Publications by authors named "Carolyn J Macmillan"
Article Synopsis
- Angiogenesis plays a key role in the inflammatory conditions of the Central Nervous System, and this study explores two specific angiogenesis inhibitors’ effects on a mouse model of Multiple Sclerosis known as EAE.
- The inhibitors B20-4.1.1 and K(1-3) were found to reduce angiogenesis in the spinal cord and improve clinical outcomes without altering local VEGF levels, suggesting effective inhibition.
- While B20-4.1.1 decreased T cell activity and the production of the Th-17 cytokine IL-17, K(1-3) did not have a significant impact on T cell dynamics or cytokine production when tested in vitro.
Angiogenesis in the animal model of multiple sclerosis experimental autoimmune encephalomyelitis (EAE) is regulated by vascular endothelial growth factor (VEGF) and angiopoietin-2. We determined whether VEGF blockade with the anti-VEGF monoclonal antibody bevacizumab could inhibit angiogenesis and affect peripheral pathogenic immune responses in EAE. Mice treated with bevacizumab from the time of onset of clinical signs showed reduced clinical and pathologic scores.
View Article and Find Full Text PDFThe regulation of angiogenesis was studied over the course of the animal model of multiple sclerosis, acute experimental autoimmune encephalomyelitis (EAE) in mice using immunohistochemistry. During EAE, angiogenesis peaked 21 days after disease induction, with significant increases in gray matter and adjacent to the leptomeninges. Angiogenesis correlated with clinical and pathologic scores.
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