TRPV1 stimulation increased oxidative neurotoxicity and apoptosis in the glia cell membrane but not in the perinuclear area: An evidence of TRPV1 subtype


ÖZ A., Cinar R., NAZIROĞLU M.

METABOLIC BRAIN DISEASE, 2022 (Peer-Reviewed Journal) identifier identifier identifier

  • Publication Type: Article / Article
  • Publication Date: 2022
  • Doi Number: 10.1007/s11011-022-01037-x
  • Journal Name: METABOLIC BRAIN DISEASE
  • Journal Indexes: Science Citation Index Expanded, Scopus, Academic Search Premier, BIOSIS, EMBASE, MEDLINE
  • Keywords: Glia, TRPV1 channels, Calcium ion, Oxidative stress, Apoptosis, DORSAL-ROOT GANGLION, INTRACELLULAR CALCIUM, TRPM2 CHANNELS, ACTIVATION, INVOLVEMENT, MICROGLIA, RELEASE, STRESS, DEATH, CONTRIBUTES

Abstract

Glia are essential neurons of the immune system in the central nervous system. The effective mission of glia depends on their activation, release of cytokines, and oxidative cleaning of debris material from neuronal cells. Accumulating evidence indicates that microglia activation-induced oxidative stress via the activation Ca2+ permeable TRPV1 channel has an essential role in the pathophysiology of neurodegenerative diseases. However, there is scarce information on the cytosolic localization of TRPV1 and the induction of oxidative cytotoxicity in the glia. Hence, we investigated the interactions between cytosolic TRPV1 expression levels and oxidative neurotoxicity in the BV2, C8-D1A, N9 glia, and DBTRG glioblastoma cells. We observed TRPV1 expression in the perinuclear area but not in the cell membrane in the BV2, C8-D1A, and N9 cells. Hence, we observed no activation of TRPV1 on the increase of mitochondrial free reactive oxygen species (mROS) and apoptosis in the cells after the capsaicin stimulation. However, we observed TRPV1 channel expression in the positive control (DBTRG) cell membranes. Hence, the Ca2+ influx, TRPV1 current density, apoptosis, and mROS levels were increased in the DBTRG cells after the capsaicin stimulation, although their levels were diminished by the treatment of the TRPV1 blocker (capsazepine). In conclusion, the presence of TRPV1 in the cell membrane of DBTRG cells induced excessive generation of mROS and apoptosis actions, although the presence of TRPV1 in the perinuclear area did not cause the actions. It seems that there is a subtype of TRPV1 in the perinuclear area, and it is not activated by the capsaicin.