# Placental Proteins and Prematurity

> **NIH NIH R21** · UNIVERSITY OF COLORADO DENVER · 2022 · $243,049

## Abstract

Each year, 12-18 million infants worldwide, representing ~10% of all births, are born preterm (before 37 weeks
of gestation). The mechanisms underpinning preterm birth are poorly understood and, with the possible
exception of progesterone, no interventions are currently available to prevent preterm labor. The management
of the preterm infant has improved over the last 30 years, however despite this progress, prematurity remains
the second most common direct cause of death among children under 5 years of age. In addition, infants born
preterm are at risk of neonatal morbidity (e.g., intraventricular hemorrhage, bronchopulmonary dysplasia and
necrotizing enterocolitis) and long-term sequelae including chronic lung disease, retinopathy, cognitive
impairment and poor neurodevelopmental outcomes. Emerging evidence show that factors secreted by the
placenta are critical for normal fetal organ development. One of the most fundamental differences between
fetal and postnatal life is the instantaneous discontinuation of the umbilical circulation at delivery, depriving the
premature infant of placental factors, such as proteins, critical for fetal organ development. However, the
identity of proteins secreted by the human placenta into the fetal circulation remain largely unknown. Using the
SOMALOGIC proteomic platform, we recently reported that 341 proteins are secreted by the human term
placenta into the fetal circulation. Remarkably, a large number of these proteins could be linked to processes
such as angiogenesis and neurogenesis, suggesting that a subset of these proteins are critical for the normal
development of fetal tissues such as the brain, lung, and cardiovascular system. However, it is currently
unknown if these or other proteins are secreted by the placenta into the fetal circulation earlier in gestation and
if supplementation of a subset of these proteins could improve outcomes in prematurity. In this high risk/high
reward proposal we will test the central hypothesis that proteins associated with the development of the brain,
lung, retina, intestine and cardiovascular system are secreted by the placenta into the fetal circulation in
extremely and very preterm infants and administration of a subset of these proteins improve outcomes in a
guinea-pig model of prematurity. Our approach will be to determine the abundance of ~5000 proteins in
umbilical artery and vein and neonatal blood of extremely and very preterm infants, using a novel Slow Off-rate
Modified Aptamer (SOMA) proteomics platform, allowing us to characterize the preterm infant plasma
proteome in unprecedented depth. We will test the ability of a small subset of these proteins to improve
outcomes using a unique premature guinea-pig model. This proposal represents a shift in the paradigm how to
approach the problem of prematurity by focusing on the intrauterine environment that the infant born preterm
has been separated prematurely from, rather than optimizing the quality of care base...

## Key facts

- **NIH application ID:** 10493397
- **Project number:** 5R21HD104914-02
- **Recipient organization:** UNIVERSITY OF COLORADO DENVER
- **Principal Investigator:** Thomas Jansson
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $243,049
- **Award type:** 5
- **Project period:** 2021-09-24 → 2024-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10493397

## Citation

> US National Institutes of Health, RePORTER application 10493397, Placental Proteins and Prematurity (5R21HD104914-02). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10493397. Licensed CC0.

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