We are analyzing https://link.springer.com/article/10.1007/s00018-013-1350-0.

Title:
Fibronectin in tissue regeneration: timely disassembly of the scaffold is necessary to complete the build | Cellular and Molecular Life Sciences
Description:
Tissue injury initiates extracellular matrix molecule expression, including fibronectin production by local cells and fibronectin leakage from plasma. To benefit tissue regeneration, fibronectin promotes opsonization of tissue debris, migration, proliferation, and contraction of cells involved in the healing process, as well as angiogenesis. When regeneration proceeds, the fibronectin matrix is fully degraded. However, in a diseased environment, fibronectin clearance is often disturbed, allowing structural variants to persist and contribute to disease progression and failure of regeneration. Here, we discuss first how fibronectin helps tissue regeneration, with a focus on normal cutaneous wound healing as an example of complete tissue recovery. Then, we continue to argue that, although the fibronectin matrix generated following cartilage and central nervous system white matter (myelin) injury initially benefits regeneration, fibronectin clearance is incomplete in chronic wounds (skin), osteoarthritis (cartilage), and multiple sclerosis (myelin). Fibronectin fragments or aggregates persist, which impair tissue regeneration. The similarities in fibronectin-mediated mechanisms of frustrated regeneration indicate that complete fibronectin clearance is a prerequisite for recovery in any tissue. Also, they provide common targets for developing therapeutic strategies in regenerative medicine.
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Keywords {🔍}

google, scholar, pubmed, cas, fibronectin, cell, matrix, wound, healing, biol, tissue, cartilage, human, extracellular, res, neurosci, cells, regeneration, plasma, van, ffrenchconstant, homandberg, oligodendrocyte, baron, multiple, fragment, sclerosis, fragments, article, expression, osteoarthritis, effects, repair, mol, zhao, integrins, sci, dermatol, integrin, alpha, chronic, chem, activation, franklin, domain, induces, receptor, chondrolysis, precursor, research,

Topics {✒️}

cooh-terminal heparin-binding fragment month download article/chapter fibronectin-fragment-induced cartilage chondrolysis collagen fragment-induced anabolic lipopolysaccharide-induced oligodendrocyte injury 45-kda collagen-binding fragment cell-fibronectin matrix interactions mapk/erk 1/2-dependent signaling interferon beta-1b decreases transforming growth factor-beta1 extracellular matrix–cytoskeleton crosstalk platelet-derived growth factor �fibronectin-integrin imbalance disorder” fibronectin-eda promotes survival fibronectin dimers cross-linked wia baron streptozotocin-induced diabetic rats build review published vitronectin-induced microglial activation full-thickness skin wounds human intervertebral disc short-term catabolic effects multiple sclerosis lesions human adult astrocytes bone tissue healing oligodendrocyte progenitor cells cell adhesion assays interleukin-1-mediated pathway matrix metalloproteinase-9 expression basement membrane proteins tumor cell invasion van der heide extracellular matrix degradation oligodendrocyte precursor cells stromelysin gene expression fibronectin extracellular matrix privacy choices/manage cookies benefit tissue regeneration impair tissue regeneration extracellular matrix interferes extracellular matrix fibrils integrin-activating peptide author information authors scientific research nwo fibronectin polymerization regulates fibronectin fragment activation cs1 domain contributes beta subunit expression bebo bf jr human articular chondrocytes

Questions {❓}

Peters JH, Loredo GA, Benton HP (2002) Is osteoarthritis a “fibronectin-integrin imbalance disorder”?
Potential significance for multiple sclerosis?
Scanzello CR, Plaas A, Crow MK (2008) Innate immune system activation in osteoarthritis: is osteoarthritis a chronic wound?
Trapp BD, Nave KA (2008) Multiple sclerosis: an immune or neurodegenerative disorder?
Widgerow AD (2013) Chronic wounds - is cellular “reception” at fault?
Van Strien ME, Breve JJ, Fratantoni S, Schreurs MW, Bol JG, Jongenelen CA, Drukarch B, van Dam AM (2011) Astrocyte-derived tissue transglutaminase interacts with fibronectin: a role in astrocyte adhesion and migration?

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