Together these results reveal that a HOTAIR/miR-34a-5p/Notch1 signaling pathway may regulate the development of IDD, potentially making HOTAIR a viable target for treatment of this disease.
Compared to the NC group, the mice in the T1DM group had increased expressions of TRPM7 and miR-34a; decreased weight and fasting insulin; increased blood glucose and levels of ICA, IAA, and GAD-Ab; prolonged escape latency; less time spent in the target quadrant; incomplete neuronal structure; reduced neuron numbers; increased cell apoptosis and expressions of activated Bax, Cyt-c, and cleaved caspase-3; but reduced Bcl-2 expression.
Taken together, our results demonstrate that upregulated miR-34a potentiates Fas-mediated endplate chondrocyte apoptosis, which is associated with IDD.