細胞外マトリクス

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 細胞間を満たす立体構造で、細胞外マトリックス等も表記される。「細胞外マトリクス」も「細胞外マトリックス」も、日本語英語的な表記である。「細胞外器質」「細胞外基質」「細胞間マトリクス」「細胞間マトリックス」等という表記もあり、バイオテクノロジーの分野での表記も必ずしも統一されてはいない。

美容医学における「細胞外マトリクス(細胞外マトリックス)」

 美容医学における「細胞外マトリクス(細胞外マトリックス)」とは、主に注射治療(メソセラピー)の方法で用いる場合の自家組織のinvivo幹細胞の活性惹起による再生を行なうための材料をいう。また、このような治療法を「細胞外マトリクス注射(細胞外マトリックス)」「細胞外マトリクス治療(細胞外マトリックス)」「細胞外マトリクス療法(細胞外マトリックス)」という。美容医学における材料としての「細胞外マトリクス(細胞外マトリックス)」ないし治療法としての「細胞外マトリクス注射(細胞外マトリックス)」「細胞外マトリクス治療(細胞外マトリックス)」「細胞外マトリクス療法(細胞外マトリックス)」を指して、「マトを使う」「マト注」等の用語を用いることがある。

細胞外マトリクス(細胞外マトリックス)による治療に対応しているクリニック(「相談のみ」のクリニックを含む)

国内外における細胞外マトリクス(細胞外マトリックス)による治療の運用

細胞外マトリクス(細胞外マトリックス)による治療は、国内外ともに、民間医療保険・公的医療保険のいずれにおいても、保険適用となることはほとんどない。そのため、一回の治療費が数十万円から数百万円に及ぶの普通となっており、一般にはほとんど普及していない。
高額な富裕層向け医療保険を販売する金融機関とバイオテクノロジーメーカーと提携した一部の海外のクリニックには、ある種の細胞外マトリクス(細胞外マトリックス)による治療を公表し、実施しているところもある。

細胞外マトリクス(細胞外マトリックス)と「多能性細胞外マトリクス(細胞外マトリックス)」

(細胞外マトリクス/細胞外マトリックス)による治療では、欠損した手の指・足の指、毛髪(毛芽及び毛包)、心筋機能、膀胱、腎臓機能の再生が確認されており、このような多様な再生能力の惹起を示す細胞外マトリクス(細胞外マトリックス)を、特に「多能性細胞外マトリクス(細胞外マトリックス)」という。
細胞外マトリクス(細胞外マトリックス)の製作調整のノウハウを有する研究医が、それぞれのプロトコルを確立しているが、それぞれのプロトコルの詳細は必ずしも公開されていない。

Pubmedにおける細胞外マトリクス(細胞外マトリックス)に関連する研究蓄積状況とクリニックにおける美容医学臨床治療における応用可能な症例

Abstract The extracellular matrix(細胞外マトリクス/細胞外マトリックス)consists of a complex mixture of structural and functional proteins and serves an important role in tissue and organ morphogenesis, maintenance of cell and tissue structure and function, and in the host response to injury. Xenogeneic and allogeneic extracellular matrix(細胞外マトリクス/細胞外マトリックス) has been used as a bioscaffold for the reconstruction of many different tissue types in both pre-clinical and human clinical studies. Common features of extracellular matrix(細胞外マトリクス/細胞外マトリックス)-associated tissue remodeling include extensive angiogenesis, recruitment of circulating progenitor cells, rapid scaffold degradation and constructive remodeling of damaged or missing tissues. The extracellular matrix(細胞外マトリクス/細胞外マトリックス)-induced remodeling response is a distinctly different phenomenon from that of scar tissue formation.

Abstract Much recent research has focused on the study of the expression of growth factor genes and on the identification of growth factor signaling mechanisms inside cells. However, growth factor signaling can also be regulated outside of cells by extracellular matrix extracellular(細胞外マトリクス/細胞外マトリックス) proteins and proteolytic enzymes. The ability of extracellular proteins to process complex information in the absence of new protein synthesis is illustrated in blood clotting and complement pathways. An increasing number of growth factors, including IGFs, FGFs, TGF-beta's, and HGF, have been found to associate with the extracellular matrix(細胞外マトリクス/細胞外マトリックス) proteins or with heparan sulfate. Rapid and localized changes in the activity of these factors can be induced by release from matrix storage and/or by activation of latent forms. These growth factors, in turn, control cell proliferation, differentiation, and synthesis and remodeling of the extracellular matrix(細胞外マトリクス/細胞外マトリックス). It is therefore likely that much of the information processing necessary for construction of complex multicellular organisms occurs in the extracellular environment. This suggests that extracellular matrix(細胞外マトリクス/細胞外マトリックス) plays a major role in the control of growth factor signaling for extracellular matrix therapy in clinic(クリニックでの細胞外マトリクス治療/細胞外マトリックス治療).
Abstract Repair of tissue after injury depends on the synthesis of a fibrous extracellular matrix(細胞外マトリクス/細胞外マトリックス) to replace lost or damaged tissue. Newly deposited extracellular matrix (細胞外マトリクス/細胞外マトリックス)is then re-modeled over time to emulate normal tissue. The extracellular matrix(細胞外マトリクス/細胞外マトリックス) directs repair by regulating the behavior of the wide variety of cell types that are mobilized to the damaged area in order to rebuild the tissue. Acute inflammation, re-epithelialization, and contraction all depend on cell-extracellular matrix (細胞外マトリクス/細胞外マトリックス)interactions and contribute to minimize infection and promote rapid wound closure. Matricellular proteins are up-regulated during wound healing where they modulate interactions between cells and the extracellular matrix(細胞外マトリクス/細胞外マトリックス) to exert control over events that are essential for efficient tissue repair. Here, we discuss how the extracellular matrix(細胞外マトリクス/細胞外マトリックス) changes during the stages of tissue repair, how matricellular(細胞外マトリクス/細胞外マトリックス) proteins affect cell-extracellular matrix (細胞外マトリクス/細胞外マトリックス)interactions, and how these proteins might be exploited for use therapeutically(細胞外マトリクス治療/細胞外マトリックス治療).
Abstract In the process of matrix assembly, multivalent extracellular matrix (細胞外マトリクス/細胞外マトリックス) proteins are induced to self-associate and to interact with other ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) proteins to form fibrillar networks. Matrix assembly is usually initiated by ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) glycoproteins binding to cell surface receptors, such as fibronectin (FN) dimers binding to α5ß1 integrin. Receptor binding stimulates FN self-association mediated by the N-terminal assembly domain and organizes the actin cytoskeleton to promote cell contractility. FN conformational changes expose additional binding sites that participate in fibril formation and in conversion of fibrils into a stabilized, insoluble form. Once assembled, the FN matrix impacts tissue organization by contributing to the assembly of other ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) proteins. Here, we describe the major steps, molecular interactions, and cellular mechanisms involved in assembling FN dimers into fibrillar matrix while highlighting important issues and major questions that require further investigation.
Abstract The extracellular matrix (細胞外マトリクス/細胞外マトリックス), and especially the connective tissue with its collagen, links tissues of the body together and plays an important role in the force transmission and tissue structure maintenance especially in tendons, ligaments, bone, and muscle. The ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) turnover is influenced by physical activity, and both collagen synthesis and degrading metalloprotease enzymes increase with mechanical loading. Both transcription and posttranslational modifications, as well as local and systemic release of growth factors, are enhanced following exercise. For tendons, metabolic activity, circulatory responses, and collagen turnover are demonstrated to be more pronounced in humans than hitherto thought. Conversely, inactivity markedly decreases collagen turnover in both tendon and muscle. Chronic loading in the form of physical training leads both to increased collagen turnover as well as, dependent on the type of collagen in question, some degree of net collagen synthesis. These changes will modify the mechanical properties and the viscoelastic characteristics of the tissue, decrease its stress, and likely make it more load resistant. Cross-linking in connective tissue involves an intimate, enzymatical interplay between collagen synthesis and ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) proteoglycan components during growth and maturation and influences the collagen-derived functional properties of the tissue. With aging, glycation contributes to additional cross-linking which modifies tissue stiffness. Physiological signaling pathways from mechanical loading to changes in ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) most likely involve feedback signaling that results in rapid alterations in the mechanical properties of the ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス). In developing skeletal muscle, an important interplay between muscle cells and the ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) is present, and some evidence from adult human muscle suggests common signaling pathways to stimulate contractile and ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) components. Unaccostumed overloading responses suggest an important role of ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) in the adaptation of myofibrillar(筋 線維) structures in adult muscle. Development of overuse injury in tendons involve morphological and biochemical changes including altered collagen typing and fibril size, hypervascularization zones, accumulation of nociceptive substances, and impaired collagen degradation activity. Counteracting these phenomena requires adjusted loading rather than absence of loading in the form of immobilization. Full understanding of these physiological processes will provide the physiological basis for understanding of tissue overloading and injury seen in both tendons and muscle with repetitive work and leisure time physical activity.
The impact of the extracellular matrix on inflammation(細胞外マトリクス/細胞外マトリックス) for extracellular matrix therapy(細胞外マトリクス治療/細胞外マトリックス治療).
Abstract The advent of in situ immunology and intravital analyses of leukocyte movement in tissues has drawn attention to the previously neglected extracellular matrix (細胞外マトリクス/細胞外マトリックス) and its role in modulating immune cell behaviour in inflamed tissues. The ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) exists in different biochemical and structural forms; both their individual components and three-dimensional ultrastructure impart specific signals to cells that modulate basic functions that are important for the early steps in inflammation, such as immune cell migration into inflamed tissues and immune cell differentiation. In chronically inflamed tissues, aberrant ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) expression and fragments of the ECM-extracellular matrix(細胞外マトリクス/細胞外マトリックス) that are derived from tissue-remodelling processes can influence immune cell activation and survival, thereby actively contributing to immune responses at these sites.