Fig. 8

Ifngas1 acts as a molecular sponge regulating miR-21a-3p to down-regulated caspase9 expression, thereby regulating Akt signaling pathway. a qRT-PCR. Changes in the expression of miR-21a-3p, miR-18b-5p, miR-10a-5p, miR-130b-5p and other ASD-related miRNAs after hADSC-Exo treated. b Firefly luciferase activity was normalized to Renilla luciferase activity (Firefly/Renilla). In 293T cells, Ifngas1 3′-UTR pmirGLO plasmid with miR-21a-3p mimic/negative control or mutant Ifngas1 (pmirGLO-Ifngas1-MUT) 3′-UTR pmirGLO plasmid with miR-21a-3p mimic/negative control was co-transfected. c Primary cultures of C57BL mice or BTBR mice neurons. BTBR mice neurons co-cultured with hADSC-Exo were transfected with Ifngas1. d Apoptosis was measured by IHC staining of cleaved caspase-3 (CC-3) in C57BL (WT) and BTBR mice neurons. BTBR mice neurons were transfected with Ifngas1 or NC mimic (negative control). e KEGG pathway enrichment diagram. f, g WB western blot. f In the neurons of BTBR mice, caspase9 and BAX levels are increased, while BCL-2 levels are decreased (relative to β-actin), which was related to a decrease in AKT phosphorylation (p-AKT), but the total level of AKT was unchanged. Transfection of Ifngas1 but not NC mimics (negative control) rescued the cortical neurons in BTBR mice. Quantification of AKT, p-AKT, caspase9, BCL-2, BAX, normalized to β-actin levels, and values were plotted. Differences in six protein values were assessed by Tukey’s multiple comparison test one-way ANOVA, error bars represent S.E.M. *p < 0.05, **p < 0.01, ***p < 0.001