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Published on: December 22, 2023
Structural differences in the umbilical vein wall after full-term and pre-term delivery
M Bagyánszki1, Z Novák, N Bódi
1Department of Physiology, Anatomy and Neuroscience, University of Szeged, Szeged, Hungary. bmarcsi@bio.u-szeged.hu
Human umbilical cords, lacking nerves, rely on cell-to-cell contact for fetoplacental circulation control. Pre-term infants show damaged smooth muscle cells and increased apoptosis in umbilical veins, impacting fetal circulation.
Area of Science:
- Obstetrics and Gynecology
- Developmental Biology
- Vascular Biology
Background:
- The human umbilical cord, largely devoid of innervation, suggests paracrine signaling is crucial for regulating fetoplacental circulation.
- Direct cell-to-cell contact between smooth muscle cells and endothelium may play a vital role in this regulation.
Purpose of the Study:
- To investigate the ultrastructure and cellular characteristics of umbilical veins in full-term and pre-term neonates.
- To examine the role of smooth muscle cell processes and endothelial cell apoptosis in umbilical cord function.
Main Methods:
- Electron microscopy was used to analyze the ultrastructure of umbilical vein smooth muscle cells.
- Immunohistochemistry was employed to assess c-kit and Bax immunoreactivity in umbilical vein tissues.
- Samples were obtained immediately following full-term and pre-term deliveries.
Main Results:
- Smooth muscle cells in the tunica media possess c-kit immunoreactive, foot-like processes.
- In full-term neonates, over 50% of these processes showed normal ultrastructure, closely associated with the lamina elastica interna.
- In pre-term infants, over 60% of processes were shrunken and detached, with increased endothelial Bax expression indicating apoptosis.
Conclusions:
- Umbilical vein smooth muscle cell processes undergo significant ultrastructural changes in pre-term infants.
- Enhanced endothelial apoptosis in pre-term umbilical veins suggests a compromised fetoplacental circulation mechanism.
- These findings highlight potential cellular mechanisms underlying circulatory issues in pre-term neonates.
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