Selenium Attenuates HPV-18 Associated Apoptosis in Embryo-Derived Trophoblastic Cells but Not Inner Cell Mass In...

Area of Science:

• Cell Biology
• Virology
• Reproductive Biology

Background:

• Human papillomaviruses (HPV) are linked to cell cycle arrest.
• Understanding HPV's impact on embryonic development is crucial.
• Antioxidants may offer protective mechanisms against viral effects.

Purpose of the Study:

• To investigate the effects of HPV-18 on early embryonic cells (trophoblasts).
• To evaluate the potential of selenomethionine (SeMet) as an antioxidant to counteract HPV-18-induced damage.
• To determine if SeMet can prevent HPV-18-associated necrosis and apoptosis.

Main Methods:

• Mouse embryos were cultured and exposed to HPV-18, SeMet, or both.
• Trophoblast integrity was assessed using morphometric analysis.
• Apoptosis and necrosis were quantified using dual-stain fluorescence assays.

Main Results:

• HPV-18 exposure led to a 29% reduction in trophoblast nuclear size.
• SeMet supplementation prevented nuclear shrinkage and maintained trophoblast viability despite HPV-18 presence.
• HPV-18 decreased overall cell viability by 44% and inner cell mass (ICM) viability by over 60%, effects attenuated by SeMet.

Conclusions:

• HPV-18 negatively impacts embryonic trophoblast size and viability.
• The antioxidant SeMet effectively mitigates HPV-18-induced nuclear shrinkage and cell death in trophoblasts.
• SeMet's protective effect on apoptosis suggests differential oxidative stress pathways in trophoblasts versus ICM cells.