Ca 2+ signals in human umbilical endothelial cells derived from pregnancy with fetal growth restriction associated with hypertensive disorder

• Published in: Biomedical reports Vol. 20; no. 5; p. 76
• Main Authors: Cortés, Magdalena P, Alonso, Catalina, Vinet, Raúl, Valdivia-Cortés, Karla, Muñoz-Sagredo, Leonel, Bahamondez-Canas, Tania F, Cárdenas, Ana María
• Format: Journal Article
• Language: English
• Published: England 01.05.2024
• Subjects: P2Y2 receptor; calcium; fetal growth restriction; store-operated Ca2+ entry; ATP; hypertensive disorders of pregnancy
• ISSN: 2049-9434; 2049-9442
• DOI: 10.3892/br.2024.1764

Fetal growth restriction associated with hypertensive disorders of pregnancy (FGR-HDP) is a prevalent pathology with a higher risk of perinatal morbimortality. In this condition, placental insufficiency and endothelial dysfunction serve key roles. The present prospective cohort study monitored 11 patients with an FGR-HDP and 15 with full-term normotensive pregnancies and studied post-natal intracellular calcium concentration ([Ca ] ) signals in human umbilical vein endothelial cells (HUVECs). Small fetuses with placental insufficiency were identified using fetal biometry with Doppler velocimetry. Mean gestational age and birth weight were 31.8±4.1 weeks and 1,260±646 g for FGR-HDP and 39.2±0.8 weeks and 3,320±336 g for normal births, respectively. Abnormal umbilical artery Doppler waveforms were found in 64% of neonates with FGR-HDP. A significant percentage (86%) of FGR newborns were admitted to the neonatal intensive care unit at Gustavo Fricke hospital, Viña del Mar, Chile, with one case of death after birth. [Ca ] signals were measured by microfluorimetry in Fluo-3-loaded HUVECs from primary cultures. Altered [Ca ] signals were observed in HUVECs from FGR-HDP, where the sustained phase of ATP-induced [Ca ] responses was significantly reduced compared with the normotensive group. Also, the [Ca ] signals induced with 10 mM Ca after depletion of internal Ca stores were significantly higher. The present study provides a better comprehension of the role of altered cytosolic Ca dynamics in endothelial dysfunction and an model to assess novel therapeutic approaches for decreasing or preventing complications in FGR-HDP.