Regulatory Role of lncRNA Silencing on Pathway in a High-Glucose-Induced Cell Model.

This study investigated the regulatory role of the long non-coding RNA maternally expressed gene 3 () in tau hyperphosphorylation and insulin signaling () under high-glucose (HG)-induced neurotoxic conditions mimicking Alzheimer's disease pathology. To explore the function of within a hyperglycemic (Hyp) model, was silenced using small interfering RNA (siRNA) assay, followed by Western blot analysis, qRT-PCR, and network analyses. The si + Hyp group had lower levels of (0.48-fold) and (0.52-fold) than did the Hyp group. In the si + Hyp group, (2.51-fold) and (2.38-fold) expressions were higher than were those in the Hyp group, while in the si group, GSK3β (4.59-fold), microtubule-associated protein (, ) (6.37-fold), interleukin (5.67-fold), (3.29-fold), and tumor necrosis factor-α () (3.06-fold) were all significantly upregulated in comparison to the control group. A higher level of p-tau protein was seen in the si group in comparison to the control group, as well as in the si + Hyp group in comparison to the Hyp group. Gene ontology analysis following administration showed that genes downstream of the pathway were suppressed, whereas genes regulating the neuroinflammatory response were upregulated. The results suggest that the lncRNA may be a promising therapeutic target in HG-induced neurodegenerative AD.