Psychological and oxidative stress induce apoptosis through TRPV1 channel activation in granulosa cells of oocyte during in vitro fertilization

Abstract

Several physiological and pathophysiological functions such as mitochondria and phagocytosis induce oxidative stress. Oxidative stress results in excessive production of reactive oxygen species (ROS). There is a high amount of psychologically and chemically stress in in vitro fertilization (IVF), because of presence stressful permanent infertility and treatment procedures (An et al. 2013). Oocytes are surrounded by granulosa cells. It is well-known that there is a direct relationship between oxidative stress contents of granulosa cells and oocyte quality (Tola et al 2013). Excessive Ca2+ influx induces excessive mitochondrial ROS production and apoptosis through activation of caspase activations. Involvement of voltage gated Ca2+ channels on oocyte quality and apoptosis in the granulosa cells has been clarified by results of several studies (Platano et al. 2013; Tola et al 2013). Transient receptor potential vanilloid 1 (TRPV1) channel is a calcium permeable and non-selective cation channel. The similar effects of voltage gated calcium channels may present between oxidative stress and TRPV1 channel activation in the oocyte, because the TRPV1 channel is activated by excessive production of ROS. The importance of TRPV1 channel on the oocyte maturation was recently reported (Cecconi et al. 2019).  In the oral presentation, I will review recent studies on apoptosis through TRPV1 channel activation in granulosa cells of oocyte during IVF.  In conclusion, current literature data indicated that psychological and oxidative stress-induced ROS, apoptosis and Ca2+ contents of oocyte and granulosa cells have very important roles on the oocyte maturation in patients with infertility during the IVF. There are some involvement clues of TRPV1 channels on the oocyte maturation and apoptosis, but the subject needs future studies.