Protheragen offers comprehensive in vivo animal model development services for Scleroderma, tailored to accelerate the discovery and evaluation of novel therapeutics. Leveraging a wide range of validated murine models, our service enables researchers to investigate disease mechanisms, assess treatment efficacy, and advance translational research with scientific rigor and reliability.
Scleroderma, or systemic sclerosis, is a complex autoimmune disorder characterized by fibrosis of the skin and internal organs. Due to its heterogeneous pathology and multifactorial etiology, robust animal models are essential for understanding disease progression and evaluating potential therapies. Protheragen utilizes various strains of Mus musculus (mouse), including Balb/c, C57BL/6, DBA/2J, NOD, and genetically modified lines, each offering distinct immunological and fibrotic responses that closely mimic aspects of human Scleroderma. These models provide critical insights into disease mechanisms and therapeutic efficacy, facilitating the translation of preclinical findings into clinical advancements.
Chemically-induced Scleroderma models are established by administering agents such as bleomycin sulfate, which triggers localized or systemic fibrosis in mice. This methodology is reproducible and enables controlled induction of Scleroderma-like pathology across multiple strains, including Balb/c, C57BL/6, DBA/2J, and NOD. Key advantages include rapid onset of symptoms, dose-dependent responses, and suitability for high-throughput drug screening. These models are primarily used for evaluating anti-fibrotic therapies, elucidating mechanisms of fibrosis, and studying immune cell involvement in disease progression.
Genetic models involve the use of transgenic or knockout mice that harbor specific gene modifications, such as the TSSK1B transgenic line on the C57BL/6 background. These models mimic genetic susceptibilities and molecular pathways implicated in Scleroderma, enabling in-depth investigation of gene function and disease pathogenesis. Advantages include the ability to study chronic and spontaneous disease development, as well as the impact of specific genetic factors. Genetic models are ideal for target validation, mechanistic studies, and long-term efficacy testing of therapeutic candidates.
Immunodeficient models, such as the NOD strain with severe combined immune deficiency (SCID), are chemically induced to develop Scleroderma-like features. These models lack functional immune responses, making them valuable for studies involving human cell or tissue engraftment, as well as evaluation of immune-modulating therapies. Advantages include reduced immune-mediated variability and enhanced translational relevance for xenograft studies. Applications include cell-based therapy testing, humanized mouse studies, and immune mechanism dissection.
Protheragen delivers a complete solution for in vivo Scleroderma research, encompassing model selection, study design, model induction, therapeutic administration, and comprehensive endpoint analysis. Key efficacy endpoints include dermal thickness measurement, collagen deposition quantification (histology and hydroxyproline assays), skin and organ fibrosis scoring, inflammatory marker profiling, and molecular analyses (qPCR, Western blot, immunohistochemistry). Our analytical capabilities extend to advanced imaging, cytokine quantification, and flow cytometry. Rigorous quality control measures, including standardized protocols, validated reagents, and reproducible methodologies, ensure data integrity and scientific validity throughout every stage of the study.
Partnering with Protheragen provides access to expertly developed, scientifically validated Scleroderma models and end-to-end research support. Our experienced team collaborates closely with clients to customize studies, accelerate timelines, and generate actionable data that drive therapeutic innovation. Contact us today to discuss your Scleroderma research needs and discover how our in vivo model services can advance your preclinical pipeline.
| Species | Strain | Characteristic (Details) |
|---|---|---|
| Mus musculus (mouse) | Balb/c | Chemical agent-induced (bleomycin sulfate) |
| Mus musculus (mouse) | C57BL/6 | Chemical agent-induced (bleomycin sulfate) |
| Mus musculus (mouse) | C57BL/6 | Chemical agent-induced (bleomycin sulfate); Transgenic (TSSK1B) |
| Mus musculus (mouse) | C57BL/6J | Chemical agent-induced (bleomycin sulfate) |
| Mus musculus (mouse) | DBA/2J | Chemical agent-induced (bleomycin sulfate) |
| Mus musculus (mouse) | NOD | Chemical agent-induced (bleomycin sulfate); Severe combined immune deficiency (SCID) |
| Mus musculus (mouse) | Chemical agent-induced (bleomycin sulfate) |
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