Expression of two neuronal markers, growth-associated protein 43 and neuron-specific enolase, in rat glial cells

Abstract

Recent studies have revealed that proteins such as growth-associated protein 43 (GAP-43) and neuron-specific enolase (NSE), believed for many years to be expressed exclusively in neurons, are also present in glial cells under some circumstances. Here we present an overview of these observations. GAP-43 is expressed both in vitro and in vivo transiently in immature rat oligodendroglial cells of the central nervous system, in Schwann cell precursors, and in non-myelin-forming Schwann cells of the peripheral nervous system. GAP-43 mRNA is also present in oligodendroglial cells and Schwann cells, indicating that GAP-43 is synthesized in these cells. GAP-43 is also expressed in type 2 astrocytes (stellate-shaped astrocytes) and in some reactive astrocytes but not in type 1 astrocytes (flat protoplasmic astrocytes). These results suggest that GAP-43 plays a more general role in neural plasticity during development of the central and peripheral nervous systems. NSE enzymatic activity and protein and mRNA have been detected in rat cultured oligodendrocytes at levels comparable to those of cultured neurons. NSE expression increases during the differentiation of oligodendrocyte precursors into oligodendrocytes. In vivo, NSE protein is expressed in differentiating oligodendrocytes and is repressed in fully mature adult cells. The upregulation of NSE in differentiating oligodendrocytes coincides with the formation of large amounts of membrane structures and of protoplasmic processes. Similarly, NSE becomes detectable in glial neoplasms and reactive glial cells at the time when these cells undergo morphological changes. The expression of the glycolytic isozyme NSE in these cells, which do not normally contain it, could reflect a response to higher energy demands. This expression may also be related to the neurotrophic and neuroprotective properties demonstrated for this enolase isoform. NSE activity and protein and mRNA have also been found in cultured rat type 1-like astrocytes but at much lower levels than in neurons and oligodendrocytes. Thus GAP-43 and NSE should be used with caution as neuron-specific markers in studies of normal and pathological neural development.

cAMP induces neuronal differentiation of mesenchymal stem cells via activation of extracellular signal-regulated kinase/MAPK

“…Importantly, forskolin treatment for 48 h dramatically increased the expression of neuron-specific proteins, NF200 and NSE. Although some NSE isoforms have been found in glial cells at certain stages of differentiation [18], the identified NSE was most likely derived from neuronaltype cells because GFAP was not expressed (data not shown) in forskolin-treated MSCs under our experimental conditions.…”

Rauwolfia vomitoria and Gongronema latifolium extracts influences cerebellar cortex

“…On the other hand, increased NSE expression in the GL and RV+GL groups, indicate injury to the neurons which the combination was unable to ameliorate successfully. Some glial cells under certain condition also express NSE [52,53]. As it was important to rule out NSE expression by these glial cells, anti-GFAP was also studied as well.…”

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

“…Patients with various systemic autoimmune diseases have been reported to have autoantibodies against α-enolase, but cross-reactivity with NSE in these diseases is rare (6). Neurons and glial cells (including oligodendrocytes) are known to express NSE (43,44); so, it is not surprising to see higher autoreactivity against NSE compared to NNE in an autoimmune disease such as MS, which primarily affects the CNS.…”