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Biological Regulation of the Chondrocytes provides a comprehensive examination of the various regulations in which cartilaginous cells are involved. The book's introductory chapter provides an overview of the different types of chondrocyte, while following chapters discuss the various biological regulations implicated in chondrocyte functions, especially the modulation of differentiative properties. Chapters 2 and 3 examine the extracellular matrix components, and Chapter 4 discusses the special case of cultured chondrocytes and the usefulness of in vitro approaches. The following three chapters focus on the complex role of cartilaginous growth factors and cytokines (FGF, TGFB, IGF, and IL1) on the modulation of the chondrocyte properties. Chapter 9 discusses the synoviocyte, and the last four chapters examine the biochemical and molecular perturbations that appear during repair, aging, rheumatic disease, and cancer. Biological Regulation of the Chondrocytes will benefit rheumatologists, pharmaceutical researchers, physiologists, connective tissue specialists, and students and other researchers in the osteoarticular field.
This book covers the proceedings of the Fifth Symposium on Mechanobiology of Cartilage and Chondrocyte. Mechanobiology can be now considered as a vigorous branch of biomechanics, biorheology and physiology mainly concerned with the study of the influence of mechanical forces on cells and tissues and their clinical or therapeutical applications. As we are now in the age of proteomics, genomics and cell micro mechanical approaches, suing methods like laser tweezers or confocal microscopy, mechanobiology brings new challenges. With such new research, mechanobiology promises new diagnostic and therapeutic approaches. In other respect there has been increasing interest over recent years in the fundamental role played by local mechanical parameters in chondrocyte regulations and cartilage dysfunctions as a first step in the development of osteoarthritis. These proceedings are sub-divided into four parts: Theoretical approaches and mechanobiology of chondrocyte; Cartilage and chondrocyte studies; Osteoarthritis: inflammation degradation and clinical approaches; and, Cartilage engineering
Insulin-like growth factors (IGFs) and inflammatory cytokines (e.g. IL-1) affect cartilage metabolism in opposite ways. The actions of IGFs in biological systems are modulated by locally produced IGF binding proteins (IGFBPs). This thesis investigated the effects of the IGFs and inflammatory cytokines on IGFBPs produced by chondrocytes and the subsequent interplay of these factors on proteoglycan production in vitro. To do this, a primary culture of ovine articular chondrocytes was used as an in vitro experimental model system. It was concluded that the IGFBP-5-mediated decrease in proteoglycan synthesis could be a relevant in vivo mechanism by which IL-1 exerts its catabolic effect and disturbs the balance between the synthesis and degradation of cartilage matrix macromolecules in pathological conditions.
Evidence generated by a number of genetic studies indicates that growth is regulated by a number of genes and that interference with their expression can have catastrophic effects on the well being of the whole organism. This work covers skeletal development and growth.
Articular cartilage is an avascular and flexible connective tissue found in joints. It produces a cushioning effect at the joints and provides low friction to protect the ends of the bones from wear and tear/damage. It has poor repair capacity and any injury can result in pain and loss of mobility. One of the common forms of articular cartilage disease which has a huge impact on patient's life is arthritis. Research on cartilage cell/tissue engineering will help patients to improve their physical activity by replacing or treating the diseased/damaged cartilage tissue. Cartilage cell, called chondrocyte is embedded in the matrix (Lacunae) and has round shape in vivo. The in vitro monolayer culture of primary chondrocyte causes morphological change characterized as dedifferentiation. Transforming growth factor-beta (TGF-[beta]), a cytokine superfamily, regulates cell function, including differentiation and proliferation. The effect of TGF-[beta]1, 2, 3, and their manipulated forms in biological regulation of primary chondrocyte was investigated in this work. A novel method was developed to isolate and purify the primary chondrocytes from knee joint of neonate Sprague-Dawley rat, and the effect of some supplementations such as hyaluronic acid and antibiotics were also investigated to provide the most appropriate condition for in vitro culture of chondrocyte cells. Addition of 0.1mg/ml hyaluronic acid in chondrocyte culture media resulted an increase in primary chondrocyte proliferation and helped the cells to maintain chondrocytic morphology. TGF-[beta]1, 2 and 3 caused chondrocytes to obtain fibroblastic phenotype, alongside an increase in apoptosis. The healing process of the wound closure assay of chondrocyte monolayers were slowed down by all three isoforms of TGF-[beta]. All three types of TGF-[beta] negatively affected the strength of chondrocyte adhesion. TGF-[beta]1, 2 and 3 up regulated the expression of collagen type-II, but decreased synthesis of collagen type-I, Chondroitin sulfate glycoprotein, and laminin. They did not show any significant change in production of S-100 protein and fibronectin. TGF-[beta]2, and 3 did not change expression of integrin-[beta]1 (CD29), but TGF-[beta]1 decreased the secretion of this adhesion protein. Manipulated TGF-[beta] showed huge impact on formation of fibroblast like morphology of chondrocytes with chondrocytic phenotype. These isoforms also decreased the expression of laminin, chondroitin sulfate glycoprotein, and collagen type-I, but they increased production of collagen type-II and did not induce synthesis of fibronectin and S-100 protein. In addition, the strength of cell adhesion on solid surface was reduced by manipulated TGF-[beta]. Only manipulated form of TGF-[beta]1 and 2 could increase the proliferation rate. Manipulation of TGF-[beta] did not up regulate the expression of integrin-[beta]1 in planar culture system. The implications of this R & D work are that the manipulation of TGF-[beta] by combination of TGF-[beta]1, 2, and 3 can be utilized in production of superficial zone of cartilage and perichondrium. The collagen, fibronectin and hyaluronic acid could be recruited for the fabrication of a biodegradable scaffold that promotes chondrocyte growth for autologous chondrocyte implantation or for formation of cartilage.
Osteoarthritis (OA), the most common form of arthritis, is generally characterized by a slowly progressive degeneration of articular cartilage, particularly in the weight-bearing joints. It has a stronger prevalence in women, and its incidence increases with age. OA is a major and growing health concern in developed countries, owing to steadily increasing life expectancy and the demand for better quality of life. Because of its chronic nature and nonfatal outcome, OA affects the growing population of the elderly over an increasing time span. Moreover, despite its relatively benign character, OA is one of the most disabling diseases; it is responsible for increasing financial and social burdens in terms of medical treatments, forced inactivity, loss of mobility, and dependence. Despite a growing awareness of OA as a medical problem that has yet to reach its maximum impact on society, there is a surprising absence of effective medical treatments beyond pain control and surgery. So far, only symptom-modifying drugs are available, while there remains a major demand for disease-modifying treatments of proven clinical efficacy. This demand will hopefully be met in the future by some of the drugs that have been pressed into development and are now at different stages of clinical investigation. Nevertheless, the current lack of effective treatments reflects a still insufficient knowledge of cartilage with respect to its metabolism, interactions with other joint tissues, and causes and mechanisms (possibly of very different nature) leading to failure of its turnover.
Osteoarthritis is a public health issue due to its impact in term of handicap. Regarded as a multi-factorial disease, mechanistic and inflammatory theories are no more opposed but, on the contrary, are framed within the same continuum: osteoarthritis, inflammation and degeneration. This book helps readers understand the secrets of this disease.
This reference work presents the origins of cells for tissue engineering and regeneration, including primary cells, tissue-specific stem cells, pluripotent stem cells and trans-differentiated or reprogrammed cells. There is particular emphasis on current understanding of tissue regeneration based on embryology and evolution studies, including mechanisms of amphibian regeneration. The book covers the use of autologous versus allogeneic cell sources, as well as various procedures used for cell isolation and cell pre-conditioning , such as cell sorting, biochemical and biophysical pre-conditioning, transfection and aggregation. It also presents cell modulation using growth factors, molecular factors, epigenetic approaches, changes in biophysical environment, cellular co-culture and other elements of the cellular microenvironment. The pathways of cell delivery are discussed with respect to specific clinical situations, including delivery of ex vivo manipulated cells via local and systemic routes, as well as activation and migration of endogenous reservoirs of reparative cells. The volume concludes with an in-depth discussion of the tracking of cells in vivo and their various regenerative activities inside the body, including differentiation, new tissue formation and actions on other cells by direct cell-to-cell communication and by secretion of biomolecules.
This book explores the latest data dealing with mechanosensitive channels research results. It was compiled by a group of internationally recognized scientists leading in the field of mechanosensitive ion channels or mechanically gated channels and signaling cascades research. Key problems of cell mechanobiology are also discussed. As a whole, the volume dwells on the major issues of mechanical stress influencing the ion channels and intracellular signaling pathways.