TRPC1- and TRPC3-dependent Ca²⁺ signaling in mouse cortical astrocytes affects injury-evoked astrogliosis in vivo.

ABSTRACT: Following brain injury astrocytes change into a reactive state, proliferate and grow into the site of lesion, a process called astrogliosis, initiated and regulated by changes in cytoplasmic Ca²⁺ . Transient receptor potential canonical (TRPC) channels may contribute to Ca²⁺ influx but their presence and possible function in astrocytes is not known. By RT-PCR and RNA sequencing we identified transcripts of Trpc1, Trpc2, Trpc3, and Trpc4 in FACS-sorted glutamate aspartate transporter (GLAST)-positive cultured mouse cortical astrocytes and subcloned full-length Trpc1 and Trpc3 cDNAs from these cells. Ca²⁺ entry in cortical astrocytes depended on TRPC3 and was increased in the absence of Trpc1. After co-expression of Trpc1 and Trpc3 in HEK-293 cells both prote

SUBMITTER: Belkacemi T 

PROVIDER: S-EPMC5526095 | biostudies-literature | 2017 Sep

REPOSITORIES: biostudies-literature