# Atypical protein kinase C signaling and placentation

> **NIH NIH R21** · UNIVERSITY OF KANSAS MEDICAL CENTER · 2020 · $229,500

## Abstract

Abstract
 Early pregnancy loss is a serious health concern. Defective development of the syncytiotrophoblast (SynT)-
lineage, which assures placentation and establishes the fetal/maternal exchange surface, is one of the leading
causes for early pregnancy loss. Furthermore, in an established pregnancy, defective development and function of
SynT-lineage could lead to pregnancy-associated complications like IUGR and preeclampsia or serve as
developmental causes for postnatal or adult diseases. Despite of the critical importance of SynTs, we have a poor
understanding of signaling mechanisms that regulate SynT development. Especially very little is known about early
human placentation process. Our studies with mouse model provide genetic evidence that loss-of atypical protein
kinase C isoform, PKCλ/ι, function in trophoblast progenitors could lead to early pregnancy due to defective
development of SynTs within the placental labyrinth zone. These observations led us to the central hypothesis of
this proposal that PKCλ/ι)-signaling mediates a conserved function in establishing SynT development across
mammalian species. The goal of this proposal is to test this hypothesis by using both transgenic mouse and
human trophoblast stem cells (human TSCs) as experimental models. Two specific aims are proposed.
In aim 1, using conditional PKCλ/ι knockout mouse models, we will test the hypothesis that cell-autonomous
function of PKCλ/ι in trophoblast progenitors is essential for SynT development and placentation.
In aim 2, using human TSCs as a model system, we will test the hypothesis that PKCλ/ι signaling is essential
for both maintenance of the stem/progenitor state in hTSCs and their differentiation towards SynT lineage.

## Key facts

- **NIH application ID:** 9903417
- **Project number:** 5R21HD098880-02
- **Recipient organization:** UNIVERSITY OF KANSAS MEDICAL CENTER
- **Principal Investigator:** Soumen Paul
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $229,500
- **Award type:** 5
- **Project period:** 2019-04-01 → 2022-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9903417

## Citation

> US National Institutes of Health, RePORTER application 9903417, Atypical protein kinase C signaling and placentation (5R21HD098880-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/9903417. Licensed CC0.

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