@article{RommelMildeEberleetal.2020,
  author    = {Rommel, Marcel G. E. and Milde, Christian and Eberle, Regina and Schulze, Harald and Modlich, Ute},
  title     = {Endothelial-platelet interactions in influenza-induced pneumonia: A potential therapeutic target},
  series = {Anatomia, Histologia, Embryologia},
  volume    = {49},
  journal   = {Anatomia, Histologia, Embryologia},
  number    = {5},
  doi       = {10.1111/ahe.12521},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-213610},
  pages     = {606 -- 619},
  year      = {2020},
  abstract  = {Every year, influenza viruses spread around the world, infecting the respiratory systems of countless humans and animals, causing illness and even death. Severe influenza infection is associated with pulmonary epithelial damage and endothelial dysfunction leading to acute lung injury (ALI). There is evidence that an aggressive cytokine storm and cell damage in lung capillaries as well as endothelial/platelet interactions contribute to vascular leakage, pro-thrombotic milieu and infiltration of immune effector cells. To date, treatments for ALI caused by influenza are limited to antiviral drugs, active ventilation or further symptomatic treatments. In this review, we summarize the mechanisms of influenza-mediated pathogenesis, permissive animal models and histopathological changes of lung tissue in both mice and men and compare it with histological and electron microscopic data from our own group. We highlight the molecular and cellular interactions between pulmonary endothelium and platelets in homeostasis and influenza-induced pathogenesis. Finally, we discuss novel therapeutic targets on platelets/endothelial interaction to reduce or resolve ALI.},
  language  = {en}
}
@article{PollittPoulterGitzetal.2014,
  author    = {Pollitt, Alice Y. and Poulter, Natalie S. and Gitz, Eelo and Navarro-Nu{\~n}ez, Leyre and Wang, Ying-Jie and Hughes, Craig E. and Thomas, Steven G. and Nieswandt, Bernhard and Douglas, Michael R. and Owen, Dylan M. and Jackson, David G. and Dustin, Michael L. and Watson, Steve P.},
  title     = {Syk and Src Family Kinases Regulate C-type Lectin Receptor 2 (CLEC-2)-mediated Clustering of Podoplanin and Platelet Adhesion to Lymphatic Endothelial Cells*},
  series = {The Journal of Biological Chemistry},
  volume    = {289},
  journal   = {The Journal of Biological Chemistry},
  number    = {52},
  doi       = {10.1074/jbc.M114.584284},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-120770},
  pages     = {35695-710},
  year      = {2014},
  abstract  = {The interaction of CLEC-2 on platelets with Podoplanin on lymphatic endothelial cells initiates platelet signalling events that are necessary for prevention of blood-lymph mixing during development. In the present study, we show that CLEC-2 signalling via Src family and Syk tyrosine kinases promotes platelet adhesion to primary mouse lymphatic endothelial cells at low shear. Using supported lipid bilayers containing mobile Podoplanin, we further show that activation of Src and Syk in platelets promotes clustering of CLEC-2 and Podoplanin. Clusters of CLEC-2-bound Podoplanin migrate rapidly to the centre of the platelet to form a single structure. Fluorescence life-time imaging demonstrates that molecules within these clusters are within 10 nm of one another and that the clusters are disrupted by inhibition of Src and Syk family kinases. CLEC-2 clusters are also seen in platelets adhered to immobilised Podoplanin using direct stochastic optical reconstruction microscopy (dSTORM). These findings provide mechanistic insight by which CLEC-2 signalling promotes adhesion to Podoplanin and regulation of Podoplanin signalling thereby contributing to lymphatic vasculature development.},
  language  = {en}
}