Fig. 7: NGFR knockdown inhibits the PI3K/Akt signaling pathway and c-Fos promotes NONRATT023402.2 expression.

A NONRATT023402.2 expression determined by qRT-PCR in the right striatum of Sham, ShNGFR, LncRNA, and LncRNA + ShNGFR rats (n = 3−5). B NGFR expression determined by qRT-PCR in the right striatum of Sham, ShNGFR, LncRNA, and LncRNA + ShNGFR rats (n = 3). C The AIM score was positively correlated with the NONRATT023402.2 expression level (n = 16). D The AIM score was positively correlated with the NGFR expression level (n = 16). E The NONRATT023402.2 expression level was positively correlated with the NGFR expression level (n = 16). F Quantification of p-PI3K, PI3K, p-Akt, Akt, and c-Fos expressions in the right striatum of Sham, ShNGFR, LncRNA, and LncRNA + ShNGFR rats (n = 3). The signal intensities of protein bands were normalized to that of GAPDH. G Representative sequence of c-Fos binding specificity queried from JASPAR (identifier MA0099.2). H Luciferase reporter assay for interactions between c-Fos and NONRATT023402.2 in HEK293FT cells. I A working model showing the mechanism of the NONRATT023402.2/ miR-3065-5p/ NGFR axis in the striatum of LID rats. NONRATT023402.2 targets miR-3065-5p/ NGFR axis as a ceRNA and activates the PI3K/Akt signaling pathway and c-Fos to aggravate AIM symptoms. The c-Fos, as a transcription factor, in turn promotes NONRATT023402.2 expression, forming a positive feedback loop in the rat model of LID. Data represent the mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001.