English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Increasing evidence has demonstrated a vital role of microRNAs (miRNAs) in diverse biological processes. However, their functions in developing brain with hypoxia-ischemia (HI) remain largely unknown. Through a miRNA microarray analysis in a P10 rat model of cerebral HI, we found that miR-30d-5p was one of the most deregulated miRNAs in neonatal brains in response to HI. MiR-30d-5p was downregulated in a time-dependent manner in brain cortex after HI, which was accompanied by increased expression of Beclin1 both at transcript and protein levels. Increase of miR-30d-5p by agomir (AG) resulted in reduction of autophagy and increase of apoptosis, whereas inhibition of miR-30d-5p by antagomir (AT) enhanced autophagy and inhibited apoptosis in rat brains after HI. Moreover, miR-30d-5p AG increased infarct volume, delayed recovery of neurological function, and impaired improvement of spatial memory ability. MiR-30d-5p AT decreased infarct volume, promoted neurological recovery, and improved behavior performance of rats subjected to HI. Collectively, these results indicated that miR-30d-5p modulated survival programs of neural cell by regulating autophagy and apoptosis.

miR-30d-5p Plays an Important Role in Autophagy and Apoptosis in Developing Rat Brains After Hypoxic–Ischemic Injury