COVID-19: the vasculature unleashed.
Ontology highlight
ABSTRACT:
SUBMITTER: Teuwen LA
PROVIDER: S-EPMC7240244 | biostudies-literature | 2020 Jul
REPOSITORIES: biostudies-literature
Publications
COVID-19: the vasculature unleashed.
Teuwen Laure-Anne LA Geldhof Vincent V Pasut Alessandra A Carmeliet Peter P
Nature reviews. Immunology 20200701 7
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Project description:Aims: SARS-CoV-2 infection causes COVID-19, which in severe cases evokes life-threatening acute respiratory distress syndrome (ARDS). Transcriptome signatures and the functional relevance of non-vascular cell types (e.g. immune and epithelial cells) in COVID-19 are becoming increasingly evident. However, despite its known contribution to vascular inflammation, recruitment/invasion of immune cells, vascular leakage and perturbed hemostasis in the lungs of severe COVID-19 patients, an in-depth interrogation of the endothelial cell (EC) compartment in lethal COVID-19 is lacking. Moreover, progressive fibrotic lung disease represents one of the complications of COVID-19 pneumonia and ARDS. Analogous features between idiopathic pulmonary fibrosis (IPF) and COVID-19 suggest partial similarities in their pathophysiology, yet, a head-to-head comparison of pulmonary cell transcriptomes between both conditions has not been implemented to date.
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Project description:In this contribution we present reactivity studies of a rare example of a titanium salt, in the form of [μ2-K(OEt2)]2[(PN)2Ti[triple bond, length as m-dash]N]2 (1) (PN- = N-(2-(diisopropylphosphino)-4-methylphenyl)-2,4,6-trimethylanilide) to produce a series of imide moieties including rare examples such as methylimido, borylimido, phosphonylimido, and a parent imido. For the latter, using various weak acids allowed us to narrow the pK a range of the NH group in (PN)2Ti[triple bond, length as m-dash]NH to be between 26-36. Complex 1 could be produced by a reductively promoted elimination of N2 from the azide precursor (PN)2TiN3, whereas reductive splitting of N2 could not be achieved using the complex (PN)2Ti[double bond, length as m-dash]N[double bond, length as m-dash]N[double bond, length as m-dash]Ti(PN)2 (2) and a strong reductant. Complete N-atom transfer reactions could also be observed when 1 was treated with ClC(O)tBu and OCCPh2 to form NCtBu and KNCCPh2, respectively, along with the terminal oxo complex (PN)2Ti[triple bond, length as m-dash]O, which was also characterized. A combination of solid state 15N NMR (MAS) and theoretical studies allowed us to understand the shielding effect of the counter cation in dimer 1, the monomer [K(18-crown-6)][(PN)2Ti[triple bond, length as m-dash]N], and the discrete salt [K(2,2,2-Kryptofix)][(PN)2Ti[triple bond, length as m-dash]N] as well as the origin of the highly downfield 15N NMR resonance when shifting from dimer to monomer to a terminal nitride (discrete salt). The upfield shift of 15Nnitride resonance in the 15N NMR spectrum was found to be linked to the K+ induced electronic structural change of the titanium-nitride functionality by using a combination of MO analysis and quantum chemical analysis of the corresponding shielding tensors.
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