Abstract
The balances between NSCs growth and differentiation, and between glial and neuronal differentiation play a key role in brain regeneration after any pathological conditions. It is well known that the nervous tissue shows a poor recovery after injury due to the factors present in the wounded microenvironment, particularly inflammatory factors, that prevent neuronal differentiation. Thus, it is essential to generate a favourable condition for NSCs and conduct them to differentiate towards functional neurons. Here, we show that neuroinflammation has no effect on NSCs proliferation but induces an aberrant neuronal differentiation that gives rise to dystrophic, non-functional neurons. This is perhaps the initial step of brain failure associated to many neurological disorders. Interestingly, we demonstrate that phosphatidylcholine (PtdCho)-enriched media enhances neuronal differentiation even under inflammatory stress by modifying the commitment of post-mitotic cells. The pro-neurogenic effect of PtdCho increases the population of healthy normal neurons. In addition, we provide evidences that this phospholipid ameliorates the damage of neurons and, in consequence, modulates neuronal plasticity. These results contribute to our understanding of NSCs behaviour under inflammatory conditions, opening up new venues to improve neurogenic capacity in the brain.
Highlights
The balances between neural stem cells (NSCs) growth and differentiation, and between glial and neuronal differentiation play a key role in brain regeneration after any pathological conditions
The balance between NSCs proliferation and differentiation is essential for tissue repair[16] and up to know is not clear how it is affected by inflammation
NSCs have a fundamental role after nervous tissue damage as they have the potential for regeneration owing to their capacity of self-renewal and differentiation into neurons[8,32]
Summary
The balances between NSCs growth and differentiation, and between glial and neuronal differentiation play a key role in brain regeneration after any pathological conditions. In response to different types of injuries that cause neurons and oligodendrocytes death, activated astrocytes and the resident immune-like glial cells, the microglia, proliferate and generate proinflammatory cytokines (such as IL-1, IL-6, IFN-γ and TNF-α), chemokines, prostaglandins, and free oxygen radicals, often leading to the development of cerebral damage, and promoting macrophages infiltration[8] Both kinds of cells act as a host defence mechanism eliminating cellular debris and releasing inflammatory factors. In response to inflammatory reactions, it was shown that the glia scar could prevent tissue regeneration by NSCs8, and that LPS-induced neuroinflammation caused synapse loss by a mechanism dependent of microglia activation and IL-1β secretion[14] In this scenario, understanding the NSCs response to these conditions and the mechanisms involved in the integration into the injured brain will be critical for the development of effective therapeutic strategies using stem cells. Addition of liposome of egg-source PtdCho further induces neuronal differentiation and rescues the morphological and functional deficit by modulating neuronal plasticity
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