Akademik Veri Yönetim Sistemi
8th International Brain Research School 22 - 28 May 2023, Isparta /Türkiye., Isparta, Türkiye, 22 - 28 Mayıs 2023, cilt.15, ss.13
Calcium ion (Ca2+) concentration is low inside of
cells (50-100 nM) as compared to the outside of the cells
(1-3 mM). Several physiological and neuronal factors
such as muscle contraction, cell proliferation, and growth
are induced by the Ca2+ influx. However, the excessive
Ca2+ influx induces cell death and apoptosis via the
activation of calcium channels. The excessive Ca2+
influx-mediated neuronal death is induced in several
diseases, including the neurodegenerative diseases.
The involvements of voltage gated calcium and
chemical channels on the Ca2+ influx in neuronal cells
have been known for a long time. In addition to the wellknown calcium channels, the new channel superfamily
namely transient receptor potential (TRP) was
discovered within last decades. The TRP superfamily
contains 28 members in mammalian, and their activation
and inhibition mechanisms are very different from the
voltage gated calcium and chemical channels.
TRP melastatin 2 (TRPM2) is a subfamily member
of the TRPs. The TRPM2 channel's protein structure
consists of an enzyme (ADP-ribose pyrophosphatase) in
the C domain (Nazıroğlu et al. 2020). When the enzyme
is activated by oxidative stress and ADP-ribose, it causes
a rise of excessive Ca2+ influx in the brain and neurons.
The increased expression of TRPM2 channels also
contributes to the rise in excessive Ca2+ influx. Numerous
molecular pathways, including increases in the
mitochondrial membrane potential and caspase (caspase3, caspase-8, and caspase-9) activations are induced by
the increased cytosolic free Ca2+ concentrations.
The apoptotic and neural death pathways are
subsequently stimulated by the activations of molecular
pathways. A new study found that the increases of
TRPM2 expression levels were found in the apoptotic
neuronal cells (An et al. 2019). Furthermore, it has been
documented that a rise in TRPM2 expression caused
neurons to death by necrosis, autophagy, and apoptosis
(Shi et al. 2021). I will go over the rise in oxidative stress
and neuronal cell death which are induced by TRPM2
channel expression in the oral presentation.
According to evidence from the most recent
research, the induction of neuronal cell death and
oxidative stress in the neurons depends critically on the
upregulation of TRPM2 expression.