Modulation of megakaryopoiesis and platelet production during inflammation.

Abstract:

:Megakaryocytes (MKs) are widely known as the progenitor cells of platelets. These large, polyploid cells are a derivative of the hematopoietic stem cell (HSC), and reside in the bone marrow, lining blood vessel walls where they release their platelet progeny into circulation. Although little is known about how MKs differ under various environmental stressors, both chronic and acute inflammation alter the differentiation and molecular content of MKs. Furthermore, evidence suggests that the release of inflammatory cytokines may induce MK rupture and rapid release of platelets as a mechanism to quickly replenish diminished platelet counts in response to inflammation. Similarities between MKs and their close relatives, white blood cells, have introduced the notion that MKs may play a role in combating infection by engulfing and presenting antigens, and passing this information to circulating platelets. In addition, MKs exposed to varying bone marrow environments produce different platelets which enter circulation primed to respond to and combat inflammation, infection, or injury. This review focuses on how inflammation alters MK production, maturation, and platelet production. In addition, it introduces the idea that inflammation reprograms MKs to create different, more pathogenic platelets and leads them to take on different roles as responders to deleterious conditions. In the future, studies determining how platelets are altered in disease states may lead to novel MK- and platelet-based therapeutic targets to mitigate inflammation-related morbidity and mortality.

journal_name

Thromb Res

journal_title

Thrombosis research

authors

Couldwell G,Machlus KR

doi

10.1016/j.thromres.2019.05.008

subject

Has Abstract

pub_date

2019-07-01 00:00:00

pages

114-120

eissn

0049-3848

issn

1879-2472

pii

S0049-3848(19)30243-9

journal_volume

179

pub_type

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