Role of the extracellular matrix in morphogenesis
Cell Biology Section, CDBRB, National Institute of Dental and Craniofacial Research/NIH, 30 Convent Drive, MSC 4370, Bethesda, MD 20892, USA. Current Opinion in Biotechnology
(Impact Factor: 7.12).
11/2003; 14(5):526-32. DOI: 10.1016/j.copbio.2003.08.002
The extracellular matrix is a complex, dynamic and critical component of all tissues. It functions as a scaffold for tissue morphogenesis, provides cues for cell proliferation and differentiation, promotes the maintenance of differentiated tissues and enhances the repair response after injury. Various amounts and types of collagens, adhesion molecules, proteoglycans, growth factors and cytokines or chemokines are present in the tissue- and temporal-specific extracellular matrices. Tissue morphogenesis is mediated by multiple extracellular matrix components and by multiple active sites on some of these components. Biologically active extracellular matrix components may have use in tissue repair, regeneration and engineering, and in programming stem cells for tissue replacement.
Available from: Dayamon D Mathew
- "These scaffolds are naturally rich in collagen, elastin, glycosaminoglycans (GAGs), laminin and fibronectin on which the cells can migrate, attach and grow. In addition, many of the bioactive degradation products released from the graft at the site of the grafting mimic growth factors required for healing (Kleinman et al., 2003). The ECM is also known to aid angiogenesis by regulating the migration, proliferation and sustenance of endothelial cells (Raines, 2000). "
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ABSTRACT: An acellular cholecyst derived extracellular matrix (p-CEM) of porcine origin was prepared using anionic biological detergent. Healing potential of (p-CEM) was compared with commercially available collagen sheet (b-CS) and open wound (C) in full-thickness skin wounds in rats. Thirty six clinically healthy adult Sprague Dawley rats of either sex were randomly divided into three equal groups. Under general anesthesia, a full-thickness skin wound (20×20mm2) was produced on the dorsum of each rat. The defect in group I was kept as open wound and was taken as control. In group II, the defect was repaired with commercially available collagen sheet (b-CS). In group III, the defect was repaired with cholecyst derived extracellular matrix of bovine origin (p-CEM). Healing was evaluated on the basis of wound contraction, gross, hematological, immunological and histopathological observations. On critical analysis of the observed parameters it was found that p-CEM has healing potential and shown better healing response than commercially available collagen sheet to reconstruct full thickness skin wounds in rats.
Available from: Wolfgang Holnthoner
- "For instance, proteins of the extracellular matrix and the arrangement of tissue fibers have been proven to support cell migration and proliferation, including gene expression and cell–cell interactions   . Despite these obvious advantages, tissue engineering approaches using decellularized material are often limited due to batch-to-batch variations of the accessible allograft raw material . "
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ABSTRACT: Statement of significance:
In the US alone more than 1million vascular grafts are needed in clinical practice every year. Despite severe disadvantages, such as donor site morbidity, autologous grafting from the patient's own arteries or veins is regarded as the gold standard for vascular tissue repair. Besides, strategies based on synthetic or natural materials have shown limited success. Tissue engineering approaches based on decellularized tissues are regarded as a promising alternative to clinically used treatments to overcome the observed limitations. However, a source for supply of non-cadaver human allograft material would be favorable. Here, we established a decellularization method of vascular tissue from the human placenta chorionic plate, a suitable human tissue source of consistent quality. The decellularized human placenta vessels can be a potent graft material for future in vivo applications and furthermore might be a versatile tool for experimental studies on vascularization.
Available from: Gerald Burgstaller
- "Many of these annotations, however, are not based on direct experimental observations or have not been comprehensively tested in vivo. Developmental signaling pathways active in tissue repair, such as the TGF-b, Wnt, Shh, or Bmp pathways, which emanate from secreted morphogens and are regulated by interacting ECM components (Kleinman et al, 2003), are often deregulated in chronic lung diseases, potentially causing persistent pulmonary fibrosis (Fernandez & Eickelberg, 2012). Bleomycin-induced lung injury, which induces robust fibrogenesis 2 weeks after injury, is the most frequently used animal model of pulmonary fibrosis (Mouratis & Aidinis, 2011; Bauer et al, 2015). "
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ABSTRACT: The extracellular matrix (ECM) is a key regulator of tissue morpho-genesis and repair. However, its composition and architecture are not well characterized. Here, we monitor remodeling of the extra-cellular niche in tissue repair in the bleomycin-induced lung injury mouse model. Mass spectrometry quantified 8,366 proteins from total tissue and bronchoalveolar lavage fluid (BALF) over the course of 8 weeks, surveying tissue composition from the onset of inflammation and fibrosis to its full recovery. Combined analysis of proteome, secretome, and transcriptome highlighted post-transcriptional events during tissue fibrogenesis and defined the composition of airway epithelial lining fluid. To comprehensively characterize the ECM, we developed a quantitative detergent solu-bility profiling (QDSP) method, which identified Emilin-2 and colla-gen-XXVIII as novel constituents of the provisional repair matrix. QDSP revealed which secreted proteins interact with the ECM, and showed drastically altered association of morphogens to the insoluble matrix upon injury. Thus, our proteomic systems biology study assigns proteins to tissue compartments and uncovers their dynamic regulation upon lung injury and repair, potentially contributing to the development of anti-fibrotic strategies.
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