Animal Models of Joint Injury and Disease
关节损伤和疾病的动物模型
基本信息
- 批准号:10602567
- 负责人:
- 金额:$ 14.9万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2019
- 资助国家:美国
- 起止时间:2019-04-15 至 2024-03-31
- 项目状态:已结题
- 来源:
- 关键词:Animal BehaviorAnimal ModelAnimal TestingAnti-Inflammatory AgentsArthralgiaArthritisAwarenessBehaviorBenchmarkingBiocompatible MaterialsBiological AssayBiological ProductsBiologyBiomechanicsCellsCollaborationsCommunitiesDataDegenerative polyarthritisDiseaseDisease ManagementDisease modelEpidemicEuthanasiaEvaluationFresh TissueFunctional disorderFundingGenesGoalsGuidelinesHealthHistologicHistologyImageImmunohistochemistryInbreedingInflammationInflammatoryInstructionJointsKnowledgeLocomotionMeasuresMechanicsMedicineModelingMolecularMouse StrainsMusMusculoskeletalPainPathologyProcessProteinsProtocols documentationQuality ControlReagentReproducibilityResearchResearch PersonnelResourcesRestRheumatoid ArthritisRodent ModelRunningSamplingSensorimotor functionsSerumSourceStandardizationSupervisionSwellingSymptomsTestingTherapeutic InterventionTimeTissuesTrainingTraining and EducationTraumatic ArthropathyUniversitiesWashingtonarthropathiesbiobankbonecohortfunctional outcomesinterestjoint functionjoint injurymouse modelnext generationnovel therapeutic interventionoutreachpain reliefpain sensitivityprogramsrepositorytreadmill
项目摘要
Rheumatoid arthritis (RA) and osteoarthritis (OA) are highly prevalent and have reached epidemic proportions
in the US and worldwide. These joint diseases are characterized by inflammation, swelling (particularly in RA),
pain, and limited mobility. Despite significant advances in developing anti-inflammatory therapies, biologics, and
symptomatic pain relief measures, significant shortcomings in treating these diseases remain, buttressing the
need for robust research to meet this urgent health predicament. A wide range of small animal models of joint
disease, including RA and OA, has been developed in recent years and helped advance our understanding of
disease pathology, underlying mechanisms, disease management and therapeutic intervention. However, the
reproducible implementation of these models is challenging, especially in the hands of non-experts and due to
scarcity of validated benchmark criteria across studies. At the same time, tests of animal behavior, sensitivity,
and musculoskeletal function have demonstrated value in identifying symptoms and joint dysfunction in rodent
models of arthritis. Yet, the full spectrum of creation of joint injury/disease models and evaluation of functional
outcomes to achieve comprehensive analysis is rarely used by most research groups due to limited availability
of essential resources. Core D will address this need by supporting model implementation and functional
assessment as an integrated resource. Our ability to do so rests on the collective expertise of the Core leaders
in inflammatory joint disease (Dr. Abu-Amer), post-traumatic OA (Drs. O’Keefe and Shen) and functional
assessment of joint pain and dysfunction (Drs. Guilak and Setton). Notably, four of these investigators joined the
WUSTL Research Community in the past few years, which has provided our Center with a unique opportunity to
develop this Resource Core. Our goal is to advance current knowledge to bridge gaps in our understanding of
the cellular, molecular and functional basis of joint arthritis, and to develop and evaluate new therapeutic
strategies. The Core will standardize protocols and support the reproducible implementation of RA and OA
models for widespread use by the Research Community. We will facilitate collaboration with Cores B and C to
enable comprehensive analyses. Importantly, the Core will organize critical resources, including a facility for
testing murine musculoskeletal function and behavior. We will establish a new, organized biomaterial resource
to collect and store tissue and serum samples from RA and OA mouse models, which will be made available as
a standard resource for histology, gene and protein screens by all investigators. Finally, the Core will provide
hands-on training and enrichment program to train the next generation of joint investigators. Our Specific Aims
are: Aim 1: Support the implementation and utilization of reproducible OA and RA mouse models. Aim 2: Provide
measures of biomechanics, behavior, and function to assess mouse joint function. Aim 3: Establish murine OA
and RA biomaterials repository. Aim 4: Provide hands-on training, outreach and enrichment.
类风湿性关节炎(RA)和骨关节炎(OA)非常普遍,已经达到流行病的程度
项目成果
期刊论文数量(0)
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会议论文数量(0)
专利数量(0)
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{{ truncateString('YOUSEF ABU-AMER', 18)}}的其他基金
Regulation of Osteoclastogenesis and Inflammatory Osteolysis
破骨细胞生成和炎性骨质溶解的调节
- 批准号:
10681786 - 财政年份:2023
- 资助金额:
$ 14.9万 - 项目类别:
Mechanisms of Physiologic and Pathologic Osteoclastogenesis
破骨细胞发生的生理和病理机制
- 批准号:
10380048 - 财政年份:2018
- 资助金额:
$ 14.9万 - 项目类别:
Mechanisms of Physiologic and Pathologic Osteoclastogenesis
破骨细胞发生的生理和病理机制
- 批准号:
9889901 - 财政年份:2018
- 资助金额:
$ 14.9万 - 项目类别:
Molecular Mechanisms Underlying Tak1 Function in Osteoclasts
破骨细胞中 Tak1 功能的分子机制
- 批准号:
8635282 - 财政年份:2008
- 资助金额:
$ 14.9万 - 项目类别:
Molecular Mechanisms Underlying Tak1 Function in Osteoclasts
破骨细胞中 Tak1 功能的分子机制
- 批准号:
8830431 - 财政年份:2008
- 资助金额:
$ 14.9万 - 项目类别:
Mechanisms of IKK Regulation of Basal and Inflammatory Osteoclastogenesis
IKK 调节基础和炎症破骨细胞生成的机制
- 批准号:
7793408 - 财政年份:2008
- 资助金额:
$ 14.9万 - 项目类别:
Molecular Mechanisms Underlying Tak1 Function in Osteoclasts
破骨细胞中 Tak1 功能的分子机制
- 批准号:
8501884 - 财政年份:2008
- 资助金额:
$ 14.9万 - 项目类别:
Mechanisms of IKK Regulation of Basal and Inflammatory Osteoclastogenesis
IKK 调节基础和炎症破骨细胞生成的机制
- 批准号:
7461161 - 财政年份:2008
- 资助金额:
$ 14.9万 - 项目类别:
Molecular Mechanisms Underlying Tak1 Function in Osteoclasts
破骨细胞中 Tak1 功能的分子机制
- 批准号:
9017945 - 财政年份:2008
- 资助金额:
$ 14.9万 - 项目类别:
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