MicroRNA-670 aggravates cerebral ischemia/reperfusion injury via the Yap pathway

Apoptosis is an important programmed cell death process involved in ischemia/reperfusion injury.MicroRNAs are considered to play an important role in the molecular mechanism underlying the regulation of cerebral ischemia and reperfusion injury.However,whether miR-670 can regulate cell growth and death in cerebral ischemia/reperfusion and the underlying mechanism are poorly understood.In this study,we established mouse models of transient middle artery occlusion and Neuro 2a cell models of oxygen-glucose deprivation and reoxygenation to investigate the potential molecular mechanism by which miR-670 exhibits its effects during cerebral ischemia/reperfusion injury both in vitro and in vivo.Our results showed that after ischemia/reperfusion injury,miR-670 expression was obviously increased.After miR-670 expression was inhibited with an miR-670 antagomir,cerebral ischemia/reperfusion injury-induced neuronal death was obviously reduced.When miR-670 overexpression was induced by an miR-670 agomir,neuronal apoptosis was increased.In addition,we also found that miR-670 could promote Yap degradation via phosphorylation and worsen neuronal apoptosis and neurological deficits.Inhibition of miR-670 reduced neurological impairments after cerebral ischemia/reperfusion injury.These results suggest that microRNA-670 aggravates cerebral ischemia/reperfusion injury through the Yap pathway,which may be a potential target for treatment of cerebral ischemia/reperfusion injury.The present study was approved by the Institutional Animal Care and Use Committee of China Medical University on February 27,2017(IRB No.2017PS035K).

Live Cells Process Exogenous Peptide as Fibronectin Fibrillogenesis In Vivo

The human body is one of the most sophisticated material systems.It is still a considerable challenge to biomimic the“life-design”process to construct a part of“life”in vivo.Herein,we mimicked the natural fibronectin(FN)fibrillogenesis system using ligand–receptor interaction-induced self-assembly to construct in situ artificial fibrous FN in vivo,based on exogenous FN mimic peptide(FNMP).We performed the in vivo study with a tumor-bearing mouse model,to which the particle formulated FNMP raw materials were delivered with high efficiency to the tumor site through intravenous(iv)administration.In the tumor,the presence of overexpressed integrin receptors on the cell surface induced the self-assembly of the FNMP into fibrous structures,thereby,creating an artificial fibrous FN.However,the FNMP-based artificial fibrous FN showed different biological functionality from the natural fibrous FN,inhibiting the growth and migration of cells,making our constructed FN able to inhibit tumor growth,invasion,and metastasis.Thus,this study opens an avenue for the precise construction of biomimetic materials for in vivo biomedical applications.