Lab AnimalPub Date : 2025-07-30DOI: 10.1038/s41684-025-01593-6
Alexandra Le Bras
{"title":"Mitochondrial trafficking","authors":"Alexandra Le Bras","doi":"10.1038/s41684-025-01593-6","DOIUrl":"https://doi.org/10.1038/s41684-025-01593-6","url":null,"abstract":"<p>Many cancers are innervated, and cancer-infiltrating neurons have been linked to higher cancer aggressiveness and metastatic potential. However, the underlying mechanisms are still unknown. A new study using mouse models of breast cancer reports that cancer-associated neurons enhance cancer cell metabolic capacity and metastatic dissemination by transferring their mitochondria. Hoover and colleagues first showed that neurotoxin-mediated denervation in a human ductal carcinoma in situ xenograft model reduced the incidence of invasive lesions compared to control mice. Then the researchers labeled the mitochondria of host mammary fat pad neurons using a lentiviral construct to induce GFP protein expression, before injecting 4T1 breast cancer cells into the fat pad. Flow cytometry analysis confirmed the presence of tumor cells exhibiting the green signal, consistent with a nerve-to-cancer transfer of mitochondria. Finally, the team developed MitoTRACER, a reporter of cell-to-cell mitochondrial transfer based on cre-lox recombination that permanently labels recipient cancer cells and their progeny. The fate mapping experiment revealed enrichment of mitochondria-recipient cancer cells or their progeny at metastatic tumor sites, indicating higher metastatic potential. These findings could guide the development of therapeutic strategies targeting nerve–cancer mitochondrial transfers to prevent metastatic disease.</p><p><b>Original reference:</b> Hoover, G. et al<i>. Nature</i> https://doi.org/10.1038/s41586-025-09176-8 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"79 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-07-30DOI: 10.1038/s41684-025-01590-9
Alexandra Le Bras
{"title":"Macaque model of inherited macular dystrophy","authors":"Alexandra Le Bras","doi":"10.1038/s41684-025-01590-9","DOIUrl":"https://doi.org/10.1038/s41684-025-01590-9","url":null,"abstract":"<p>Inherited macular dystrophies are a group of genetic disorders resulting in progressive damage to the cells in the macula, leading to vision loss. Although gene- and cell-based therapies offer promising approaches for these conditions, progress is hindered by the lack of animal models that recapitulate the macular changes observed in patients. In <i>JCI insight</i>, Xialin Liu’s team reports the first spontaneous nonhuman primate model of inherited macular dystrophy. Few years ago, while performing ocular biometric measurements in a cohort of <i>Macaca fascicularis</i> using advanced imaging techniques, the team identified a 6.8-year-old male with macular abnormalities. Whole-genome sequencing data revealed that the animal was carrying a <i>BEST1p.Q327E</i> variant. In humans, mutations in the <i>BEST1</i> gene give rise to Best vitelliform macular dystrophy (BVMD), one of the most common inherited macular dystrophies. Longitudinal imaging of the animal over two years revealed progressive macular changes, lipid-rich deposit accumulation, retinal pigment epithelium disruption and photoreceptor degeneration, recapitulating early human BVMD pathology. Histological analysis also indicated a buildup of damaged cone mitochondria. The model, which provides new insights into the pathophysiological processes involved in macular diseases, could be valuable for testing potential therapies.</p><p><b>Original reference:</b> Yi, W. et al. <i>JCI Insight</i> <b>10</b>, e190807 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"26 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-07-30DOI: 10.1038/s41684-025-01597-2
Jorge Ferreira
{"title":"Sex-specific effects of adolescence social isolation","authors":"Jorge Ferreira","doi":"10.1038/s41684-025-01597-2","DOIUrl":"https://doi.org/10.1038/s41684-025-01597-2","url":null,"abstract":"<p>Adolescence is a critical period for the maturation of brain circuits regulating social behavior, including the mesocorticolimbic dopamine system. Social experiences have long-lasting consequences in the development of individuals. However, the impact of social isolation during adolescence is still unclear. A study in <i>Behavioral Brain Research</i> examines how social instability stress (SS) during adolescence affects social reward motivation and dopamine receptor expression in rats. Using an operant conditioning task and mRNA analysis, researchers found that SS reduces social reward motivation in female rats—but only in adulthood—while male rats showed no such effect when compared to non-isolated rats. Interestingly, SS increased D2 dopamine receptor expression—a key protein in the dopamine signaling system—in important brain regions connected to reward and motivation compared to control rats. Overall, these results show clear evidence that social stress during adolescence has lasting effects, changing how dopamine works and affecting social behavior in adult males and females differently.</p><p><b>Original reference:</b> Leonetti, A. M. et al. <i>Behav. Brain Res</i>. <b>493</b>, 115702 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"41 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-07-30DOI: 10.1038/s41684-025-01595-4
Jorge Ferreira
{"title":"Dog Duchenne muscular dystrophy characterization","authors":"Jorge Ferreira","doi":"10.1038/s41684-025-01595-4","DOIUrl":"https://doi.org/10.1038/s41684-025-01595-4","url":null,"abstract":"<p>Duchenne muscular dystrophy (DMD) is a severe, inherited muscle-wasting disorder caused by mutations in the <i>DMD</i> gene, leading to dystrophin deficiency and downstream pathological cascades, including calcium overload, muscle necrosis, fibrosis, and progressive cardiac and skeletal muscle dysfunction. While mouse models are commonly used, they fail to fully model the human disease. The canine DMD model offers a more accurate representation of the disease, exhibiting progressive muscle weakness, respiratory decline, and cardiomyopathy. In a study in <i>Disease Models & Mechanisms</i>, researchers addressed an important technical limitation by developing a custom antibody specific to canine Dwarf open reading frame (DWORF), a micropeptide implicated in calcium handling and muscle function. Using this tool, they found that DWORF expression—previously demonstrated to have a protective role in muscular wasting diseases—is reduced in the skeletal and cardiac muscles of adult DMD dogs. This is the first characterization of DWORF protein in a large-animal model of DMD, providing groundwork for preclinical evaluation of DWORF-targeted therapies in a system that more accurately reflects human DMD pathology.</p><p><b>Original reference:</b> Gibson, A.M. et al. <i>Dis. Model & Mech</i>. <b>18</b>, dmm052285 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"26 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-07-30DOI: 10.1038/s41684-025-01592-7
Alexandra Le Bras
{"title":"Health benefits of early-life exercise","authors":"Alexandra Le Bras","doi":"10.1038/s41684-025-01592-7","DOIUrl":"https://doi.org/10.1038/s41684-025-01592-7","url":null,"abstract":"<p>Although accumulating evidence indicates that exercise has a positive impact on healthspan, the influence of early-life exercise on adult health has been understudied. The matter is important as recent reports suggest that most adolescents do not meet current physical activity guidelines. New research published in <i>Nature Communications</i> demonstrates that 3 months of early-life exercise results in lasting health benefits in both male and female mice. The researchers subjected male and female C57BL/6J mice to either sedentary conditions or swimming exercise (90 min per day for 3 months) at 1–4 months of age before rearing the animals without exercise for the rest of their life. While early-life exercise did not extend the overall lifespan of the mice, evaluation of various health parameters revealed that it enhanced systemic metabolism, cardiovascular function and improved musculoskeletal health in aged mice. Early-life exercise also reduced systemic inflammation and frailty, two fundamental hallmarks of aging. Notably, early-life exercise was associated with a reduction in alopecia and fur color loss in aged mice. Further studies are needed to explore the mechanisms underlying the long-term health effects of early-life exercise and to translate these findings to human populations.</p><p><b>Original reference:</b> Feng, M. et al<i>. Nat. Commun</i>. <b>16</b>, 6328 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"27 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-07-30DOI: 10.1038/s41684-025-01591-8
Alexandra Le Bras
{"title":"A new humanized pig model","authors":"Alexandra Le Bras","doi":"10.1038/s41684-025-01591-8","DOIUrl":"https://doi.org/10.1038/s41684-025-01591-8","url":null,"abstract":"<p>Humanized mice engrafted with human hematopoietic stem and progenitor cells (HSPCs) are valuable models for exploring human immunology. However, the small size and short lifespan of the mouse models limit their translational value. Pigs are suitable large animal models for preclinical research, but existing immunodeficient pig models show limited human HSPC engraftment and multilineage differentiation. A new study reports the development of an immunodeficient pig model that supports robust human HSPC engraftment and blood cell formation, offering a valuable preclinical tool for studying human immunology. The researchers used CRISPR-Cas9 technology to inactivate <i>RAG1</i> and <i>IL2RG</i> in Bama pig fibroblasts and generated the immunodeficient pigs via somatic cell nuclear transfer and embryo transfer. The team also deleted <i>CD47</i>, a gene encoding a cell surface protein that regulates macrophage-mediated phagocytosis with the aim of preventing rejection of human cells by pig macrophages. Using multiple approaches to characterize human cell development in the engineered pigs, the researchers found that the triple-knockout pigs (<i>RAG2/IL2RG/CD47</i>) showed long-term human HSPC engraftment in the bone marrow, robust thymopoiesis and T cell development in the thymus, and repopulation with multilineage human hematopoietic cells throughout tissues.</p><p><b>Original reference:</b> Hu, Z. et al<i>. Nat. Biomed. Eng</i>. https://doi.org/10.1038/s41551-025-01397-6 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"5 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-07-30DOI: 10.1038/s41684-025-01600-w
Jorge Ferreira
{"title":"How do mice prefer to be handled?","authors":"Jorge Ferreira","doi":"10.1038/s41684-025-01600-w","DOIUrl":"https://doi.org/10.1038/s41684-025-01600-w","url":null,"abstract":"","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"26 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144748119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-07-30DOI: 10.1038/s41684-025-01596-3
Jorge Ferreira
{"title":"New glioblastoma therapeutic targets","authors":"Jorge Ferreira","doi":"10.1038/s41684-025-01596-3","DOIUrl":"https://doi.org/10.1038/s41684-025-01596-3","url":null,"abstract":"<p>Glioblastoma (GBM) is an aggressive brain tumor marked by cellular heterogeneity, complicating treatment strategies. A study in <i>Communications Biology</i> employs single-nucleus RNA sequencing (snRNA-Seq) and spatial transcriptomics to profile the tumor microenvironment (TME) in the GL261-GSC syngeneic mouse model of GBM—a model that allows the study of the immune system and has been previously used to study multiple therapeutic targets. The study shows the analyses of 14 in vivo tumor samples and 5 cultured GBM cell samples, mapping cellular states across disease stages. The use of snRNA-Seq preserves sensitive cell populations, offering a more accurate representation of the TME than conventional scRNA-Seq. The study also compares snRNA-Seq with two single-cell RNA sequencing methods to assess technical biases. Treatments included temozolomide, the current standard of care, and the experimental peptide Tat-Cx43<sub>266–283</sub>, which showed significant anti-tumor effects. The findings highlight potential therapeutic targets and reveal molecular similarities between the GL261-GSC GBM model and TME<sup>Med</sup> GBM, the most common human GBM subtype, validating its translational relevance.</p><p><b>Original reference:</b> García-Vicente, L. et al. <i>Commun. Biol</i>. <b>8</b>, 671 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"19 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lab AnimalPub Date : 2025-07-30DOI: 10.1038/s41684-025-01594-5
Jorge Ferreira
{"title":"A new zebrafish epilepsy model","authors":"Jorge Ferreira","doi":"10.1038/s41684-025-01594-5","DOIUrl":"https://doi.org/10.1038/s41684-025-01594-5","url":null,"abstract":"<p>Epilepsy affects approximately 70 million people globally, with 30–40% of patients experiencing drug-resistant seizures despite treatment with multiple antiseizure medications (ASMs). To address this issue, in a study in <i>Disease Models & Mechanisms</i>, the team developed a novel zebrafish model targeting <i>slc25a22a</i>, the ortholog of human <i>SLC25A22</i>—a gene associated with a range of epileptic conditions. Unlike existing zebrafish models, which often rely on gene knockdowns and show weak seizure phenotypes, the new CRISPR-Cas9–generated <i>slc25a22a</i> knockout exhibits robust epilepsy traits, including spontaneous seizures, behavioral hyperactivity and electrophysiological hyperexcitability. Importantly, treatment with valproic acid effectively suppressed these phenotypes, highlighting the model’s relevance for both mechanistic studies and drug screening. These findings indicate that <i>slc25a22a</i> can be a promising therapeutic target for refractory epilepsy and establish this zebrafish line as a valuable platform for preclinical research into novel ASMs.</p><p><b>Original reference:</b> Lee, S.-H. et al. <i>Dis. Model & Mech</i>. <b>18</b>, dmm052275 (2025)</p>","PeriodicalId":17936,"journal":{"name":"Lab Animal","volume":"13 1","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144747307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
求助内容：
应助结果提醒方式：