Apoptotic Chondrocytes and Osteoarthritis
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".
Deadline for manuscript submissions: closed (28 February 2017) | Viewed by 170382
Special Issue Editors
Interests: inflammation; apoptosis; arthritis; chondrocytes; matrix metalloproteinases; signal transduction; pro-inflammatory; anti-inflammatory & anabolic cytokines
Special Issues, Collections and Topics in MDPI journals
Interests: cartilage biology; arthritis biomarkers; comparative medicine/comparative physiology; Techniques: quantitative immunohistochemical and immunomorhological techniques; post-genomic techniques including tissue microarray technology; proteomics; metabolomics and bioinformatics
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The loss of chondrocyte vitality is a significant hallmark of the changes that occur in articular cartilage in human osteoarthritis (OA). Theoretically, a population of mesenchymal stem cells (MSCs) could potentially replace those chondrocytes lost during the OA process, but their presence or absence remains controversial. If these MSCs are eventually confirmed to exist, then provided with the correct growth factors and/or supplements these MSCs could develop into chondrocytes which have been lost in OA. In addition, these MSCs could also be engineered to “resist” apoptosis and behave as authentic articular chondrocytes to replace extracellular matrix proteins degraded and removed from cartilage in OA, as well as to assist damaged articular cartilage to regenerate. Numerous previously published histochemical, biochemical and molecular analyses have indicated that there is an elevated frequency of apoptotic chondrocytes in OA, although to this day these findings also remain controversial. What is known, is that several of the pro-inflammatory cytokines, including TNF-α, IL-1β, as well as some soluble mediators, such as nitric oxide (NO), all of which are present at elevated levels in OA synovial fluid, have the capacity to induce apoptosis in chondrocyte cultures. Importantly, the signal transduction pathways activated by TNF-α, IL-1β and NO which also appears to involve nuclear factor kappaB (NF-κB) activation have also been identified in cultured chondrocytes. Therefore, downstream signaling is very likely to regulate both chondrocyte pro-apoptotic and anti-apoptotic protein gene expression during the OA process. However, the extent to which these signaling pathways can be genetically or chemically modified to prevent or suppress chondrocyte apoptosis in OA remains to be fully elucidated.
Mohamed N. Rahaman
Prof. Dr. Ali Mobasheri
Guest Editor
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Keywords
- articular cartilage
- apoptosis
- chondrocytes
- cytokines
- osteoarthritis
- signal transduction
- soluble mediators
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