98%
921
2 minutes
20
The dramatic increase in myotomal muscle mass in teleosts appears to be related to their sustained ability to produce new fibres in the growing myotomal muscle. To describe muscle fibre input dynamics in trout (Oncorhynchus mykiss), we generated a stable transgenic line carrying green fluorescent protein (GFP) cDNA driven by the myogenin promoter. In this myog:GFP transgenic line, muscle cell recruitment is revealed by the appearance of fluorescent, small, nascent muscle fibres. The myog:GFP transgenic line displayed fibre formation patterns in the developing trout and showed that the production of new fluorescent myofibres (muscle hyperplasia) is prevalent in the juvenile stage but progressively decreases to eventually cease at approximately 18 months post-fertilisation. However, fluorescent, nascent myofibres were formed de novo in injured muscle of aged trout, indicating that the inhibition of myofibre formation associated with trout ageing cannot be attributed to the lack of recruitable myogenic cells but rather to changes in the myogenic cell microenvironment. Additionally, the myog:GFP transgenic line demonstrated that myofibre production persists during starvation.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1242/jeb.113704 | DOI Listing |
Mol Ther Methods Clin Dev
June 2025
Université Paris-Saclay, University Evry, Inserm, Genethon, Integrare Research Unit UMR_S951, 91000 Evry, France.
Pompe disease is a glycogen storage disorder caused by mutations in the acid α-glucosidase (GAA) gene, leading to reduced GAA activity and glycogen accumulation in heart and skeletal muscles. Enzyme replacement therapy with recombinant GAA, the standard of care for Pompe disease, is limited by poor skeletal muscle distribution and immune responses after repeated administrations. The expression of GAA in muscle with adeno-associated virus (AAV) vectors has shown limitations, mainly the low targeting efficiency and immune responses to the transgene.
View Article and Find Full Text PDFFront Immunol
September 2025
Department of Pathological Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, United States.
Oncolytic virotherapy (OVT) has emerged as a promising and innovative cancer treatment strategy that harnesses engineered viruses to selectively infect, replicate within, and destroys malignant cells while sparing healthy tissues. Beyond direct oncolysis, oncolytic viruses (OVs) exploit tumor-specific metabolic, antiviral, and immunological vulnerabilities to reshape the tumor microenvironment (TME) and initiate systemic antitumor immunity. Despite promising results from preclinical and clinical studies, several barriers, including inefficient intratumoral virus delivery, immune clearance, and tumor heterogeneity, continue to limit the therapeutic advantages of OVT as a standalone modality and hindered its clinical success.
View Article and Find Full Text PDFFront Immunol
September 2025
Division of Allergy and Clinical Immunology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
NSG-SGM3 humanized mouse models are well-suited for studying human immune physiology but are technically challenging and expensive. We previously characterized a simplified NSG-SGM3 mouse, engrafted with human donor CD34 hematopoietic stem cells without receiving prior bone marrow ablation or human secondary lymphoid tissue implantation, that still retains human mast cell- and basophil-dependent passive anaphylaxis responses. Its capacities for human antibody production and human B cell maturation, however, remain unknown.
View Article and Find Full Text PDFMol Ther Methods Clin Dev
September 2025
Office of Gene Therapy, Office of Therapeutic Products, Center for Biologics Evaluation and Research, U.S. Food and Drug Administration, Silver Spring, MD 20993, USA.
genome editing with CRISPR-Cas9 systems is generating worldwide attention and enthusiasm for the possible treatment of genetic disorders. However, the consequences of potential immunogenicity of the bacterial Cas9 protein and the AAV capsid have been the subject of considerable debate. Here, we model the antigen presentation in cells after gene editing by transduction of a human cell line with an AAV2 vector that delivers the Cas9 transgene.
View Article and Find Full Text PDFBiochem Biophys Rep
June 2025
Department of Public Health, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Background: Synaptic dysfunction and synapse loss occur in Alzheimer's disease (AD). The current study aimed to identify synaptic-related genes with diagnostic potential for AD.
Methods: Differentially expressed genes (DEGs) were overlapped with phenotype-associated module selected through weighted gene co-expression network analysis (WGCNA), and synaptic-related genes.