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The publication highlights an important role for antibodies that block the activity of Semaphorin 4D (SEMA4D) in reducing three causes of neuroinflammatory disease including the breakdown of the blood-brain barrier, apoptosis (programmed cell death) of oligodendrocytes precursor cells important for maintaining the myelin coating on neurons, and activation of microglia, innate inflammatory cells of the central nervous system.
In contrast, neither the shortest VEGF121 isoform, which does not bind NRP-1 and thus does not recruit BM cells, nor semaphorin 3A, which attracts cells but inhibits endothelial activation, is capable of sustaining arterial formation (6).
Third, two classes of molecular inhibitors to growth are present in the lesioned CNS to actively block axonal growth: inhibitory extracellular matrix proteins, including chondroitin sulfate proteoglycans, and inhibitory proteins present on adult myelin, including Nogo, myelin-associated glycoprotein, oligodendrocyte-myelin glycoprotein, netrin, semaphorins, Wnt proteins, and others [64-66].
Axons--the long extensions formed by growing brain cells--display neuropilin-1, which reacts to proteins called semaphorins or collapsins, which serve as axonal stop signs.
Scatter-factor and semaphorin receptors: cell signaling for invasive growth.
Transcriptome analysis indicated that five semaphorin receptors (e.
Semaphorin 7A plays a critical role in TGF-beta1-induced pulmonary fibrosis.
This common variant lies on chromosome 5 near a gene known as semaphorin 5A, which is thought to help guide the growth of neurons and their long projections called axons.