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Altered angiogenesis in low birth weight individuals: a role for anti-angiogenic circulating factors
Isabelle Ligi1, Stéphanie Simoncini, Edwige Tellier
1Department of Neonatology, La Conception Hospital , Marseille , France .
Insights
Low birth weight babies exhibit impaired endothelial progenitor cell function due to antiangiogenic factors in their serum, potentially impacting future cardiovascular health.
Area of Science:
- Neonatal research
- Vascular biology
- Cardiovascular health
Background:
- Low birth weight (LBW) is a known risk factor for adult hypertension.
- Endothelial progenitor cells (EPCs) show dysfunction in LBW neonates.
- Investigating angiogenic factors in LBW neonates is crucial.
Purpose of the Study:
- To determine if plasma pro- or anti-angiogenic factors are linked to EPC dysfunction in LBW neonates.
- To explore the association between these factors and impaired angiogenesis.
Main Methods:
- Umbilical cord blood was collected from normal and LBW neonates.
- Endothelial colony-forming cells (ECFCs) from controls were cultured with serum from both groups.
Main Results:
- LBW serum significantly reduced ECFC proliferation and migration.
- VEGF levels were lower, while sVEGFR and PF4 were higher in LBW neonates.
- Adding VEGF reversed the inhibitory effects of LBW serum on ECFCs.
Conclusions:
- LBW infant serum contains antiangiogenic factors affecting ECFCs.
- The VEGF/sVEGF/PF4 pathway is implicated in LBW-associated EPC dysfunction.
Objective:
Low birth weight (LBW) is a risk factor for hypertension at adulthood. Endothelial progenitor cells (EPCs) dysfunction has been characterized in LBW neonates. We hypothesized that changes in soluble, plasma pro- or anti-angiogenic factors are associated with EPCs dysfunction and impaired angiogenesis in LBW neonates.
Method:
Venous umbilical cord blood was collected from 42 normal, term neonates and 75 LBW neonates. Cord blood endothelial colony forming cells (ECFC) from control patients were cultured in the presence of 10% of serum obtained from both groups.
Results:
The proliferation and the migration of ECFC were significantly reduced when cultured with 10% of serum of LBW neonates compared to serum of control neonates. Matrigel invasion assay was not significantly altered. Umbilical vein plasma VEGF concentration was significantly reduced in LBW neonates while that of sVEGFR and PF4 were significantly higher. Addition of VEGF corrected the inhibitory effect of LBW serum on normal ECFC proliferation.
Conclusions:
Serum obtained from LBW babies contains factors that exhibit an antiangiogenic effect on ECFC proliferation and migration. VEGF/sVEGF/PF4 pathway seems to be involved in the EPCs dysfunction in LBW neonates.
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