids were detected in the vitrified CCs. Pathway enrichment implicated autophagy, glycerophospholipid metabolism, etc. A joint analysis of metabolomic and transcriptomic data revealed four enrichment pathways, including cholesterol metabolism, fat digestion and absorption, regulation of lipolysis in adipocytes, and metabolic pathways. Notably, the supplementation of lysophosphatidylcholine during IVM attenuated oxidative stress, enhanced mitochondrial activity, and enhanced the viability and embryonic development of cryopreserved porcine oocytes. The results indicate that vitrification alters lipids in oocytes and CCs, and the supplementation of lipids plays a role in improving the quality of vitrified oocytes.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 8","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13114417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Maternal Inflammation Alters Nuclear and Mitochondrial DNA Methylation Patterns in Neonatal Brain Monocytes. 母体炎症改变新生儿脑单核细胞的核和线粒体DNA甲基化模式。

IF 5.2 2区生物学

Cells Pub Date : 2026-04-18 DOI: 10.3390/cells15080714

Andrew T Ebenezer, Jonathan R Hicks, Brooke Hollander, Alexander Hone, Mona Batish, Robert Akins, Adam Marsh, Elizabeth Wright-Jin

{"title":"Maternal Inflammation Alters Nuclear and Mitochondrial DNA Methylation Patterns in Neonatal Brain Monocytes.","authors":"Andrew T Ebenezer, Jonathan R Hicks, Brooke Hollander, Alexander Hone, Mona Batish, Robert Akins, Adam Marsh, Elizabeth Wright-Jin","doi":"10.3390/cells15080714","DOIUrl":"https://doi.org/10.3390/cells15080714","url":null,"abstract":"Neonatal hypoxic ischemic encephalopathy (HIE) is a common birth complication that can cause death or lifelong disabling conditions like cerebral palsy, epilepsy, and autism. It is well established that maternal infection and inflammation are significant risk factors for HIE but reasons for this increase in neurological risk to the offspring remain unknown. Inflammation or infection are associated with epigenetic changes and may contribute to the increased risk of neurodevelopmental disability in exposed offspring. Here, we analyzed and compared DNA methylation patterns in brain monocytes isolated from control, maternal immune activation (MIA), and an inflammation sensitized HIE (IS-HIE) CF-1 mouse model at postnatal day 7. We found that maternal inflammation induced significant methylation differences in neonates relative to control samples in both MIA and IS-HIE samples with no significant differences identified between the MIA and IS-HIE groups. MIA samples showed hypermethylation at loci involving craniofacial development and transcription factors important for regulating neurodevelopment and immune function. MIA samples also demonstrated significant hypermethylation at multiple mitochondrial genome CpGs. These findings suggest that maternal inflammation induces epigenetic alterations in fetal brain immune cells that are detectable in neonates. These changes may contribute to heightened neurodevelopmental risk in offspring following hypoxic injury, highlighting potential molecular pathways for future therapeutic targeting.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 8","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115308/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147762666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cellular, Molecular, and Behavioural Sequelae of Early-Life Continuous Low-Dose-Rate Irradiation in Mice. 小鼠早期连续低剂量率辐射的细胞、分子和行为后遗症。

IF 5.2 2区生物学

Cells Pub Date : 2026-04-17 DOI: 10.3390/cells15080711

Feng Ru Tang, Hong Wang, Salihah Lau, Amanda Tan

{"title":"Cellular, Molecular, and Behavioural Sequelae of Early-Life Continuous Low-Dose-Rate Irradiation in Mice.","authors":"Feng Ru Tang, Hong Wang, Salihah Lau, Amanda Tan","doi":"10.3390/cells15080711","DOIUrl":"https://doi.org/10.3390/cells15080711","url":null,"abstract":"The Fukushima nuclear accident highlighted that evacuation-related psychosocial harm can outweigh direct radiation risks, underscoring the need to define the health impacts of chronic low-dose-rate (LDR) radiation and evidence-based thresholds for intervention. This study investigated the effects of continuous, postnatal LDR gamma irradiation (1.2 mGy/h, cumulative dose: 5 Gy) in male mice. While no changes in body weight, hippocampal neurogenesis, or major glial and neuronal populations were observed, persistent DNA damage (γ-H2AX foci) in dentate gyrus granule cells occurred in both irradiated male and female mice. Irradiated male mice developed anxiety-like behaviour, a phenotype not observed in a previously published study of female mice subjected to an identical irradiation protocol. Molecular profiling revealed two novel, dysregulated miRNA/mRNA axes in the hippocampus linking DNA damage to behaviour: a maladaptive miR-466i-5p/Tfcp2l1 pathway associated with genomic instability, and a potentially adaptive miR-101a-5p/BMP6 pathway promoting neuronal survival. Venn analysis further identified miR-124b-3p and novel-miR489-3p as conserved exposure biomarkers, altered in both the hippocampus and blood of irradiated animals. Our results show that a high cumulative dose of chronic LDR induces markedly less severe hippocampal pathology than has been reported for equivalent acute doses. These findings support the concept of dose-rate-dependent threshold dose and contribute to the evidence base for developing countermeasures following nuclear incidents or other radiation exposures.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 8","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13114697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Small Subset, Big Impact: Regulatory Function of γδ T Cells in Arteriogenesis. 小亚群，大影响：γδ T细胞在动脉发生中的调节功能。

IF 5.2 2区生物学

Cells Pub Date : 2026-04-17 DOI: 10.3390/cells15080709

Kira-Sofie Wimmer, Carolin Baur, Matthias Kübler, Christoph Arnholdt, Konda Kumaraswami, Franziska Heim, Katharina Elbs, Michael Reha Rohrmoser, Daphne Merkus, Elisabeth Deindl

{"title":"Small Subset, Big Impact: Regulatory Function of γδ T Cells in Arteriogenesis.","authors":"Kira-Sofie Wimmer, Carolin Baur, Matthias Kübler, Christoph Arnholdt, Konda Kumaraswami, Franziska Heim, Katharina Elbs, Michael Reha Rohrmoser, Daphne Merkus, Elisabeth Deindl","doi":"10.3390/cells15080709","DOIUrl":"https://doi.org/10.3390/cells15080709","url":null,"abstract":"Despite the identification of several mediators of arteriogenesis, the growth of natural bypass, the role of lymphocytes, particularly T cells, in this process remains poorly defined. Among these, γδ T cells, which express alternative T cell receptors, have emerged as a key immune component. This study examined the roles of αβ and γδ T cells in arteriogenesis using a murine hindlimb model. While the absence of αβ T cells did not affect arteriogenesis, γδ T cell depletion markedly reduced vascular cell proliferation and perfusion recovery. Early phase analyses revealed impaired mast cell activation, whereas platelet-neutrophil aggregates and neutrophil extravasation were unaffected. In the later proliferative phase, γδ T cell depletion hindered perivascular M2-like (MRC1+) macrophage accumulation. Flow cytometric analysis of whole blood in wildtype mice revealed a temporal shift in γδ T cell populations from a CD27+/CD39- phenotype, commonly associated with pro-inflammatory functions and IFNγ production, to CD39+ phenotypes, which have been linked to anti-inflammatory properties and IL-10 production. In rescue experiments, administration of IFNγ to γδ T cell-depleted mice restored mast cell activation, whereas IL-10 treatment reestablished M2-like (MRC1+) macrophage accumulation. These findings collectively identify γδ T cells as critical regulators of both early and late phases of arteriogenesis through coordinated inflammatory and regenerative mechanisms.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 8","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Ultrastructural Signs of High Functional Activity of Neuromuscular Synapses in Aging Rats After Photobiomodulation. 光生物调节后老龄大鼠神经肌肉突触高功能活动的超微结构征象。

IF 5.2 2区生物学

Cells Pub Date : 2026-04-17 DOI: 10.3390/cells15080710

Tatyana Vasyagina, Daria Nefedova, Andrey Seliverstov, Natalya Shchelchkova, Marina Bugrova, Anna Bavrina

{"title":"Ultrastructural Signs of High Functional Activity of Neuromuscular Synapses in Aging Rats After Photobiomodulation.","authors":"Tatyana Vasyagina, Daria Nefedova, Andrey Seliverstov, Natalya Shchelchkova, Marina Bugrova, Anna Bavrina","doi":"10.3390/cells15080710","DOIUrl":"https://doi.org/10.3390/cells15080710","url":null,"abstract":"Aging is characterized by progressive degeneration of neuromuscular junctions (NMJs), which significantly contributes to muscle weakness and the development of sarcopenia. Photobiomodulation (PBM), a non-invasive therapeutic method based on the use of low-intensity light, has shown promising results in mitigating muscle degeneration in both experimental and clinical studies. The aim of this study was to evaluate the ultrastructural effects of photobiomodulation on neuromuscular junctions and skeletal muscle fibers in the m. vastus lateralis muscle of aged rats using light and transmission electron microscopy. Male Wistar rats (18 months old, body weight 650-800 g, n = 10) were subjected to photobiomodulation of the right m. vastus lateralis muscle (650 nm, 6 J/cm2, four consecutive daily sessions of 3 min each). The contralateral left limb served as an untreated control. Muscle samples were analyzed by light and transmission electron microscopy. Histological examination revealed typical age-related changes in control muscles, including variability in muscle fiber diameter, centrally located nuclei, and an increased volume of connective tissue. Ultrastructural analysis confirmed signs of skeletal muscle aging, such as myofibril fragmentation, sarcomere disorganization, lipofuscin accumulation, and tubular aggregate formation. Morphometric analysis of neuromuscular junctions after photobiomodulation showed an increase in the number of active zones on the presynaptic membrane, elongation of the postsynaptic membrane, and a reduction in the width of the synaptic cleft. In addition, mitochondrial hyperplasia was observed in presynaptic terminals, while the total number of synaptic vesicles decreased. These findings indicate a compensatory reorganization of neuromuscular junctions and suggest that photobiomodulation can enhance their functional activity in aged skeletal muscle.","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 8","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13115259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

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