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Journal article
Identification of Chondrocyte Genes and Signaling Pathways in Response to Acute Joint Inflammation
Scientific reports, v 9(1), pp 93-93
14 Jan 2019
PMID: 30643177
Featured in Collection : UN Sustainable Development Goals @ Drexel
Abstract
Traumatic joint injuries often result in elevated proinflammatory cytokine (such as IL-1β) levels in the joint cavity, which can increase the catabolic activities of chondrocytes and damage cartilage. This study investigated the early genetic responses of healthy in situ chondrocytes under IL-1β attack with a focus on cell cycle and calcium signaling pathways. RNA sequencing analysis identified 2,232 significantly changed genes by IL-1β, with 1,259 upregulated and 973 downregulated genes. Catabolic genes related to ECM degeneration were promoted by IL-1β, consistent with our observations of matrix protein loss and mechanical property decrease during 24-day in vitro culture of cartilage explants. IL-1β altered the cell cycle (108 genes) and Rho GTPases signaling (72 genes) in chondrocytes, while chondrocyte phenotypic shift was observed with histology, cell volume measurement, and MTT assay. IL-1β inhibited the spontaneous calcium signaling in chondrocytes, a fundamental signaling event in chondrocyte metabolic activities. The expression of 24 genes from 6 calcium-signaling related pathways were changed by IL-1β exposure. This study provided a comprehensive list of differentially expressed genes of healthy in situ chondrocytes in response to IL-1β attack, which represents a useful reference to verify and guide future cartilage studies related to the acute inflammation after joint trauma.
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Details
- Title
- Identification of Chondrocyte Genes and Signaling Pathways in Response to Acute Joint Inflammation
- Creators
- Mengxi Lv - University of DelawareYilu Zhou - University of DelawareShawn W Polson - University of DelawareLeo Q Wan - Rensselaer Polytechnic InstituteMeiqing Wang - Air Force Medical UniversityLin Han - School of Biomedical Engineering, Science, and Health Systems, Drexel University, Philadelphia, PA, United StatesLiyun Wang - University of DelawareX Lucas Lu - University of Delaware
- Publication Details
- Scientific reports, v 9(1), pp 93-93
- Publisher
- Springer Nature
- Grant note
- W81XWH-13-1-0148 / U.S. Department of Defense (United States Department of Defense) P20 GM103446 / NIGMS NIH HHS AR054385 / Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.) AR066824 / Foundation for the National Institutes of Health (Foundation for the National Institutes of Health, Inc.)
- Resource Type
- Journal article
- Language
- English
- Academic Unit
- School of Biomedical Engineering, Science, and Health Systems
- Web of Science ID
- WOS:000455592300014
- Scopus ID
- 2-s2.0-85060038097
- Other Identifier
- 991019168464704721
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- Collaboration types
- Domestic collaboration
- International collaboration
- Web of Science research areas
- Rheumatology