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Updated: Jan 28, 2026
Induction of Endothelial Differentiation in Cardiac Progenitor Cells Under Low Serum Conditions
Published on: January 7, 2019
CD133+/C-kit+Lin- endothelial progenitor cells in fetal circulation demonstrate impaired differentiation potency in
Yejin Park1, Hwa Jin Lee1, Yun Ji Jung1
1Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Institute of Women's Medical Life Science, Placenta-derived Stem Cell Genomic Research Lab, Yonsei University College of Medicine, Seoul, Republic of Korea.
Insights
Preeclampsia exposure irreversibly impairs endothelial progenitor cell (EPC) differentiation and function in offspring, linked to epigenetic changes. This may explain long-term cardiovascular risks in these individuals.
Area of Science:
- Cardiovascular biology
- Epigenetics
- Perinatal medicine
Background:
- Preeclampsia survivors face increased long-term cardiovascular and metabolic disease risk.
- Aberrant fetal cell reprogramming in utero is a suspected cause.
- Endothelial progenitor cells (EPCs) are crucial for vascular health.
Purpose of the Study:
- To investigate functional and epigenetic changes in EPCs from offspring of preeclamptic pregnancies.
- To assess the impact of the in-utero environment on EPC development.
- To explore potential irreversible epigenetic alterations.
Main Methods:
- Compared CD133+/C-kit+/Lin- (CKL-) EPCs from normal and preeclamptic pregnancies (n=10 each).
- Assessed EPC differentiation into outgrowth endothelial cells (OECs) and OEC angiogenic functions (migration, adhesion, tube formation).
- Analyzed EPC H3K4, H3K9, and H3K27 trimethylation levels.
Main Results:
- Preeclampsia-derived EPCs showed reduced H3K4 and H3K9 trimethylation.
- Significantly delayed EPC differentiation and reduced OEC colony formation were observed.
- OECs from preeclampsia-exposed offspring exhibited impaired migration, adhesion, and tube formation.
Conclusions:
- Preeclampsia exposure causes significant and irreversible impairment of EPC differentiation and OEC angiogenic function.
- These functional deficits are likely due to irreversible epigenetic changes incurred during gestation.
- Findings suggest a mechanism for the increased cardiovascular risk in offspring from preeclamptic pregnancies.
Objectives:
Individuals delivered from preeclamptic pregnancies exhibit a long-term increased risk of developing cardiovascular and metabolic diseases, likely caused by aberrant fetal cell reprogramming incurred in utero. The present study investigated the functional impairment and epigenetic changes exhibited by endothelial progenitor cells derived from offspring born to preeclamptic pregnancies.
Study Design:
The capacity of CD133+/C-kit+/Lin- (CKL-) human umbilical cord blood endothelial progenitor cells (EPCs) derived from gestationally matched normal and preeclamptic (n = 10 each) pregnancies to differentiate to form outgrowth endothelial cells (OECs) was assessed by observing both their morphology, and the number and size of generated OECs colonies. Likewise, OECs angiogenic function was evaluated via migration, adhesion, and tube-formation assays. EPCs from preeclampsia were cultured in normal-, and preeclampsia-derived serum-conditioned media to assess the effects of environmental factors on EPC differentiation potency and OEC angiogenic function, and finally, EPCs H3K4, H3K9, and H3K27 trimethylation levels were assayed.
Results:
The preeclampsia-derived CKL- EPCs exhibited decreased H3K4 and H3K9 trimethylation levels, significantly delayed differentiation times, and a significant reduction in both their number of generated OECs colonies, and exhibited reduced OECs migration, adhesion, and tube formation activities compared to those achieved by the normal-derived EPCs. Interestingly, the reduced differentiation potency of the preeclampsia-derived EPCs was not rescued via exposure to normal serum.
Conclusions:
Exposure to preeclampsia significantly and irreversibly reduced CKL- EPC differentiation potency and OEC angiogenic function, likely reflecting incurred irreversible epigenetic changes.
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