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Neuroinflammation is widely regarded as chronic, as opposed to acute, inflammation of the central nervous system. [5] Acute inflammation usually follows injury to the central nervous system immediately, and is characterized by inflammatory molecules, endothelial cell activation, platelet deposition, and tissue edema. [6]
Stellate cells are neurons in the central nervous system, named for their star-like shape formed by dendritic processes radiating from the cell body. These cells play significant roles in various brain functions, including inhibition in the cerebellum and excitation in the cortex, and are involved in synaptic plasticity and neurovascular coupling.
Glial fibrillary acidic protein (GFAP) is a protein that is encoded by the GFAP gene in humans. [5] It is a type III intermediate filament (IF) protein that is expressed by numerous cell types of the central nervous system (CNS), including astrocytes [6] and ependymal cells during development. [7]
FS cells having a main role in moderating the neuro-immune/endocrine regulation of inflammation is backed up by data in conjunction with depicting C3a, C5a receptors (which are the main factors of the innate immune system), secreting IL-6 and MIF (inflammatory cytokines), and controlling the release of these cytokines via anti-inflammatory ...
The cells of the neurovascular unit also make up the blood–brain barrier (BBB), which plays an important role in maintaining the microenvironment of the brain. [11] In addition to regulating the exit and entrance of blood, the blood–brain barrier also filters toxins that may cause inflammation, injury, and disease. [12]
The activated stellate cell is characterized by proliferation, contractility, and chemotaxis. This change is seen as a transdifferentiation whereby the cells lose their stellate shape and acquire that of myofibroblasts. [8] [6] This state of the stellate cell is the main source of extracellular matrix production in liver injury. [9]
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