Analysis of extracellular superoxide dismutase and Akt in ascending aortic aneurysm with tricuspid or bicuspid aortic valve
Author(s) -
Alessandro Arcucci,
Maria Rosaria Ruocco,
F. Albano,
G. Granato,
Vito Romano,
Gaetano Corso,
Ciro Bancone,
Emmanuele De Vendittis,
Alessandro Della Corte,
Stefania Montagnani
Publication year - 2014
Publication title -
european journal of histochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.754
H-Index - 42
eISSN - 2038-8306
pISSN - 1121-760X
DOI - 10.4081/ejh.2014.2383
Subject(s) - bicuspid aortic valve , protein kinase b , elastin , aortic valve , extracellular matrix , medicine , aortic aneurysm , phosphorylation , pathology , chemistry , endocrinology , aorta , biochemistry
Ascending aortic aneurysm (AsAA) is a consequence of medial degeneration (MD), deriving from apoptotic loss of smooth muscle cells (SMC) and fragmentation of elastin and collagen fibers. Alterations of extracellular matrix structure and protein composition, typical of medial degeneration, can modulate intracellular pathways. In this study we examined the relevance of extracellular superoxide dismutase (SOD3) and Akt in AsAA pathogenesis, evaluating their tissue distribution and protein levels in ascending aortic tissues from controls (n=6), patients affected by AsAA associated to tricuspid aortic valve (TAV, n=9) or bicuspid aortic valve (BAV, n=9). The results showed a significant reduction of SOD3, phospho-Akt and Akt protein levels in AsAA tissues from patients with BAV, compared to controls, whereas the differences observed between controls and patients with TAV were not significant. The decreased levels of SOD3 and Akt in BAV aortic tissues are associated with decreased Erk1/Erk2 phosphorylation and MMP-9 levels increase. The authors suggest a role of decreased SOD3 protein levels in the progression of AsAA with BAV and a link between ECM modifications of aortic media layer and impaired Erk1/Erk2 and Akt signaling in the late stages of the aortopathy associated with BAV.
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