Abstract
Traumatic brain injury (TBI) is a heterogeneous disorder that involves brain damage due to external forces. TBI is the main factor of death and morbidity in young males with a high incidence worldwide. TBI causes central nervous system (CNS) damage under a variety of mechanisms, including synaptic dysfunction, protein aggregation, mitochondrial dysfunction, oxidative stress, and neuroinflammation. Glial cells comprise most cells in CNS, which are mediators in the brain’s response to TBI. In the CNS are present astrocytes, microglia, oligodendrocytes, and polydendrocytes (NG2 cells). Astrocytes play critical roles in brain’s ion and water homeostasis, energy metabolism, blood-brain barrier, and immune response. In response to TBI, astrocytes change their morphology and protein expression. Microglia are the primary immune cells in the CNS with phagocytic activity. After TBI, microglia also change their morphology and release both pro and anti-inflammatory mediators. Oligodendrocytes are the myelin producers of the CNS, promoting axonal support. TBI causes oligodendrocyte apoptosis, demyelination, and axonal transport disruption. There are also various interactions between these glial cells and neurons in response to TBI that contribute to the pathophysiology of TBI. In this review, we summarize several glial hallmarks relevant for understanding the brain injury and neuronal damage under TBI conditions.
Highlights
Specialty section: This article was submitted toRedox Physiology, a section of the journal Frontiers in PhysiologyReceived: 13 July 2021 Accepted: 20 September 2021Published: 22 October 2021Citation: Mira RG, Lira M and Cerpa W (2021) Traumatic Brain Injury: Mechanisms of Glial Response.Front
The immunoreactivity of the astrocytic marker glial acidic fibrillary protein (GFAP) (Luo et al, 2014) and the microglial marker ionized calcium-binding adaptor molecule 1 (Iba-1) (Aungst et al, 2014; Chen et al, 2014; Mouzon et al, 2014; Broussard et al, 2018) increase in response to Traumatic brain injury (TBI) In addition, periphery immune cells migrate to the site of damage such as neutrophils (Clark et al, 1994), inflammatory leukocytes (Soares et al, 1995; Schwarzmaier et al, 2013), macrophages, dendritic cells, and T cells (Jin et al, 2012) that contribute in brain damage (Chou et al, 2018; Kramer et al, 2019)
Traumatic brain injury is a critical health problem worldwide leading to death, and a risk factor in the development of neurodegenerative diseases
Summary
In the CNS, we can find several types of glial cells: astrocytes, microglia, oligodendrocytes, and Neuron Glia-antigen two positive cells (NG2 + or polydendrocytes, or oligodendrocyte progenitor cells) (Peters, 2004). Microglia express a set of immune receptors to recognize pathogens, cytokine, chemokines, and complement receptors to develop their function. These cells are highly dynamic, and once activated, they can suffer morphological changes along with changes in protein expression and secretion, releasing pro and anti-inflammatory mediators (Colonna and Butovsky, 2017). NG2 cells are progenitor cells for oligodendrocytes, but they can localize in brain areas where myelination is not required These cells express voltage-gated channels to generate and propagate action potentials; this issue is still debated (Peters, 2004; Eugenin-von Bernhardi and Dimou, 2016; von Bernhardi et al, 2016).
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