Signaling Pathways in Cartilage Repair

Abstract

In adult healthy cartilage, chondrocytes are in a quiescent phase characterized by a fine balance between anabolic and catabolic activities. In ageing, degenerative joint diseases and traumatic injuries of cartilage, a loss of homeostatic conditions and an up-regulation of catabolic pathways occur. Since cartilage differentiation and maintenance of homeostasis are finely tuned by a complex network of signaling molecules and biophysical factors, shedding light on these mechanisms appears to be extremely relevant for both the identification of pathogenic key factors, as specific therapeutic targets, and the development of biological approaches for cartilage regeneration. This review will focus on the main signaling pathways that can activate cellular and molecular processes, regulating the functional behavior of cartilage in both physiological and pathological conditions. These networks may be relevant in the crosstalk among joint compartments and increased knowledge in this field may lead to the development of more effective strategies for inducing cartilage repair.

Ex vivo culture platform for assessment of cartilage repair treatment strategies

“…It is difficult to explain which exact mechanism is responsible for maintaining cartilage tissue content and properties in case of separation of bone and cartilage tissues and using tissue-specific medium. It has been shown before that cartilage homeostasis and function strongly depend on the crosstalk between cartilage and bone (Mariani et al, 2014). It is likely that cartilage and bone cells perform optimally when they receive the specific factors they require for their metabolism, which in turn can lead to positive signaling between the two tissues.…”

Different response of human chondrocytes from healthy looking areas and damaged regions to IL1β stimulation under different oxygen tension

“…The hypoxic response is mainly mediated by hypoxia inducible factors (HIF) ‐1α and HIF‐2α in chondrocyte development. HIF‐1a, is reported to promote chondrogenesis of MSCs, in part by activating SOX9 . The chondrogenic and anti‐catabolic effect of hypoxia could be blocked by HIF‐1α inhibitor .…”

Immunohistochemistry Evaluation of TGF-β1, SOX-9, Type II Collagen and Aggrecan in Cartilage Lesions Treated with Conditioned Medium of Umbilical Cord Mesencyhmal Stem Cells in Wistar Mice (Rattus novergicus)

“…In our study, we analyzed a group of proteins that are potentially found in the medium and have a potential to be beneficial in cartilage repair. The growth, development, maintenance, and improvement of articular cartilages are strictly regulated by multiple signaling pathways performed by several bioactive factors [11]. TGF-β1 is an especially significant factor in the chondrogenic differentiation of MSCs.…”