Wissenschaftliche Gesellschaft Freiburg

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    Restoring genetic diversity to facilitate the implementation of the EU Nature Restoration Law

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    Governments and economic blocs are recognising that the world faces a biodiversity crisis. The restoration of biodiversity to the levels prior to widespread human induced damage has been incorporated as a crucial component of conservation in the Global Biodiversity Framework of the Convention of Biological Diversity. The Nature Restoration Law (NRL) forms part of the European Union's response and after its adoption by the European Parliament and the Council of the European Union, it has formally become the Nature Restoration Regulation (NRR). The NRL aims to play a role in restoring ecosystems, habitats and species but does not expressly include genetic diversity, the third biodiversity component. Considering genetic diversity in strategic biodiversity planning is important to help nature adapt to rapid anthropogenic change. We have reviewed the text of the NRL and note opportunities to incorporate genetic diversity in National Restoration Plans to augment its implementation. In particular, genetic diversity assessments are well aligned with the NRL's aspiration to enhance connectivity, and genetic indicators can assess the effectiveness of its implementation. Here we give examples where restoration has incorporated genetic diversity to ensure long term wide-reaching success. This is of relevance beyond the NRL and applies generally to policy for nature restoration efforts globally, especially those related to the Global Biodiversity Framework

    Choroidal neovascularization is suppressed with activation of TREM2 in mononuclear phagocytes - brief report

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    BACKGROUND:Mononuclear phagocytes contribute to pathological angiogenesis in age-related macular degeneration, a leading worldwide cause of visual impairment. However, the mechanisms that orchestrate the functions of mononuclear phagocytes remain poorly understood. TREM2 (triggering receptor on myeloid cells 2) has been shown to be crucial for the activation of mononuclear phagocytes in atherosclerosis, fatty liver disease, and Alzheimer disease. The objective of this study was to investigate the role of TREM2 in pathological angiogenesis in age-related macular degeneration.METHODS:C57BL/6J and Trem2 knockout mice were subjected to laser-induced choroidal neovascularization, a model of choroidal neovascular age-related macular degeneration. Purified bovine sulfatide and agonist anti-TREM2 antibody was used to activate TREM2 signaling. The expression of TREM2 or downstream signals were assessed with immunohistochemistry or real-time quantitative PCR. In vitro murine macrophage RAW264.7 cells were used to investigate the direct impact of sulfatide on inflammatory and phagocytic responses.RESULTS:We found that pharmacological activation of TREM2 suppressed laser-induced choroidal neovessel formation. The activation of TREM2 in mononuclear phagocytes suppressed TNF (tumor necrosis factor) and subsequently promoted phagocytosis.CONCLUSIONS:These findings demonstrate that activation of TREM2 in mononuclear phagocytes suppresses the proinflammatory response, promotes phagocytosis, and impedes choroidal neovessel formation. Our study provides insight into the critical role of TREM2 in pathological angiogenesis

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