Publication: Visualizing TGF-ß and BMP signaling in human atherosclerosis: a histological evaluation based on Smad activation
Authors
van Dijk, R.A. ; Engels, C.C ; Schaapherder, A.F ; Mulder-Stapel, A. ; ten Dijke, P. ; Hamming, J.F ; Lindeman, J.H.N.
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Publisher
F. Hernandez y JuanF. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología.
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Background: The TGF-ß superfamily members Transforming Growth Factor-ß (TGF-ß/Activin) and Bone Morphogenetic Proteins (BMP) have been implicated in the pathogenesis of atherosclerosis. However, their role in human disease remains controversial. In this study we used Smad phosphorylation as a read out for TGF-ß and BMP signaling during the initiation, progression and (de)stabilization of human atherosclerotic disease. Material and methods: A systematic analysis was performed in 114 peri-renal aortic patches (stained with Movat Pentachrome, H&E, pSmad2, pSmad1,5,8 and PAI-1) covering the entire atherosclerotic spectrum (van Dijk, 2010). Immunostaining against T-cells (CD3) and monocytes and macrophages (CD68) was used to explore a putative association between TGF-ß and BMP signaling and vascular inflammation.
Results: Smad phosphorylation was present within the normal arterial wall in approximately 10% of the endothelial cells and intimal smooth muscle cells. A significant increase in pSmad2 and pSmad1,5,8 positivity was found in non-progressive lesions (>50% positivity). No further increase or decrease was found in the progressive atherosclerotic lesions, vulnerable and stabilized lesions. No association was found between TGF-ß and BMP signaling and CD3 and CD68 expression, nor cap thickness.
Conclusion: Activation of the TGF-ß and BMP pathways is an early event in atherosclerotic lesion formation. No significant relationships were found between Smad phosphorylation and vessel wall inflammation or plaque vulnerability.
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Citation
Histology and Histopatholgy. Volume 27, number 3 (March), 2012
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