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Updated: May 13, 2026

Isolation of Endothelial Progenitor Cells from Healthy Volunteers and Their Migratory Potential Influenced by Serum Samples After Cardiac Surgery

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Published on: February 14, 2017

Differential stem- and progenitor-cell trafficking by prostaglandin E2.

Jonathan Hoggatt¹, Khalid S Mohammad, Pratibha Singh

¹Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.

|March 15, 2013

Summary

Non-steroidal anti-inflammatory drugs (NSAIDs) promote hematopoietic stem cell (HSC) egress from bone marrow niches by inhibiting prostaglandin E2 (PGE2) signaling. This enhances HSC engraftment, offering a therapeutic strategy for transplantation.

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Directed Differentiation of Hemogenic Endothelial Cells from Human Pluripotent Stem Cells

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Published on: March 31, 2021

Area of Science:

Hematology
Stem Cell Biology
Immunology

Background:

Hematopoietic stem cells (HSCs) require niche regulation for lifelong blood production.
Prostaglandin E2 (PGE2) has a known ex vivo role in HSC function.
The in vivo regulation of HSCs within the bone marrow niche is not fully understood.

Purpose of the Study:

To investigate the role of endogenous prostaglandin E2 (PGE2) in regulating hematopoietic stem cell (HSC) behavior within the bone marrow niche.
To determine if non-steroidal anti-inflammatory drug (NSAID) treatment affects HSC mobilization and engraftment.
To explore the therapeutic potential of NSAID-mediated HSC mobilization.

Main Methods:

NSAID treatment in mice to inhibit endogenous PGE2.
Analysis of HSC egress from the bone marrow and peripheral blood.
Assessment of stem and progenitor cell mobilization mechanisms.
Evaluation of hematopoietic graft repopulating ability and long-term engraftment.
NSAID treatment in non-human primates and human volunteers.
PGE2 receptor (EP4) knockout mouse studies.

Main Results:

NSAID treatment induced modest HSC egress from the bone marrow, independent of the SDF-1-CXCR4 axis.
HSC egress was linked to niche attenuation and reduced osteopontin levels.
NSAID-mobilized hematopoietic grafts showed superior repopulating ability and engraftment.
NSAID-mediated egress was confirmed across species, including humans.
Reduced E-prostanoid 4 (EP4) receptor signaling impaired progenitor expansion and promoted stem/progenitor egress.

Conclusions:

Endogenous PGE2, signaling through EP4 receptors, plays a critical role in retaining HSCs within the bone marrow niche.
NSAID treatment represents a viable strategy to mobilize HSCs for enhanced therapeutic transplantation.
This study uncovers a novel regulatory mechanism for HSC retention and mobilization.