The mutual interaction between the host spinal cord and grafted undifferentiated stem cells fosters the production of a lesion-induced secretome
Krisztián Pajer
Tamás Bellák
Antal Nógrádi
1.Department of Anatomy, Histology and Embryology, Faculty of Medicine, University of Szeged, Szeged, Hungary2.Department of Anatomy, Histology and Embryology, Faculty of Medicine, University of Szeged, Szeged, Hungary3.Department of Anatomy, Histology and Embryology, Faculty of Medicine, University of Szeged, Szeged, Hungary
摘要：Pathophysiology of spinal cord injury: Injury to the spinal cord results in loss of gray and white matter i.e., it produces a segmental spinal cord lesion and, as a consequence leads to a fatal loss of motor, sensory and autonomic functions. Spinal cord injuries in humans and other mammals are not followed by the replacement of lost neurons and oligodendrocytes and regrowth of injured axons, instead they lead to permanent, fatal and incurable functional deficits. The prima-ry physical injury is followed by a cascade of tissue-decaying events, called secondary injury, which leads to ischemia, vascular disruption, neuroinflammation, excitotoxicity, demyelination and death of neurons and glial cells (Silva et al., 2014; Figure 1A). The direct mechanical disruption of the vasculature results in the increased permeability of the blood-spinal cord barrier. Due to the leakiness of blood-spinal cord barrier and production of cytokines by activated microglia, a number of various immune cells (T lymphocytes, neutrophils and monocytes) invade the injury site. The macrophages generate a set of inflammatory cytokines such as tumor necrosis factor-α, interleukin (IL)-1α, IL-1β, and IL-6, which may further augment the secondary events (Ahuja et al., 2017). In addition, a number of other disruptive processes contrib-ute to the heterogeneous and time-sensitive pathophysiology of spinal cord injury.
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论文发表日期：2020-10-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：3( 1844-1846 )