Amyloid‐beta induces different expression pattern of tissue transglutaminase and its isoforms on olfactory ensheathing cells: Modulatory effect of indicaxanthin

Abstract

Herein, we assessed the effect of full native peptide of amyloid‐beta (Aβ) (1‐42) and its fragments (25‐35 and 35‐25) on tissue transglutaminase (TG2) and its isoforms (TG2‐Long and TG2‐ Short) expression levels on olfactory ensheathing cells (OECs). Vimentin and glial fibrillary acid protein (GFAP) were also studied. The effect of the pre‐treatment with indicaxanthin from Opuntia ficus‐indica fruit on TG2 expression levels and its isoforms, cell viability, total reactive oxygen species (ROS), superoxide anion (O2−), and apoptotic pathway activation was assessed. The levels of Nestin and cyclin D1 were also evaluated. Our findings highlight that OECs exposure to Aβ(1‐ 42) and its fragments induced an increase in TG2 expression levels and a different expression pattern of its isoforms. Indicaxanthin pre‐treatment reduced TG2 overexpression, modulating the expression of TG2 isoforms. It reduced total ROS and O2− production, GFAP and Vimentin levels, inhibiting apoptotic pathway activation. It also induced an increase in the Nestin and cyclin D1 expression levels. Our data demonstrated that indicaxanthin pre‐treatment stimulated OECs self-renewal through the reparative activity played by TG2. They also suggest that Aβ might modify TG2 conformation in OECs and that indicaxanthin pre‐treatment might modulate TG2 conformation, stimulating neural regeneration in Alzheimer’s disease.