TRAIL-related neurotoxicity implies interaction with the Wnt pathway in human neuronal cells in vitro.

Tumor necrosis factor related apoptosis inducing ligand (TRAIL) is involved in amyloid beta dependent neurotoxicity via the extrinsic pathway. Recently, several genes modulating TRAIL cytotoxicity have been characterized, providing evidence for a role of wingless-type mouse mammary tumor virus integration site family (Wnt), Jun-N-terminal kinase and other pathways in increased cell susceptibility to the cytokine. We investigated whether neurotoxic effects of TRAIL could be due to modulation of the Wnt signaling pathway.

Levels of matrix metalloproteinases 1 and 2 in human gingival crevicular fluid during initial tooth movement.

Introduction: During orthodontic treatment, the early response of periodontal tissues to mechanical stress involves several metabolic changes that allow tooth movement. Many studies have evaluated these modifications through the analysis of various metabolites released into gingival crevicular fluid (GCF). The purpose of this investigation was to evaluate matrix metalloproteinase (MMP)-1 and MMP-2 in the GCF of human teeth exposed to orthodontic force on both the tension and compression sides in the initial phase of orthodontic tooth movement.

Trail interacts redundantly with nitric oxide in rat astrocytes: potential contribution to neurodegenerative processes.

The proapoptotic cytokine TRAIL has been shown to enhance amyloid-beta-dependent neurotoxicity. Here are reported interactions between TRAIL and nitric oxide (NO) in cultured rat astrocytes in vitro. Rat astrocytes expressed all TRAIL receptor mRNAs and proteins.