Traumatic Brain Injury and Stem Cell: Pathophysiology and Update on Recent Treatment Modalities

Figure 1

After TBI, exogenous stem stimulate proliferation of endogenous neural stem cells (a). After TBI, there is induction of neurogenesis (b) post-TBI infusion of VEGF. After TBI and rupture of the blood-brain barrier, macrophages will stimulate an initial phase of phagocytic, proteolytic, and proinflammatory functions, while the second phase is characterized by anti-inflammatory functions, which includes regeneration, growth, angiogenesis, and matrix deposition. Microglia initiate inflammatory events. This figure also demonstrates neutrophil invasion and their impact on pathological processes of brain trauma, which includes alteration of vascular permeability and contribution to oxidative damage via secretion of lysosomal enzymes, and changes in cerebral blood flow. In addition, neutrophils act by releasing inflammatory cytokines such as IL-6, IL-1, and tumor necrosis factor alpha (TNF-α) (c). Microglia, monocytes, macrophages, and neutrophils invade areas exhibiting blood-brain barrier damage, and there is extensive upregulation of neutrophil adhesion factors including integrin receptors. Gerry Shaw, microglia and neurons, 25 July 2005, by Creative Commons; hematologist, segmented neutrophils, 31 August 2009, Creative Commons; microphages by Patho via Wikimedia Commons; microglia by Frontier in Cellular Neuroscience, 30 January 2013, Creative Commons.