2 edition of Signal transduction mechanisms regulating chondrocyte production of collagenase. found in the catalog.
Signal transduction mechanisms regulating chondrocyte production of collagenase.
Written in English
|The Physical Object|
|Number of Pages||201|
Methods. Articular chondrocytes were isolated from adult bovine patellae and cultured in high density for 7 days. To study matrix protein expression, cells cultured in the absence or presence of specific calcium pathway inhibitors were exposed to a capacitively coupled electrical field (60 kHz, 20 mV/cm): for aggrecan 1 h at 50% duty cycle and for type II collagen 6 h at % duty :// In particular, the mechanisms of stiffness sensing and the downstream signal transduction involved in the ensuing gene regulation are yet to be clarified. Recent reports have shown that Wnt
Introduction. Osteoarthritis (OA) is a multifactorial disease characterized by a progressive loss of matrix proteins in human articular cartilage and subsequent chondrocyte cell death, with age as the strongest risk free radical theory of aging suggests that an accumulation of reactive oxygen species (ROS) causes irreparable damage to cells and tissues over time; however, the exact It has been reported that (a) high fluid shear stress activates COX-2 and the production of PGs at various time points; 3,4,5,6 (b) PGE 2 and 15d-PGJ 2 are involved in regulating the expression
Our understanding of basic cellular mechanisms regulating chondrocyte responses to inflammatory cytokines has been inferred from numerous studies in vitro with cultures of cartilage fragments or isolated chondrocytes and is supported by studies in experimental models of inflammatory arthritis such as collagen-induced arthritis (CIA) and antigen Osteoarthritis and rheumatoid arthritis are common cartilage and joint diseases that globally affect more than million and 20 million people, respectively. Several transcription factors have been implicated in the onset and progression of osteoarthritis, including Runx2, C/EBPβ, HIF2α, Sox4, and Sox Interleukin-1 β (IL-1β) leads to osteoarthritis through NF-ĸB, IκB&zeta
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Report on the proceedings of the ASGES Workshop on Safety Analyses and Oil Drift Models.
Regulation of senescence associated signaling mechanisms in chondrocytes for cartilage tissue regeneration the vital genes regulating chondrocyte biology and Signal transduction by the TGF Signal transduction through chondrocyte integrin receptors induces matrix metalloproteinase synthesis and synergizes with interleukin Arner EC(1), Tortorella MD.
Author information: (1)Du Pont Merck Pharmaceutical Company, Wilmington, DE:// Regulation of senescence associated signaling mechanisms in chondrocytes for cartilage tissue regeneration.
SOX9 is one of the vital genes regulating chondrocyte biology and its downregulation is involved in the indirect induction of senescence and dedifferentiation. J.L. WranaSignal transduction by the TGF-beta :// Collagenase production by chondrocytes appears to play a major role in the development of osteoarthritis.
Although the mechanisms regulating collagenase production by Matrix Metalloproteinase-9 Production by Immortalized Human Chondrocyte Lines of those signal transduction pathways that are of the mechanisms regulating expression of these key enzymes MMP degrades aggrecan and collagen II (Inada et al., ), Ihh increases non-hypertrophic chondrocyte proliferation (Van Donkelaar and Huiskes, ), collagen X facilities the mineralisation Chondrocytes communicate with each other mainly via diffusible signals rather than direct cell-to-cell contact.
The chondrogenic differentiation of mesenchymal stem cells (MSCs) is well regulated by the interactions of varieties of growth factors, cytokines, and signaling molecules.
A number of critical signaling molecules have been identified to regulate the differentiation of chondrocyte It has been established that ERK signal transduction pathway is involved in the regulation of cell growth and differentiation.
ERK-1 and -2 form the central component in the MAPK cascade. ERK-1/2 activation induces chondrocyte dedifferentiation and inhibits NO-induced :// Mechanisms for T3 regulation of chondrocyte differentiation.
T3 can modulate local actions of growth factors such as IGF-I, FGFs, Wnts, Ihh and PTHrp to regulate proliferation and differentiation Matrix metalloproteinase (MMP)-1, MMP-8 and MMP are interstitial collagenases that degrade type II collagen in cartilage; this is a committed step in the progression of rheumatoid arthritis and osteoarthritis.
Of these enzymes, the expression of MMP-1 and MMP is substantially increased in response to IL-1 and tumor necrosis factor-α, and elevated levels of these collagenases are Comparison was made with collagenase sThe human OA chondrocyte population could be divided into 2 categories: the L chondrocytes, showing low collagenase 3 It is also not known if integrin signaling activates MAP kinases in chondrocytes as in other cell types or what specific role such signaling may play in regulating chondrocyte MMP‐13 production.
Recent studies have demonstrated that IL‐1 induction of MMP‐13 requires p38 and JNK activation (19). Suppressor of cytokine signaling 3 (SOCS3) is a key regulator of cytokine signaling in macrophages and T cells.
Although SOCS3 seems to contribute to the balance between the pro-inflammatory actions of IL-6 family of cytokines and anti-inflammatory signaling of IL by negatively regulating gp/Jak/Stat3 signal transduction, how and the molecular mechanisms whereby SOCS3 controls the a key role for SOCS-3 in regulating chondrocyte re-sponses during inflammatory arthritis.
Within the gp cytokine family, OSM is a potent stimulus of chondrocyte responses, while IL-6 probably signals via trans-signaling. The gp cytokine–driven production of RANKL in chondrocytes may link chondrocyte acti- The results of this study highlight a key role for SOCS‐3 in regulating chondrocyte responses during inflammatory arthritis.
Within the gp cytokine family, OSM is a potent stimulus of chondrocyte responses, while IL‐6 probably signals via trans‐signaling. The gp cytokine–driven production of RANKL in chondrocytes may link Working synergistically with Wnt signal pathways, TGF-β stimulates chondrocyte differentiation from mesenchymal cells.
Wnt 7 may be a critical mediator of this process (93 – 95). In chicken upper sternal chondrocytes, TGF-β inhibits the expression of Wnt 4, 5, 8, and The signal transduction mechanisms of IL-1 remain obscure, and little is known of the early events following receptor binding.
The later events following interaction of IL-1 with the chondrocyte cell surface have been studied more :// Corresponding author: Mary B Goldring 0 0 0 Research Division of the Hospital for Special Surgery, Weill College of Medicine of Cornell University, Caspary Research Building, E.
70th Street, New York, NYUSA Rheumatoid arthritis (RA) is one of the inflammatory joint diseases in a heterogeneous group of disorders that share features of destruction of the extracellular matrices of Chondrocyte death observed on poly-l-lysine requires activation of PKC.
To further delineate the cell signaling mechanisms regulating chondrocyte survival under these conditions, we screened a large series of cell signaling regulators at various concentrations, from nanomolar to high micromolar values (Table 2).
To further study the effect of RA on the expression of collagenase-3, we first used primary chondrocyte cultures. Cells were treated with 10 −6 M RA, and total RNA was obtained at different times and analyzed by Northern blot using a specific collagenase-3 probe.
As shown in Fig. 2 a, RA induced the accumulation of a kb mRNA transcript corresponding to collagenase-3, the maximal effect. Nonetheless, the signal-transduction pathways and the transcriptional and post-transcriptional mechanisms regulating MMP gene expression are complex and often inter-connected, underscoring the difficulties inherent in designing successful ://Another strategy for improving cartilage tissue engineering is the transduction of the chondrogenic transcription factor Sox9, alone or together with L‐Sox5 and Sox6, into MSCs ex vivo or into joint tissues in vivo to induce cartilage formation (Ikeda et al., ; Tew et al., ).Backgroud.
Osteoarthritis (OA) is a common disease caused by chondrocyte dysfunction. KLF10 is a member of the Sp1-like transcription factor family that is involved in regulating osteoblasts, but its expression and regulatory mechanism(s) in chondrocytes are unclear.
In the present study, we aimed to investigate the regulatory role of KLF10 on the pathological process of ://