Protection by Neuroglobin Expression in Brain Pathologies

Abstract

Astrocytes play an important role in physiological, metabolic, and structural functions, and when impaired, they can be involved in various pathologies including Alzheimer, focal ischemic stroke, and traumatic brain injury. These disorders involve an imbalance in the blood flow and nutrients such as glucose and lactate, leading to biochemical and molecular changes that cause neuronal damage, which is followed by loss of cognitive and motor functions. Previous studies have shown that astrocytes are more resilient than neurons during brain insults as a consequence of their more effective antioxidant systems, transporters, and enzymes, which made them less susceptible to excitotoxicity. In addition, astrocytes synthesize and release different protective molecules for neurons, including neuroglobin, a member of the globin family of proteins. After brain injury, neuroglobin expression is induced in astrocytes. Since neuroglobin promotes neuronal survival, its increased expression in astrocytes after brain injury may represent an endogenous neuroprotective mechanism. Here, we review the role of neuroglobin in the central nervous system, its relationship with different pathologies, and the role of different factors that regulate its expression in astrocytes.

Keywords: astrocytes; brain injury; mitochondria; neuroglobin; neuroprotection.

Figure 1

Representative microphotographs of astrocyte-like cells (T98G cell line) expressing neuroglobin. Data generated in our group showed that in cells subjected to metabolic insult by adding a balanced salt solution devoid of glucose (BSS0), neuroglobin expression is enhanced and homogeneously distributed in the cytoplasm (left). The control condition (BSS5) was the same as BSS0, but adding 5-mM glucose; in this case, neuroglobin expression was decreased in comparison with BSS0 and located in proximity of the cell nucleus (center). Under basal culture conditions with DMEM medium, Ngb expression was similar to that of BSS5.