Abstract
Endothelial cell injury and activation in the placenta are features of placental vascular disease (PVD). While advances in PVD have been made, the pathogenesis of this disease is still unknown. The objective of this study was to pursue potential risk factors and signal transcription pathways involved in PVD pathogenesis. Gene expression in subjects with PVD and with normal pregnancies was compared using a two-channel microarray technique. Higher expression of HSPA6 and HSPA1A was exhibited in PVD subjects. HSPA6 and HSPA1A both encode HSP70, and, therefore, we localized HSP70 expression in placental tissue. Using quantitative polymerase chain reaction (PCR) and Western blot, we observed a significant upregulation of HSP70 in both mRNA and protein levels in placental tissue and microvascular endothelial cells of PVD subjects when compared with normal pregnancies (P< 0.05). HSP70 mRNA and protein expression also correlated negatively with infant birth weight (P< 0.05). HSP70 was expressed mainly in endothelial cells and smooth muscle cells in the placental microvessels. We therefore conclude that HSP70 may mediate endothelial activation and play a role in pathogenesis of PVD.
Highlights
The placenta plays a pivotal role in the acceptance of the fetal-placental unit by the maternal immune system
Since both HSPA6 and HSPA1A encode the protein HSP70, and both were upregulated in placentas from subjects with Placental vascular disease (PVD), we examined placental tissue and microvascular endothelial cells for the presence of HSP70 mRNA
Having shown an upregulation of HSPA6 and HSPA1A genes, the presence of HSP70 mRNA and protein in PVD placentas, and localization of HSP70 to endothelial and smooth muscle cells of the placenta, we examined whether these factors could contribute to any negative outcomes between normal and PVD subjects
Summary
The placenta plays a pivotal role in the acceptance of the fetal-placental unit by the maternal immune system. Placental vascular disease (PVD) induces complications in human pregnancy such as preeclampsia (PE) and fetal intrauterine growth restriction (IUGR) [1]. Heat shock proteins (HSPs) are highly conserved and are found in all cell types. They may be expressed as a result of temperature increase or of stressful environmental, pathological, or physiological stimuli [5]. The HSP genes A6 and A1A both encode the protein HSP70 This frequently studied member of the HSP family has been detected in placental tissue, no expression level difference was observed between preterm and term pregnancies [8,9]. Higher levels of HSP70 have been found in the peripheral circulation of patients with severe preeclampsia as well as in patients with peripheral and renal vascular disease [10,11]
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