# Pathway maps of platelet phenotype and function

> **NIH NIH R01** · OREGON HEALTH & SCIENCE UNIVERSITY · 2022 · $385,000

## Abstract

PROJECT SUMMARY
As the primary cellular mediators of hemostasis, platelets are optimized to limit bleeding through rapid
adhesion, secretion and aggregation responses at sites of endothelial injury. Platelets also adhere to
dysfunctional endothelium, where they secrete proinflammatory molecules and form aggregates with
leukocytes to progress vascular inflammation in a manner relevant to the pathogenesis of chronic diseases,
including atherosclerosis. Ongoing efforts aiming to understand and target platelet activities specific to disease
have characterized a spectrum of platelet functional phenotypes associated with inflammatory, thrombotic and
other conditions. Despite the identification of key molecular alterations that highlight differences between these
phenotypes, it remains unclear how different platelet phenotypes develop, how they should be defined, and,
ultimately, how they should be targeted. We hypothesize that platelet hemostatic, inflammatory and other
phenotypes are determined by the systematic activation of intracellular signaling pathways and effectors that
result in specific platelet functional outputs in response to physiological context. We aim to systematically
define intracellular signaling events that progress platelet adhesion (Aim 1), secretion (Aim 2) and aggregation
(Aim 3) in hemostatic programs and to determine how these responses mechanistically differ in the context of
vascular inflammation. We will engage these studies through the use of a high-throughput, proteomics-based
workflow that measures and maps intracellular signaling events and pathways underlying platelet function in
specific experimental and physiological contexts. We now use this set of proteomics, computational and cell
biological tools to build pathway maps intracellular signaling relations in platelet activation programs. In this
proposal, we use this first-in-class pathway mapping methodology together with other physiological and
systems biology tools to address how platelet signaling programs specify platelet phenotypes favoring
hemostatic and inflammatory responses. Ultimately, this work will generate knowledge as well as a conceptual
means to define and understand systems level mechanisms of platelet regulation in hemostasis as well as in
inflammation and the manifestation of disease.

## Key facts

- **NIH application ID:** 10378765
- **Project number:** 5R01HL146549-04
- **Recipient organization:** OREGON HEALTH & SCIENCE UNIVERSITY
- **Principal Investigator:** Joseph E Aslan
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $385,000
- **Award type:** 5
- **Project period:** 2019-04-01 → 2024-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10378765

## Citation

> US National Institutes of Health, RePORTER application 10378765, Pathway maps of platelet phenotype and function (5R01HL146549-04). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10378765. Licensed CC0.

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