Abstract

Yes-associated protein (YAP) is proved to increase miR-29a in the present study, but the relevant molecular mechanism is not clear. Also, growing evidence indicates that the high-level miR-29a promotes the neurite outgrowth by decreasing PTEN (phosphatase and tensin homologue deleted on chromosome 10). Results show that the expression of miR-29a increases but the PTEN decreases during transfecting the N2a cells with the YAP plasmid. Meanwhile, the advancement of neurite outgrowth is presented via using multiple methods to detect the expression of GAP-43 and NF-200, which have a strong association with neurite outgrowth. The expression of miR-29a, GAP-43, and NF-200 shows an opposite tendency compared to the PTEN when YAP is downregulated. By treating N2a cells with miR-29a mimic and inhibitor, we also find the same conclusion. For in silico analysis of miR-29a, its promoter may have a binding site for YAP. Based on a luciferase reporter assay and a chromatin immunoprecipitation (ChIP) experiment, we demonstrate that YAP could increase the expression of miR-29a by targeting the promoter of miR-29a. In conclusion, the results identify that YAP promotes the neurite outgrowth via targeting the promoter of miR-29a, and it may be an effective therapeutic medicine for the neural disease.

Highlights

  • Growing studies reveal that the Hippo signaling pathway plays a crucial role in regulating tissue and organ development [1, 2]

  • TEAD as an important transcription factor plays a crucial role in the regulation of gene expression [17]

  • TEAD which emerged as the main partner of Yes-associated protein (YAP) on DNA has been reported to interact with YAP to regulate gene expression [18, 19]

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Summary

Introduction

Growing studies reveal that the Hippo signaling pathway plays a crucial role in regulating tissue and organ development [1, 2]. We acquire significant information that YAP increases the expression of miR-29 family, which links YAP and neural growth. MiR-29a as a newfound regulatory factor is confirmed to target PTEN on promoting neurite outgrowth. PTEN which is a target of miR-29 family is closely combined with neurite outgrowth [11,12,13]. Further study shows that miR-29a promotes neurite outgrowth by downregulating PTEN expression and increasing the Akt phosphorylation level. Our data further confirm that YAP could inhibit PTEN expression by overexpressing miR-29a. TEAD as an important transcription factor plays a crucial role in the regulation of gene expression [17]. TEAD which emerged as the main partner of YAP on DNA has been reported to interact with YAP to regulate gene expression [18, 19]

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