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Spinal cord injury (SCI) is a devastating disease. Strategies that enhance the intrinsic regenerative ability are very important for the recovery of SCI to radically prevent the occurrence of sensory disorders. Epidermal growth factor (EGF) showed a limited effect on the growth of primary sensory neuron neurites due to the degradation of phosphorylated‐epidermal growth factor receptor (p‐EGFR) in a manner dependent on Casitas B‐lineage lymphoma (CBL) (an E3 ubiquitin‐protein ligase). MiR‐22‐3p predicted from four databases could target CBL to inhibit the expression of CBL, increase p‐EGFR levels and neurites length via STAT3/GAP43 pathway rather than Erk1/2 axis. EGF, EGFR, and miR‐22‐3p were downregulated sharply after injury. In vivo miR‐22‐3p Agomir application could regulate CBL/p‐EGFR/p‐STAT3/GAP43/p‐GAP43 axis, and restore spinal cord sensory conductive function. This study clarified the mechanism of the limited promotion effect of EGF on adult primary sensory neuron neurite and targeting miR‐22‐3p could be a novel strategy to treat sensory dysfunction after SCI. [ABSTRACT FROM AUTHOR]

NLRP3, as a crucial inflammasome component, plays important roles in age‐related macular degeneration. Though some activators of NLRP3 have been studied, microRNAs (miRNAs) which potentially regulate NLRP3 messenger RNA (mRNA) have not been fully explored in retinal pigment epithelial (RPE) cells and retinopathy. In this study, by miRNA microarray profiling and bioinformatic analysis, we identified that four miRNAs, miR‐4286, miR‐223‐3p, miR‐365a, miR‐22‐3p, may target NLRP3 mRNA in RPE inflammatory damage in vivo. Further, real‐time polymerase chain reaction verified that only miR‐22‐3p was significantly decreased, which was associated with NLRP3 upregulation in blue‐light‐induced retinopathy. Mechanistically, the dual‐fluorescent reporter suggested miR‐22‐3p directly binds NLRP3 mRNA. Moreover, overexpression of miR‐22‐3p could significantly reduce whereas inhibition miR‐22‐3p could increase the mRNA and protein expressions of NLRP3, Caspase‐1, and mature IL‐1β. Collectively, our results indicate that miR‐22‐3p plays a suppressive role in RPE damage by targeting NLRP3, which provides new insights into the future intervention to retinopathy. [ABSTRACT FROM AUTHOR]