CLEC-2 and Syk in the megakaryocytic/platelet lineage are essential for development.
Blood
; 119(7): 1747-56, 2012 Feb 16.
Article
em En
| MEDLINE
| ID: mdl-22186994
ABSTRACT
The C-type lectin receptor CLEC-2 signals through a pathway that is critically dependent on the tyrosine kinase Syk. We show that homozygous loss of either protein results in defects in brain vascular and lymphatic development, lung inflation, and perinatal lethality. Furthermore, we find that conditional deletion of Syk in the hematopoietic lineage, or conditional deletion of CLEC-2 or Syk in the megakaryocyte/platelet lineage, also causes defects in brain vascular and lymphatic development, although the mice are viable. In contrast, conditional deletion of Syk in other hematopoietic lineages had no effect on viability or brain vasculature and lymphatic development. We show that platelets, but not platelet releasate, modulate the migration and intercellular adhesion of lymphatic endothelial cells through a pathway that depends on CLEC-2 and Syk. These studies found that megakaryocyte/platelet expression of CLEC-2 and Syk is required for normal brain vasculature and lymphatic development and that platelet CLEC-2 and Syk directly modulate lymphatic endothelial cell behavior in vitro.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Plaquetas
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Proteínas Tirosina Quinases
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Megacariócitos
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Linhagem da Célula
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Lectinas Tipo C
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Peptídeos e Proteínas de Sinalização Intracelular
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Crescimento e Desenvolvimento
Limite:
Animals
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Pregnancy
Idioma:
En
Ano de publicação:
2012
Tipo de documento:
Article