RTN1-C mediates cerebral ischemia/reperfusion injury via modulating autophagy.

It has been widely accepted that autophagic cell death exacerbates the progression of cerebral ischemia/reperfusion (I/R). Our previous study revealed that overexpression of reticulon protein 1-C (RTN1-C) is involved in cerebral I/R injury. However, the underlying mechanisms have not been studied intensively.

RTN1-C is involved in high glucose-aggravated neuronal cell subjected to oxygen-glucose deprivation and reoxygenation injury via endoplasmic reticulum stress.

Background: Patients suffering from diabetes mellitus experience poor outcomes after ischemic stroke. RTN1-C, ER-associated proteins localized in endoplasmic reticulum (ER) membrane, plays an important role in ER stress-induced apoptosis and regulates cellular susceptibility to different apoptosis pathways. Overexpression of RTN1-C can aggravate cerebral ischemia/reperfusion injury (IRI).

RTN1-C mediates cerebral ischemia/reperfusion injury via ER stress and mitochondria-associated apoptosis pathways.

The reticulon family has been found to induce apoptosis, inhibit axon regeneration and regulate protein trafficking. However, little is known about the mechanisms of how reticulon proteins are involved in neuronal death-promoting processes during ischemia. Here, we report that the expression of Reticulon Protein 1-C (RTN1-C) was associated with the progression of cerebral ischemia/reperfusion (I/R) injury.