# Endothelial Glycocalyx Disintegrity: Repairing the Damage caused by Trauma-Hemorrhage

> **NIH NIH R35** · UNIVERSITY OF ALABAMA AT BIRMINGHAM · 2020 · $340,101

## Abstract

PROJECT SUMMARY/ABSTRACT
The aim of this R35 application is to develop a high quality, translational research program in inflammation-
induced endothelial damage and organ dysfunction. Dysregulation of microvascular function contributes to the
pathophysiology of indirect organ injury after trauma. In particular, damage to the endothelial glycocalyx occurs
within minutes of traumatic injury and is associated with increased microvascular permeability resulting in multi-
organ failure and increased mortality. Strategies that attenuate glycocalyx disintegrity by preventing its cleavage
and/or facilitating its repair hold significant promise for minimizing microvascular dysfunction and post-traumatic
organ injury. The long-term objective of our research program is to establish basic science and translational
studies that focus on the identification of novel therapeutic targets that will (1) prevent glycocalyx damage, (2)
repair glycocalyx integrity or (3) inhibit dysregulation of endothelial cell permeability that occurs as a result of
glycocalyx disintegrity. The specific programmatic areas of focus will include studies to identify the role of
heparanase in regulating glycocalyx (dis)integrity after trauma-hemorrhage and on mechanisms that mediate
glycocalyx synthesis. Additionally, our proposed studies will identify signaling pathways that regulate endothelial
barrier function that are effected by loss of cell surface glycosaminoglycans, heparan sulfate and hyaluronic acid,
which are primary constituents of the glycocalyx layer. Our research program will focus on the endothelial cell-
specific response to trauma-hemorrhage in organ systems that are most susceptible to secondary injury (e.g.,
kidney, lung and intestines) with the over-arching goal of determining how resuscitation strategies mediate
glycocalyx-dependent mechanisms in each organ. These programmatic areas of research hold promise for
significantly impacting the current resuscitation paradigm for patients in hemorrhagic shock by aiding in the
discovery of novel therapeutic targets that can be used to inhibit glycocalyx dysfunction, facilitate its repair or
reverse the downstream consequences of glycocalyx disintegrity.

## Key facts

- **NIH application ID:** 10027428
- **Project number:** 1R35GM137958-01
- **Recipient organization:** UNIVERSITY OF ALABAMA AT BIRMINGHAM
- **Principal Investigator:** Jillian Rouse Richter
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $340,101
- **Award type:** 1
- **Project period:** 2020-09-01 → 2025-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10027428

## Citation

> US National Institutes of Health, RePORTER application 10027428, Endothelial Glycocalyx Disintegrity: Repairing the Damage caused by Trauma-Hemorrhage (1R35GM137958-01). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10027428. Licensed CC0.

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