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Comment
. 2022 May;20(5):1073-1076.
doi: 10.1111/jth.15683.

Another piece of knowledge in the puzzle of procoagulant COAT platelets

Alessandro Aliotta  1 , Lorenzo Alberio  1
Affiliations
Comment

Another piece of knowledge in the puzzle of procoagulant COAT platelets

Alessandro Aliotta et al. J Thromb Haemost. 2022 May.

Erratum in

  • Corrigendum.
    [No authors listed] [No authors listed] J Thromb Haemost. 2022 Aug;20(8):1941. doi: 10.1111/jth.15783. J Thromb Haemost. 2022. PMID: 35859287 Free PMC article. No abstract available.
No abstract available

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Conflict of interest statement

The authors have no conflict of interest.

Figures

FIGURE 1
FIGURE 1
Agonist‐dependent platelet activation phenotypes. Platelet activation by thrombin or convulxin/collagen as single agonists induces a moderate increase in cytosolic calcium ([Ca2+]cyt) and “typical” endpoints, such as activation of the fibrinogen receptor integrin αIIbβ3 and granule secretion. Under these conditions, only minimal expression of negatively charged phospholipids and no externalization of cytosolic FXIII‐A are observed. Calcium ionophore is able to induce very high [Ca2+]cyt, thus mediating externalization of phosphatidylserine. However, no cytosolic FXIII‐A is present at the platelet surface. The strong activation with convulxin‐plus‐thrombin generates a subpopulation of procoagulant COAT platelets, which begins to differentiate from aggregating ones about 2 min after activation. Differentiation between COAT and non‐COAT platelets relies on the action of the sodium‐calcium exchanger (NCX). Non‐COAT platelets use forward‐mode NCX, pumping calcium out of the platelet cytosol and moving sodium in, whereas COAT platelets rely on reverse NCX function, which pumps additional calcium into the cytosol, by extruding sodium. The COAT platelet subpopulation progressively downregulates activated αIIbβ3, depolarizes mitochondria, reaches sustained and elevated [Ca2+]cyt resulting in surface expression of substantial quantities of phosphatidylserine to eventually assemble a functional prothrombinase complex, and retains on its surface α‐granule proteins (in a serotonin‐ and transglutaminase‐dependent mechanism) as well as cytosolic FXIII‐A. According to the publication by Somodi et al., surface externalization of cytosolic FXIII‐A depends on high [Ca2+]cyt and a functioning RhoA. This figure was created using templates from Servier Medical Art (CC BY 3.0 license). COAT, collagen‐and‐thrombin‐activated; F, factor.
See this image and copyright information in PMC

Comment on

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