Neuroglobin, a Factor Playing for Nerve Cell Survival

Abstract

Cell death represents the final outcome of several pathological conditions of the central nervous system and available evidence suggests that in both acute injuries and neurodegenerative diseases it is often associated with mitochondrial dysfunction. Thus, the possibility to prevent mitochondrial events involved in cell death might represent efficient tools to limit neuronal damage. In recent years, increased attention has been paid to the endogenous protein neuroglobin, since accumulating evidence showed that its high expression was associated with preserved mitochondrial function and to an increased survival of nerve cells in vitro and in vivo in a variety of experimental models of cell insult. The biological and structural features of neuroglobin and the mitochondria-related mechanisms of neuroglobin-induced neuroprotection will be here briefly discussed. In this respect, the inhibition of the intrinsic pathway of apoptosis emerges as a key neuroprotective effect induced by the protein. These findings could open the possibility to develop efficient neuroglobin-mediated therapeutic strategies aimed at minimizing the neuronal cell death occurring in impacting neurological pathologies like stroke and neurodegenerative diseases.

The Neuroprotective Effect of Hemin and the Related Mechanism in Sevoflurane Exposed Neonatal Rats

“…The antioxidant and antiapoptotic molecular properties of Ngb may be used as a potential treatment for alleviating neuronal damage, and its increased expression after brain injury may have endogenous neuroprotective effects. Perhaps in the future, we could improve the expression of Ngb by pharmacological induction or gene therapy to alleviate the brain damage caused by sevoflurane exposure (Baez et al, 2016; Guidolin et al, 2016). Interestingly, the expression level of Ngb in the sevoflurane group was also elevated, which may indicate an endogenous protective effect of Ngb.…”

Neuroglobin Can Prevent or Reverse Glaucomatous Progression in DBA/2J Mice

“…In rodent or human retinas, NGB is differentially distributed in the retinal cell layers, with an increased abundance in the GCL and especially in RGCs, 18 , 20 , 50, 51, 52 as we showed in retinas from DBA/2J mice. A recent article reviewed the available data on the neuroprotective role of NGB in a range of pathologic conditions 53 . The possible mechanism of action that leads to the beneficial effect of NGB on nerve-cell survival appears to be linked to mitochondrial function by (1) the preservation of the ATP synthesis rate, ROS homeostasis, and mitochondrial membrane potential and (2) the modulation of death signaling via the shutdown of the apoptotic cascade 53 .…”

“…A recent article reviewed the available data on the neuroprotective role of NGB in a range of pathologic conditions 53 . The possible mechanism of action that leads to the beneficial effect of NGB on nerve-cell survival appears to be linked to mitochondrial function by (1) the preservation of the ATP synthesis rate, ROS homeostasis, and mitochondrial membrane potential and (2) the modulation of death signaling via the shutdown of the apoptotic cascade 53 . For instance, the human NGB protein can efficiently scavenge a variety of ROS (superoxide anions, hydrogen peroxide, and hydroxyl radicals) 15 and also reactive nitrogen species (RNS), such as nitric oxide 54 .…”

Adeno-associated virus-mediated neuroglobin overexpression ameliorates the N-methyl-N-nitrosourea-induced retinal impairments: a novel therapeutic strategy against photoreceptor degeneration

“… 24 NGB is present at a 100-fold greater concentration in the retina than in the brain, implying that the retina may be the most important site of NGB function. 13 , 25 However, evidence on the etiological contribution of NGB is just emerging in retinal diseases. Therefore, we examined the retinal NGB expression in MNU-administered mice.…”