Serum Amyloid A Is Present in Human Saccular Intracranial Aneurysm Walls and Associates With Aneurysm Rupture
Huuska, N., Netti, E., Tulamo, R., Lehti, S., Jahromi, B. R., Kovanen, P. T., & Niemelä, M. (2021). Serum Amyloid A Is Present in Human Saccular Intracranial Aneurysm Walls and Associates With Aneurysm Rupture. Journal of Neuropathology and Experimental Neurology, 80(10), 966-974. https://doi.org/10.1093/jnen/nlab086
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Journal of Neuropathology and Experimental NeurologyAuthors
Date
2021Discipline
Gerontologian tutkimuskeskusHyvinvoinnin tutkimuksen yhteisöGerontology Research CenterSchool of WellbeingCopyright
© The Author(s) 2021. Published by Oxford University Press on behalf of American Association of Neuropathologists, Inc.
Saccular intracranial aneurysm (sIA) rupture leads to a disabling subarachnoid hemorrhage. Chronic inflammation and lipid accumulation in the sIA wall contribute to wall degenerative remodeling that precedes its rupture. A better understanding of the pathobiological process is essential for improved future treatment of patients carrying sIAs. Serum amyloid A (SAA) is an acute-phase protein produced in response to acute and chronic inflammation and tissue damage. Here, we studied the presence and the potential role of SAA in 36 intraoperatively resected sIAs (16 unruptured and 20 ruptured), that had previously been studied by histology and immunohistochemistry. SAA was present in all sIAs, but the extent of immunopositivity varied greatly. SAA immunopositivity correlated with wall degeneration (p = 0.028) and rupture (p = 0.004), with numbers of CD163-positive and CD68-positive macrophages and CD3-positive T lymphocytes (all p < 0.001), and with the expression of myeloperoxidase, matrix metalloproteinase-9, prostaglandin E-2 receptor, and cyclo-oxygenase 2 in the sIA wall. Moreover, SAA positivity correlated with the accumulation of apolipoproteins A-1 and B-100. In conclusion, SAA occurs in the sIA wall and, as an inflammation-related factor, may contribute to the development of a rupture-prone sIA.
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This work was supported by the Helsinki University Hospital EVO grantTYH2018316, Maire Taponen Foundation, the Finnish Medical Founda-tion, and Petri Honkanen Foundation. Wihuri Research Institute is main-tained by the Jenny and Antti Wihuri Foundation.License
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