Schematic of the effects of interleukin (IL)1-beta/IL1R1 on megakaryocyte and platelet function. A high fat diet will cause megakaryocytes to produce platelets with an increase in both inflammatory and thrombotic genes. IL1-beta in circulation as a result of increased body weight will bind IL1R1 on megakaryocytes. This interaction leads to the activation of the nuclear factor (NF)kB, PI3K/Akt, and mitogen activated protein kinase (MAPK) (ERK and p38) pathways. As a result, there is an increase in megakarycoyte maturation, including increased adhesion, increases in ploidy, and increases in mRNA production of inflammatory and thrombotic genes. IL1-beta can also bind IL1R1 on platelets and either enhance aggregation induced by agonists or promote adhesion and heterotypic aggregate formation. Some of the data used to create the pathway was generated in mouse (noted in pathway), however the pathway represents human homologs of those genes. Proteins on this pathway have targeted assays available via the [https://assays.cancer.gov/available_assays?wp_id=WP2865 CPTAC Assay Portal]

Authors

Kristina Hanspers , Marianthi Kalafati , Jonathan Mlius , Andika Tan , Susan Coort , and Egon Willighagen

Cited In

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Organism

Homo sapiens

Communities

Diseases

Annotations

Disease Ontology: overnutrition obesity

Pathway Ontology: obesity pathway interleukin-1 signaling pathway

Participants

References

1. Beaulieu LM, Lin E, Mick E, Koupenova M, Weinberg EO, Kramer CD, et al. Interleukin 1 receptor 1 and interleukin 1β regulate megakaryocyte maturation, platelet activation, and transcript profile during inflammation in mice and humans. Arterioscler Thromb Vasc Biol. 2014 Mar;34(3):552–64. PubMed Europe PMC Scholia