Amyloid-β regulates gap junction protein connexin 43 trafficking in cultured primary astrocytes.

ABSTRACT: Altered expression and function of astroglial gap junction protein connexin 43 (Cx43) has increasingly been associated to neurotoxicity in Alzheimer disease (AD). Although earlier studies have examined the effect of increased β-amyloid (Aβ) on Cx43 expression and function leading to neuronal damage, underlying mechanisms by which Aβ modulates Cx43 in astrocytes remain elusive. Here, using mouse primary astrocyte cultures, we have examined the cellular processes by which Aβ can alter Cx43 gap junctions. We show that Aβ_25-35 impairs functional gap junction coupling yet increases hemichannel activity. Interestingly, Aβ_25-35 increased the intracellular pool of Cx43 with a parallel decrease in gap junction assembly at the surface. Intracellular Cx43 was found to be partly

SUBMITTER: Maulik M 

PROVIDER: S-EPMC7606679 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature