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  • American Association for the Advancement of Science (AAAS)  (5)
  • Eming, Sabine A.  (5)
  • 1
    Online Resource
    Online Resource
    Engineering the Growth Factor Microenvironment with Fibronectin Domains to Promote Wound and Bone Tissue Healing
    American Association for the Advancement of Science (AAAS) ; 2011
    In:  Science Translational Medicine Vol. 3, No. 100 ( 2011-09-14)
    Details
    In: Science Translational Medicine, American Association for the Advancement of Science (AAAS), Vol. 3, No. 100 ( 2011-09-14)
    Abstract: Although growth factors naturally exert their morphogenetic influences within the context of the extracellular matrix microenvironment, the interactions among growth factors, their receptors, and other extracellular matrix components are typically ignored in clinical delivery of growth factors. We present an approach for engineering the cellular microenvironment to greatly accentuate the effects of vascular endothelial growth factor–A (VEGF-A) and platelet-derived growth factor–BB (PDGF-BB) for skin repair, and of bone morphogenetic protein–2 (BMP-2) and PDGF-BB for bone repair. A multifunctional recombinant fragment of fibronectin (FN) was engineered to comprise (i) a factor XIIIa substrate fibrin-binding sequence, (ii) the 9th to 10th type III FN repeat (FN III9-10) containing the major integrin-binding domain, and (iii) the 12th to 14th type III FN repeat (FN III12-14), which binds growth factors promiscuously, including VEGF-A165, PDGF-BB, and BMP-2. We show potent synergistic signaling and morphogenesis between α 5 β 1 integrin and the growth factor receptors, but only when FN III9-10 and FN III12-14 are proximally presented in the same polypeptide chain (FN III9-10/12-14). The multifunctional FN III9-10/12-14 greatly enhanced the regenerative effects of the growth factors in vivo in a diabetic mouse model of chronic wounds (primarily through an angiogenic mechanism) and in a rat model of critical-size bone defects (through a mesenchymal stem cell recruitment mechanism) at doses where the growth factors delivered within fibrin only had no significant effects.
    Type of Medium: Online Resource
    ISSN: 1946-6234 , 1946-6242
    URL: Article
    DOI: 10.1126/scitranslmed.3002614
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2011
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  • 2
    Online Resource
    Online Resource
    Inflammation and metabolism in tissue repair and regeneration
    American Association for the Advancement of Science (AAAS) ; 2017
    In:  Science Vol. 356, No. 6342 ( 2017-06-09), p. 1026-1030
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 356, No. 6342 ( 2017-06-09), p. 1026-1030
    Abstract: Tissue repair after injury is a complex, metabolically demanding process. Depending on the tissue’s regenerative capacity and the quality of the inflammatory response, the outcome is generally imperfect, with some degree of fibrosis, which is defined by aberrant accumulation of collagenous connective tissue. Inflammatory cells multitask at the wound site by facilitating wound debridement and producing chemokines, metabolites, and growth factors. If this well-orchestrated response becomes dysregulated, the wound can become chronic or progressively fibrotic, with both outcomes impairing tissue function, which can ultimately lead to organ failure and death. Here we review the current understanding of the role of inflammation and cell metabolism in tissue-regenerative responses, highlight emerging concepts that may expand therapeutic perspectives, and briefly discuss where important knowledge gaps remain.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.aam7928
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2017
    detail.hit.zdb_id: 128410-1
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    SSG: 11
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  • 3
    Online Resource
    Online Resource
    A common framework of monocyte-derived macrophage activation
    American Association for the Advancement of Science (AAAS) ; 2022
    In:  Science Immunology Vol. 7, No. 70 ( 2022-04-15)
    Details
    In: Science Immunology, American Association for the Advancement of Science (AAAS), Vol. 7, No. 70 ( 2022-04-15)
    Abstract: Monocytes infiltrating tissues in response to infection or inflammation rapidly differentiate into macrophages that can display a wide range of activation states. Using single-cell transcriptomics, Sanin et al . develop a framework for classifying macrophage activation states across different tissues and stimuli. On the basis of analysis of adipose tissue macrophages collected from mice infected with Listeria monocytogenes or the helminth Heligmosomoides polygyrus , the authors defined four activation paths including “phagocytic,” “inflammatory,” “oxidative stress,” and “remodeling” paths. Transient RELMα expression occurring independently of IL-4 signaling was a conserved feature of all early-infiltrating macrophages. This predictive framework was validated using a large-scale, integrated analysis of published transcriptomic data, highlighting that specific features of macrophage activation are conserved across a wide range of tissues and disease states (see the related Focus commentary by Loke et al .).
    Type of Medium: Online Resource
    ISSN: 2470-9468
    URL: Article
    DOI: 10.1126/sciimmunol.abl7482
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2022
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  • 4
    Online Resource
    Online Resource
    Wound repair and regeneration: Mechanisms, signaling, and translation
    American Association for the Advancement of Science (AAAS) ; 2014
    In:  Science Translational Medicine Vol. 6, No. 265 ( 2014-12-03)
    Details
    In: Science Translational Medicine, American Association for the Advancement of Science (AAAS), Vol. 6, No. 265 ( 2014-12-03)
    Abstract: The cellular and molecular mechanisms underpinning tissue repair and its failure to heal are still poorly understood, and current therapies are limited. Poor wound healing after trauma, surgery, acute illness, or chronic disease conditions affects millions of people worldwide each year and is the consequence of poorly regulated elements of the healthy tissue repair response, including inflammation, angiogenesis, matrix deposition, and cell recruitment. Failure of one or several of these cellular processes is generally linked to an underlying clinical condition, such as vascular disease, diabetes, or aging, which are all frequently associated with healing pathologies. The search for clinical strategies that might improve the body’s natural repair mechanisms will need to be based on a thorough understanding of the basic biology of repair and regeneration. In this review, we highlight emerging concepts in tissue regeneration and repair, and provide some perspectives on how to translate current knowledge into viable clinical approaches for treating patients with wound-healing pathologies.
    Type of Medium: Online Resource
    ISSN: 1946-6234 , 1946-6242
    URL: Article
    DOI: 10.1126/scitranslmed.3009337
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2014
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  • 5
    Online Resource
    Online Resource
    Cellular networks in wound healing
    American Association for the Advancement of Science (AAAS) ; 2018
    In:  Science Vol. 362, No. 6417 ( 2018-11-23), p. 891-892
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 362, No. 6417 ( 2018-11-23), p. 891-892
    Abstract: Restoration of tissue integrity and homeostasis after injury is fundamental to most organisms. Throughout evolution, there is diversity in whether the healing response replaces the damaged tissue through regeneration or by depositing collagenous connective tissue, defined as fibrosis. The molecular basis that underlies the repair response is complex. The postnatal decline of regenerative capacity in mammals as well as the regenerative heterogeneity among diverse organs is an unresolved obstacle in medicine. Limited fibrosis to temporarily stabilize newly forming tissue is important for healing but ultimately impairs tissue function. Disorders characterized by excessive fibrosis—including interstitial lung disease; fibrosis of the liver or kidney; sclerosing skin diseases; and localized fibrotic manifestations associated with, for example, late stage venous insufficiency, skin fragility disorders, trauma, or cancer—contribute considerably to patient discomfort and morbidity as well as high numbers of deaths worldwide. Nonetheless, progression in the development of antifibrotic therapeutics is slow ( 1 ). On page 909 of this issue, Shook et al. ( 2 ) identify a critical role of fibroblast and immune cell heterogeneity and communication in promoting efficient skin wound healing. These findings add to the understanding of fibrosis and could guide us toward better treatments for fibrosing diseases.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.aav5542
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2018
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    SSG: 11
    Location Call Number Limitation Availability
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