Inhibition of Poly(ADP-Ribose) Polymerase Activity Modulates Autophagy Induced by Experimental Spinal Cord Trauma

Several studies have shown that autophagic cell death occurs in several pathological conditions . Recent studies have suggested the existence of a biochemical mechanism of crosstalk between apoptosis and autophagic cell death. Interestingly, much attention has been paid on the potential involvement of autophagy in neurodegenerative disorders, such as Parkinson and Alzheimer diseases, where autophagy is supposed to exert a protective mechanism. Earlier studies also demonstrated increased autophagic activity at lesion sites after cerebral hypoxia‐ischemia injury, intracerebral haemorrhage, and traumatic brain injury (TBI). However, it has to be clarified whether an increased autophagy might worsen neuronal diseases (by inducing cell death) or it may be part of an endogenous protective response. Spinal cord injury (SCI) is a serious and debilitating health problem provoking lifelong disability and leading to neurological dysfunction at and/or below the level of the injury. Autophagy is rising as a significant process in pathological states and engages in cross talk with ROS and RNS in both cell signalling and protein damage. Common recognized features of neurodegenerative diseases, among which SCI, consist of impaired mitochondrial function, oxidative unbalance, accumulation of protein aggregates and the autophagic process. The functional role of autophagy in SCI is currently under intense investigation, and prior studies have characterized this process both in vitro and in vivo. Interestingly, up regulation of autophagy has been reported to both contribute as well as to cause cell death in the spine.