The ion channel TRPM4 in murine experimental autoimmune encephalomyelitis and in a model of glutamate-induced neuronal degeneration.

ABSTRACT: Transient receptor potential melastatin member 4 (TRPM4), a Ca²⁺-activated nonselective cation channel, has been found to mediate cell membrane depolarization in immune response, insulin secretion, cardiovascular diseases, and cancer. In murine experimental autoimmune encephalomyelitis (EAE), TRPM4 deletion and administration of glibenclamide were found to ameliorate clinical symptoms and attenuate disease progression. However, the exact role of TRPM4 in EAE, as well as the molecular mechanisms underlining TRPM4 contribution in EAE, remain largely unclear. In the present study, EAE was induced in WT C57BL/6 N mice using myelin oligodendrocyte glycoprotein 35-55 (MOG_35-55) and TRPM4 protein and mRNA expression were examined in spinal cord membrane extracts. Our results

SUBMITTER: Bianchi B 

PROVIDER: S-EPMC6042389 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature