Differential expression of proteins related to smooth muscle cells and myofibroblasts in human thoracic aortic aneurysm

Amalia Forte, Alessandro Della Corte, Mario Grossi, Ciro Bancone, Ciro Maiello, Umberto Galderisi, Marilena Cipollaro

Research output: Contribution to journalArticlepeer-review

Abstract

Objectives: Increasing knowledge is required for a better comprehension of the etiology of thoracic aortic aneurysm (TAA). The aim of this study was to highlight the modulations in vascular cell phenotypes, including myofibroblasts (MFs), in human TAA specimens compared to healthy aortas. Methods: histology, RT-PCR and immunohistochemical analysis of a panel of molecules, including EDA Fibronectin (Fn), smoothelin, CD34 and alpha-smooth muscle actin (alpha-SMA), selected on the basis of their informative potential as markers of smooth muscle cells (SMCs) and MF phenotypic modulation, were performed on all samples. Results: The media of TAAs was characterized by the absence of smoothelin, the unaltered expression of alpha-SMA accompanied by an alteration of its distribution pattern, and by the activated expression of the ED-A isoform of Fn. We found a concentration of round-shaped cells exclusively in the adventitia and in the perivascular tissue of TAAs, also rich in vasa vasorum, largely expressing alpha-SMA, while a sub-population also expressed ED-A Fn and CD34. CD34 was expressed by several cells in the intima of TAAs, together with cells expressing cytoplasmatic EDA Fn and alpha-SMA in comparison to healthy aortas. Conclusion: TAA specimens show an altered expression and localization of SMC and MF differentiation markers in comparison to healthy aortas, with possible implications on remodeling.
Original languageEnglish
Pages (from-to)795-803
JournalHistology and Histopathology
Volume28
Issue number6
Publication statusPublished - 2013

Subject classification (UKÄ)

  • Physiology

Free keywords

  • Thoracic aortic aneurysm
  • Myofibroblasts
  • Fibronectin
  • CD34
  • Smoothelin
  • Alpha-smooth muscle actin

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