# Translational assessment of sulfonylurea receptor-1 as a biomarker and therapeutic target for cerebral edema in traumatic brain injury

> **NIH NIH K23** · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · 2020 · $125,157

## Abstract

PROJECT ABSTRACT
There is a fundamental gap in translating preclinical work on complex underlying mechanisms of cerebral edema in
traumatic brain injury (TBI) to critically needed biomarkers and targeted/preventive therapies for improving outcomes in
humans. This is an important problem because indiscriminate clinical approaches to cerebral edema remain reactionary
and morbid - compounding a problem that is a fundamental contributor to death and disability in TBI. The long-term
research goal is to better understand the roles and interactions of edema pathways in human TBI. This will focus
innovation of successful targeted treatments. The overall objective of this K23 is to develop a comprehensive approach
towards understanding a unique, key pathway of cerebral edema in human TBI involving a transmembrane protein:
Sulfonylurea Receptor-1 (Sur1). Founded on the central dogma of biology, this proposal evaluates the Sur1-cerebral
edema relationship in TBI from multiple angles by investigating Sur1 expression and genetic variability in humans, and
complementing this with a clinically relevant, unique, edema-generating mouse-model. The central hypotheses are that 1)
Sur1 levels and genetic variability influence cerebral edema and 2) Sur1 expression patterns guide treatment efficacy. The
hypotheses have been formulated upon preliminary data generated by the applicant that strongly suggest feasibility. The
rationale for the proposal is that complementing Sur1 expression and genetics in human TBI with a relevant animal
model, has the potential to directly translate to improving clinical care and outcomes. This is expected to inform patient
risk stratification, monitoring, prognosis, and targeting/developing specific therapies. Aim 1 evaluates the relationship
between human Sur1 expression (detected in cerebrospinal fluid, CSF, by enzyme linked immunosorbent assay, ELISA),
cerebral edema, and TBI outcomes. Aim 2 evaluates the human Sur1 gene (ABCC8) tag-single nucleotide polymorphism
(SNP) associations with cerebral edema in TBI. Aim 3 generates a temporo-spatial map of Sur1 expression (by validated
techniques) and quantifies effects of Sur1 inhibition by glyburide in an edema-generating mouse-model of TBI. The
approach is innovative, in the applicant's opinion, because it molecularly complements generic intracranial pressure (ICP)
monitoring and responses to cerebral edema by focusing on a key pathway, and uses a multifaceted approach to bridge the
gap between animal models and human disease. These aims are expected to establish the utility of Sur1 as a novel
biomarker and evaluate it as a preventive therapeutic target against edema. The proposed work is significant because it
has potential groundbreaking implications for monitoring and preventing cerebral edema that may reduce morbidity and
mortality, not just in TBI, but in many other neurological disorders. The research plan is augmented by expert mentoring
and rigorous didactic training. Together, thi...

## Key facts

- **NIH application ID:** 10396240
- **Project number:** 7K23NS101036-05
- **Recipient organization:** ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER
- **Principal Investigator:** Ruchira Menka Jha
- **Activity code:** K23 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $125,157
- **Award type:** 7
- **Project period:** 2017-06-15 → 2022-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10396240

## Citation

> US National Institutes of Health, RePORTER application 10396240, Translational assessment of sulfonylurea receptor-1 as a biomarker and therapeutic target for cerebral edema in traumatic brain injury (7K23NS101036-05). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10396240. Licensed CC0.

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