1. Lower ERVW-1 and higher VEGF, FLT-1 and HIF-1 gene expression in placentae of low birth babies from Indonesia.
- Author
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Nurtanio, Teresa, Nabila, Bilqis Zahra, Fachiroh, Jajah, Nuraini, Neti, and Purnomosari, Dewajani
- Abstract
Poor placental angiogenesis is associated with several pregnancy complications including fetal growth restriction (FGR), which causes low birth weight (LBW) babies to have a high risk of growth disorders and metabolic disorders in adulthood. Recent research using syncytin knock-out mice showed significant disruption in the growth of placental vascularization. Syncytin-1 which encoded by ERVW-1 gene, is proposed to have a role in placental angiogenesis, but its relationship with other proangiogenic factors such as vascular endothelial growth factor (VEGF) in the placenta of LBW babies has not yet been determined. By knowing the mechanisms of FGR, more proactive preventive and therapeutic measures can be taken in the future. This study aimed to determine the expression of ERVW-1 , proangiogenic gene VEGF and its receptor (FLT-1), and hypoxia inducible factor-1 (HIF-1) in LBW placentas, and investigate the relationship between these genes' expression in the placenta of LBW babies. Total RNA was extracted from placental tissue. Total RNA is used as a cDNA synthesis template, followed by qRT-PCR. Correlations of ERVW-1, VEGF, FLT-1 and HIF-1 genes' expression were analyzed by linear regression. The age and body mass index of mothers with LBW and normal birth weight (NBW) babies were not significantly different. ERVW-1 expression in LBW placentas was lower than in NBW placentas, but VEGF, FLT-1 and HIF-1 expressions were higher. ERVW-1 was negatively correlated with HIF-1 and VEGF. Low expression of ERVW-1 in the placenta of LBW babies may result in impaired placental angiogenesis and possibly lead to hypoxia. • Lower expression of ERVW-1 was found in the placenta of Low Birth Weight babies. • Low ERVW-1 expression leads to hypoxia, as indicated by high HIF-1 expression. • Hypoxic conditions are compensated by upregulation of VEGF and its receptor, FLT-1. [ABSTRACT FROM AUTHOR]
- Published
- 2024
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