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RESEARCH PRODUCT

Serum Amyloid A Is Present in Human Saccular Intracranial Aneurysm Walls and Associates With Aneurysm Rupture

Eliisa NettiPetri T. KovanenRiikka TulamoSatu LehtiMika NiemeläNora HuuskaBehnam Rezai Jahromi

subject

MECHANISMPathologybiomarkkeritAneurysm Ruptured3124 Neurology and psychiatrychemistry.chemical_compoundverisuonitaudit0302 clinical medicineMedicineapolipoproteiinitSerum Amyloid A Protein0303 health sciencesbiologytulehdusaneurysmaINDUCTIONGeneral MedicineC-REACTIVE PROTEINSAANeurologyMyeloperoxidaseImmunohistochemistryInflammation Mediatorsmedicine.symptomSaccular intracranial aneurysmEXPRESSIONmedicine.medical_specialtySubarachnoid hemorrhagelipoproteiinitProstaglandinInflammationLDLPathology and Forensic MedicineLIPOPROTEINS03 medical and health sciencesCellular and Molecular NeuroscienceAneurysmHUMAN MAST-CELLSHumansSerum amyloid Akallonsisäinen aneurysma030304 developmental biologyInflammationSerum Amyloid A Proteinbusiness.industry3112 NeurosciencesIntracranial AneurysmCEREBRAL ANEURYSMS3126 Surgery anesthesiology intensive care radiologymedicine.diseaseAneurysmchemistryDENSITYbiology.proteinEndothelium Vascular3111 BiomedicineNeurology (clinical)business030217 neurology & neurosurgerySerum amyloid A

description

AbstractSaccular 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.

yearjournalcountryeditionlanguage
2021-10-01
http://urn.fi/URN:NBN:fi:jyu-202208264375