Collagens are the most abundant proteins in mammals. The collagen family comprises 28 members that contain at least one triple-helical domain. Collagens are deposited in the extracellular matrix where most of them form supramolecular assemblies. Four collagens are type II membrane proteins that also exist in a soluble form released from the cell surface by shedding. Collagens play structural roles and contribute to mechanical properties, organization, and shape of tissues. They interact with cells via several receptor families and regulate their proliferation, migration, and differentiation. Some collagens have a restricted tissue distribution and hence specific biological functions.

The Collagen Family

The extracellular matrix in development and morphogenesis: a dynamic view.

Significance: Fibroblasts play a critical role in normal wound healing. Various extracellular matrix (ECM) components, including collagens, fibrin, fibronectin, proteoglycans, glycosaminoglycans, and matricellular proteins, can be considered potent protagonists of fibroblast survival, migration, and metabolism. Recent Advances: Advances in tissue culture, tissue engineering, and ex vivo models have made the examination and precise measurements of ECM components in wound healing possible. Likewise, the development of specific transgenic animal models has created the opportunity to characterize the role of various ECM molecules in healing wounds. In addition, the recent characterization of new ECM molecules, including matricellular proteins, dermatopontin, and FACIT collagens (Fibril-Associated Collagens with Interrupted Triple helices), further demonstrates our cursory knowledge of the ECM in coordinated wound healing. Critical Issues: The manipulation and augmentation of ECM components in the healing wound is emerging in patient care, as demonstrated by the use of acellular dermal matrices, tissue scaffolds, and wound dressings or topical products bearing ECM proteins such as collagen, hyaluronan (HA), or elastin. Once thought of as neutral structural proteins, these molecules are now known to directly influence many aspects of cellular wound healing. Future Directions: The role that ECM molecules, such as CCN2, osteopontin, and secreted protein, acidic and rich in cysteine, play in signaling homing of fibroblast progenitor cells to sites of injury invites future research as we continue investigating the heterotopic origin of certain populations of fibroblasts in a healing wound. Likewise, research into differently sized fragments of the same polymeric ECM molecule is warranted as we learn that fragments of molecules such as HA and tenascin-C can have opposing effects on dermal fibroblasts.

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Extracellular Matrix and Dermal Fibroblast Function in the Healing Wound

Biologics for tendon repair.

The intrinsic pathogenetic mechanisms of tendinopathies are largely unknown and whether inflammation or degeneration has the prominent role is still a matter of debate. Assuming that there is a continuum from physiology to pathology, overuse may be considered as the initial disease factor; in this context, microruptures of tendon fibers occur and several molecules are expressed, some of which promote the healing process, while others, including inflammatory cytokines, act as disease mediators. Neural in-growth that accompanies the neovessels explains the occurrence of pain and triggers neurogenic-mediated inflammation. It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies.

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Pathogenesis of tendinopathies: inflammation or degeneration?

Type XIV Collagen Regulates Fibrillogenesis: PREMATURE COLLAGEN FIBRIL GROWTH AND TISSUE DYSFUNCTION IN NULL MICE*

Dysfunctional tendon collagen fibrillogenesis in collagen VI null mice.

Purpose. The term tendinopathy describes non-ruptured tendon injuries. While several important studies have evaluated the aetiology, pathogenesis, and treatment of this common condition, further study is needed. Several animal models, which allow for full tissue evaluation on different organizational levels and stages of disease, have been used to investigate tendinopathy.Method. A literature review was conducted to identify and evaluate animal models that have been developed and used to study the aetiology and pathology of tendinopathy.Results. Animal models of tendinopathy fit into two general categories based on the mode of injury application: (i) models that induce tendinopathy through a change in the mechanical environment, and (ii) models that induce tendinopathy through a chemical agent. The cost, difficulty, invasiveness, reproducibility and time required to induce injury in these models varies. Mechanically-induced models are beneficial since they induce injury through repetitive mechanical loadi...

Animal models of tendinopathy.

During post-natal development, tendons undergo a well orchestrated process whereby extensive structural and compositional changes occur in synchrony to produce a normal tissue. Conversely, during the repair response to injury, structural and compositional changes occur, but in this case, a mechanically inferior tendon is produced. As a result, the process of development has been postulated as a potential paradigm through which improved adult tissue healing may occur. In this study we measured the mechanical, compositional, and structural properties in the post-natal mouse Achilles tendon at 4, 7, 10, 14, 21, and 28 days old. Throughout post-natal development, the mechanical properties, collagen content, fibril diameter mean, and fibril diameter standard deviation increased. Biglycan expression decreased and decorin expression and fiber organization were unchanged. This study provides a new mouse model that can be used to quantitatively examine mechanical development, as well as compositional and structural changes and biological mechanisms, during post-natal tendon development. This model is advantageous due to the large number of genetically modified mice and commercially available assays that are not available in other animal models. A mouse model therefore allows future mechanistic studies to build on this work.

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Heather L. Ansorge

Papers

Type XIV Collagen Regulates Fibrillogenesis: PREMATURE COLLAGEN FIBRIL GROWTH AND TISSUE DYSFUNCTION IN NULL MICE*

Dysfunctional tendon collagen fibrillogenesis in collagen VI null mice.

Animal models of tendinopathy.

Mechanical, compositional, and structural properties of the post-natal mouse Achilles tendon.

Autologous fat processing via the Revolve system: quality and quantity of fat retention evaluated in an animal model.