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  • 1
    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
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  • 2
    Online Resource
    Online Resource
    Externalized histones fuel pulmonary fibrosis via a platelet-macrophage circuit of TGFβ1 and IL-27
    Proceedings of the National Academy of Sciences ; 2023
    In:  Proceedings of the National Academy of Sciences Vol. 120, No. 40 ( 2023-10-03)
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 120, No. 40 ( 2023-10-03)
    Abstract: Externalized histones erupt from the nucleus as extracellular traps, are associated with several acute and chronic lung disorders, but their implications in the molecular pathogenesis of interstitial lung disease are incompletely defined. To investigate the role and molecular mechanisms of externalized histones within the immunologic networks of pulmonary fibrosis, we studied externalized histones in human and animal bronchoalveolar lavage (BAL) samples of lung fibrosis. Neutralizing anti-histone antibodies were administered in bleomycin-induced fibrosis of C57BL/6 J mice, and subsequent studies used conditional/constitutive knockout mouse strains for TGFβ and IL-27 signaling along with isolated platelets and cultured macrophages. We found that externalized histones (citH3) were significantly ( P 〈 0.01) increased in cell-free BAL fluids of patients with idiopathic pulmonary fibrosis (IPF; n = 29) as compared to healthy controls ( n = 10). The pulmonary sources of externalized histones were Ly6G + CD11b + neutrophils and nonhematopoietic cells after bleomycin in mice. Neutralizing monoclonal anti-histone H2A/H4 antibodies reduced the pulmonary collagen accumulation and hydroxyproline concentration. Histones activated platelets to release TGFβ1, which signaled through the TGFbRI/TGFbRII receptor complex on LysM + cells to antagonize macrophage-derived IL-27 production. TGFβ1 evoked multiple downstream mechanisms in macrophages, including p38 MAPK, tristetraprolin, IL-10, and binding of SMAD3 to the IL-27 promotor regions. IL-27RA-deficient mice displayed more severe collagen depositions suggesting that intact IL-27 signaling limits fibrosis. In conclusion, externalized histones inactivate a safety switch of antifibrotic, macrophage-derived IL-27 by boosting platelet-derived TGFβ1. Externalized histones are accessible to neutralizing antibodies for improving the severity of experimental pulmonary fibrosis.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.2215421120
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2023
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    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Immunization of hu-PBL–SCID mice and the rescue of human monoclonal Fab fragments through combinatorial libraries
    Springer Science and Business Media LLC ; 1992
    In:  Nature Vol. 355, No. 6357 ( 1992-1), p. 258-262
    Details
    In: Nature, Springer Science and Business Media LLC, Vol. 355, No. 6357 ( 1992-1), p. 258-262
    Type of Medium: Online Resource
    ISSN: 0028-0836 , 1476-4687
    URL: Article
    DOI: 10.1038/355258a0
    RVK:
    TA 1000
    RVK:
    UA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1992
    detail.hit.zdb_id: 120714-3
    detail.hit.zdb_id: 1413423-8
    SSG: 11
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  • 4
    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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    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
    Location Call Number Limitation Availability
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    Online Resource
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