KFU. Card publication. Red blood cell aggregation within a blood clot causes platelet-independent clot shrinkage.

KAZAN
FEDERAL UNIVERSITY

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RED BLOOD CELL AGGREGATION WITHIN A BLOOD CLOT CAUSES PLATELET-INDEPENDENT CLOT SHRINKAGE.

Form of presentation

Articles in international journals and collections

Year of publication

2025

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Authors, employees of KFU

Khismatullin Rafael Rafikovich, author

Bibliographic description in the original language

Peshkova, A. D., Rednikova, E. K., Khismatullin, R. R., Kim, O. V., Muzykantov, V. R., Purohit, P. K., Litvinov, R. I., & Weisel, J. W. (2025). Red blood cell aggregation within a blood clot causes platelet-independent clot shrinkage. Blood advances, 9(14), 3418–3428. https://doi.org/10.1182/bloodadvances.2024015533

Annotation

Platelet-driven blood clot contraction (retraction) is important for hemostasis and thrombosis. RBCs occupy about half of the clot volume, but their possible active contribution to contraction is unknown. The work was aimed at elucidating the ability of RBCs to promote clot shrinkage. To distinguish effects of platelets and RBCs, we formed thrombin-induced clots from reconstituted human samples containing platelet-free plasma and platelet-depleted RBCs, followed by tracking the clot size. The clots before and after RBC-induced shrinkage were analyzed using histology and scanning electron microscopy. Tension developed in the RBC-containing plasma clots was measured with rheometry and theoretical modeling was used to elucidate the clot shrinkage mechanisms. Platelet-depleted clots formed in the presence of RBCs exhibited >20% volume shrinkage within one hour. This process was insensitive to blebbistatin, latrunculin A, and abciximab. At a higher RBC count clot shrinkage increased, whereas in the absence of RBCs no plasma clot shrinkage was observed. At low platelet counts RBCs stimulated clot contraction proportionately to the platelet level. Inside the shrunken clots, RBCs formed aggregates. The average tensile force per one RBC was ~120?100 pN. Clots from purified fibrinogen formed in the presence of RBCs did not change in size, but underwent shrinkage in the presence of osmotically active dextran. Blood clot shrinkage can be caused by RBCs alone and this effect is due to the RBC aggregation driven mainly by osmotic depletion. The RBC-induced clot shrinkage may reinforce platelet-driven blood clot contraction and promote clot compaction when there are few and/or dysfunctional platelets.

Keywords

RBCs, RBC aggregation, blood clotting, blood clot contraction

The name of the journal

Blood Advances

URL

https://ashpublications.org/bloodadvances/article/9/14/3418/536731/Red-blood-cell-aggregation-within-a-blood-clot

Please use this ID to quote from or refer to the card

https://repository.kpfu.ru/eng/?p_id=313830&p_lang=2

Resource files

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F_blooda_adv_2024_015533_main.pdf	4,54	pdf	show / download

Full metadata record

Field DC	Value	Language
dc.contributor.author	Khismatullin Rafael Rafikovich	ru_RU
dc.date.accessioned	2025-01-01T00:00:00Z	ru_RU
dc.date.available	2025-01-01T00:00:00Z	ru_RU
dc.date.issued	2025	ru_RU
dc.identifier.citation	Peshkova, A. D., Rednikova, E. K., Khismatullin, R. R., Kim, O. V., Muzykantov, V. R., Purohit, P. K., Litvinov, R. I., & Weisel, J. W. (2025). Red blood cell aggregation within a blood clot causes platelet-independent clot shrinkage. Blood advances, 9(14), 3418–3428. https://doi.org/10.1182/bloodadvances.2024015533	ru_RU
dc.identifier.uri	https://repository.kpfu.ru/eng/?p_id=313830&p_lang=2	ru_RU
dc.description.abstract	Blood Advances	ru_RU
dc.description.abstract	Platelet-driven blood clot contraction (retraction) is important for hemostasis and thrombosis. RBCs occupy about half of the clot volume, but their possible active contribution to contraction is unknown. The work was aimed at elucidating the ability of RBCs to promote clot shrinkage. To distinguish effects of platelets and RBCs, we formed thrombin-induced clots from reconstituted human samples containing platelet-free plasma and platelet-depleted RBCs, followed by tracking the clot size. The clots before and after RBC-induced shrinkage were analyzed using histology and scanning electron microscopy. Tension developed in the RBC-containing plasma clots was measured with rheometry and theoretical modeling was used to elucidate the clot shrinkage mechanisms. Platelet-depleted clots formed in the presence of RBCs exhibited >20% volume shrinkage within one hour. This process was insensitive to blebbistatin, latrunculin A, and abciximab. At a higher RBC count clot shrinkage increased, whereas in the absence of RBCs no plasma clot shrinkage was observed. At low platelet counts RBCs stimulated clot contraction proportionately to the platelet level. Inside the shrunken clots, RBCs formed aggregates. The average tensile force per one RBC was ~120?100 pN. Clots from purified fibrinogen formed in the presence of RBCs did not change in size, but underwent shrinkage in the presence of osmotically active dextran. Blood clot shrinkage can be caused by RBCs alone and this effect is due to the RBC aggregation driven mainly by osmotic depletion. The RBC-induced clot shrinkage may reinforce platelet-driven blood clot contraction and promote clot compaction when there are few and/or dysfunctional platelets.	ru_RU
dc.language.iso	ru	ru_RU
dc.subject	RBCs	ru_RU
dc.subject	RBC aggregation	ru_RU
dc.subject	blood clotting	ru_RU
dc.subject	blood clot contraction	ru_RU
dc.title	Red blood cell aggregation within a blood clot causes platelet-independent clot shrinkage.	ru_RU
dc.type	Articles in international journals and collections	ru_RU