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Abstract
Curcumin is a well known natural polyphenol product isolated from the rhizome of the plant Curcuma longa, anti-inflammatory agent for arthritis by inhibiting synthesis of inflammatory prostaglandins. However, the mechanisms by which curcumin regulates the functions of chondroprogenitor, such as proliferation, precartilage condensation, cytoskeletal organization or overall chondrogenic behavior, are largely unknown. In the present report, we investigated the effects and signaling mechanism of curcumin on the regulation of chondrogenesis. Treating chick limb bud mesenchymal cells with curcumin suppressed chondrogenesis by stimulating apoptotic cell death. It also inhibited reorganization of the actin cytoskeleton into a cortical pattern concomitant with rounding of chondrogenic competent cells and down-regulation of integrin beta1 and focal adhesion kinase (FAK) phosphorylation. Curcumin suppressed the phosphorylation of Akt leading to Akt inactivation. Activation of Akt by introducing a myristoylated, constitutively active form of Akt reversed the inhibitory actions of curcumin during chondrogenesis. In summary, for the first time, we describe biological properties of curcumin during chondrogenic differentiation of chick limb bud mesenchymal cells. Curcumin suppressed chondrogenesis by stimulating apoptotic cell death and down-regulating integrin-mediated reorganization of actin cytoskeleton via modulation of Akt signaling.
Highlights
The progressive degeneration of articular cartilage, indicating a disruption of the balance between anabolic and catabolic activities of the chondrocytes, results in osteoarthritis, a painful, debilitating disease of the synovial joints
We found that curcumin suppressed chondrogenesis by stimulating apoptotic cell death, down-regulating integrin β1 and lowering the phosphorylation level of focal adhesion kinase (FAK)
To determine any effects of curcumin on chondrogenesis, chondroblasts isolated from wing buds were cultured at a density of 2 × 107 cells/ml and stimulated with varying concentrations of curcumin
Summary
The progressive degeneration of articular cartilage, indicating a disruption of the balance between anabolic and catabolic activities of the chondrocytes, results in osteoarthritis, a painful, debilitating disease of the synovial joints. Several events are known to play significant roles for the initiation and progression of joint diseases, including dysregulation of pro-inflammatory cytokines, pro-inflammatory enzymes that mediate the production of prostaglandins and leukotrienes (e.g. lipo-oxygenase), together with the expressions of adhesion molecules and matrix metalloproteinases. Most bones form by endochondral ossification, in which bones are first laid down as cartilage precursors (Karsenty and Wagner, 2002). This is a precise series of events that includes aggregation and differentiation of mesenchymal cells, proliferation, hypertrophy and death of chondrocytes (DeLise et al, 2000). Chondrogenesis is characterized by 2 dramatic changes in cellular condensation that are mediated by cell-cell and cell-matrix adhesion molecules (Sandell and Adler, 1999; DeLise et al., 2000; Knudson and Knudson, 2001) and cell shape changes from fibroblastoid to round or polygonal morphologies (von der Mark and von der Mark, 1977)
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