Inhibition of transcription factor NFAT activity in activated platelets enhances their aggregation and exacerbates gram-negative bacterial septicemia

Valentina Poli
Harvard Medical School
December 20, 2021
Immunity
https://pubmed.ncbi.nlm.nih.gov/34995475

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/34995475

Research summary

This study investigates how NFAT transcription factors in platelets regulate immune and thrombotic responses during sepsis. Using the iNFATuation mouse model, the authors showed that platelet-specific inhibition of NFAT increases platelet aggregation, promotes neutrophil extracellular trap (NET) formation, and worsens outcomes in gram-negative septicemia.

Key outcome of the study

NFAT inhibition in platelets leads to excessive aggregation and immune activation, exacerbating sepsis, and revealing a non-transcriptional regulatory role for NFAT in platelets.

Mouse model

iNFATuation mouse model with Cre-inducible expression of VIVIT peptide inserted into the Rosa26 locus using FLEx technology; activated in platelets via Pf4-Cre.

TARGET:
Nfatc1, Nfatc2, Nfatc3, Nfatc4
NFAT1, NFAT2, NFAT3, NFAT4

Keywords

Sepsis, Platelet activation, NFAT signaling, Inflammation, NETs, Thrombosis

Technical specifications

Knockin, Rosa26 locus, FLEx technology, Cre-inducible, Platelet-specific expression, VIVIT peptide

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