Not simply misshapen red cells: multimolecular and cellular events in sickle vaso-occlusion
Gregory M. Vercellotti, John D. Belcher
Gregory M. Vercellotti, John D. Belcher
Published March 18, 2014
Citation Information: J Clin Invest. 2014;124(4):1462-1465. https://doi.org/10.1172/JCI75238.
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Commentary

Not simply misshapen red cells: multimolecular and cellular events in sickle vaso-occlusion

Abstract

Thromboinflammatory diseases result from the interactions of vascular endothelial cells, inflammatory cells, and platelets with cellular adhesion molecules, plasma proteins, and lipids. Tipping the balance toward a prothrombotic, proinflammatory phenotype results from multicellular activation signals. In this issue of the JCI, Li et al. explore the regulation of heterotypic neutrophil-platelet contacts in response to TNF-α–induced venular inflammation with relevance to sickle cell disease (SCD).

Authors

Gregory M. Vercellotti, John D. Belcher

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Figure 1

Histology of a venule in the dorsal skin of transgenic sickle mice after 1 hour of hypoxia and 1 hour of reoxygenation.

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Histology of a venule in the dorsal skin of transgenic sickle mice after...
Dorsal skin samples were taken for histological analysis after S+S-Antilles sickle mice were exposed to 1 hour of hypoxia and 1 hour of reoxygenation. Skin samples were fixed overnight in formalin, cut into 5-μm sections, embedded in paraffin, mounted on slides, and stained with hematoxylin and eosin before microscopic examination. The image shows a venule with a suspected vascular obstruction. White arrowheads point to leukocytes that appear to be adherent to the vascular endothelium, and white arrows point to misshapen rbcs inside the venule. Reprinted with permission from American Journal of Hematology (24).