Objective: Thoracic aortic aneurysm (TAA) reflects the local expansion of the thoracic aorta; the underlying causal molecular mechanism of TAA is not well understood. Recent studies have shown the importance of transforming growth factor beta (TGFβ) signaling in Marfan and Loeys-Dietz syndromes; however, its role in non-familial, non-syndromic TAA remains unclear. Materials and Methods: We performed histochemical and immunohistochemical analyses for activated (phosphorylated) SMAD2 (P-SMAD2) as an indicator of TGFβ signaling activities in the ascending TAA tissue as well as in the ascending aortic tissue with a normal diameter obtained from 7 patients without any clinical findings suggesting familial or syndromic TAA. Results: TAA samples showed a higher P-SMAD2-positive area than samples with a normal diameter. P-SMAD2 signal was higher in the outer zone of the aortic and TAA walls. Within the TAA tissue, P-SMAD2 staining showed the following two distinct patterns: layer-like staining at the border of the medial layer and the thickened intima and a spot-like staining within the medial layer surrounding the microvessels. Conclusion: These findings suggested that TGFβ signaling is activated in several distinct histopathological contexts in TAA, suggesting a complex role of TGFβ.
Objective: Thoracic aortic aneurysm (TAA) reflects the local expansion of the thoracic aorta; the underlying causal molecular mechanism of TAA is not well understood. Recent studies have shown the importance of transforming growth factor beta (TGFβ) signaling in Marfan and Loeys-Dietz syndromes; however, its role in non-familial, non-syndromic TAA remains unclear. Materials and Methods: We performed histochemical and immunohistochemical analyses for activated (phosphorylated) SMAD2 (P-SMAD2) as an indicator of TGFβ signaling activities in the ascending TAA tissue as well as in the ascending aortic tissue with a normal diameter obtained from 7 patients without any clinical findings suggesting familial or syndromic TAA. Results: TAA samples showed a higher P-SMAD2-positive area than samples with a normal diameter. P-SMAD2 signal was higher in the outer zone of the aortic and TAA walls. Within the TAA tissue, P-SMAD2 staining showed the following two distinct patterns: layer-like staining at the border of the medial layer and the thickened intima and a spot-like staining within the medial layer surrounding the microvessels. Conclusion: These findings suggested that TGFβ signaling is activated in several distinct histopathological contexts in TAA, suggesting a complex role of TGFβ.
Authors: Jason R Cook; Nicholas P Clayton; Luca Carta; Josephine Galatioto; Emily Chiu; Silvia Smaldone; Carol A Nelson; Seng H Cheng; Bruce M Wentworth; Francesco Ramirez Journal: Arterioscler Thromb Vasc Biol Date: 2015-01-22 Impact factor: 8.311
Authors: Benjamin S Brooke; Jennifer P Habashi; Daniel P Judge; Nishant Patel; Bart Loeys; Harry C Dietz Journal: N Engl J Med Date: 2008-06-26 Impact factor: 91.245
Authors: A IJpma; L Te Riet; K M van de Luijtgaarden; P M van Heijningen; J Burger; D Majoor-Krakauer; E V Rouwet; J Essers; H J M Verhagen; I van der Pluijm Journal: J Cardiovasc Dev Dis Date: 2019-11-01