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Ann Thorac Surg 2009;88:506-513. doi:10.1016/j.athoracsur.2009.04.030
© 2009 The Society of Thoracic Surgeons
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Ioannis K. Toumpoulis
Constantine E. Anagnostopoulos
Chris K. Rokkas
Dimitrios C. Angouras
Richard J. Shemin
Sidney Levitsky
James D. McCully
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Original Articles: Adult Cardiac

Differential Expression of Collagen Type V and XI {alpha}-1 in Human Ascending Thoracic Aortic Aneurysms

Ioannis K. Toumpoulis, MDa, Julia Thom Oxford, PhDe, Douglas B. Cowan, PhDc, Constantine E. Anagnostopoulos, MDf, Chris K. Rokkas, MDg, Themistocles P. Chamogeorgakis, MDg, Dimitrios C. Angouras, MDg, Richard J. Shemin, MDh, Mohamad Navab, PhDi, Maria Ericsson, BScd, Micheline Federman, PhDb, Sidney Levitsky, MDa, James D. McCully, PhDa,*

a Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts
b Department of Pathology, Beth Israel Deaconess Medical Center, Boston, Massachusetts
c Department of Anesthesiology, Children's Hospital Boston, Boston, Massachusetts
d Electron Microscopy Core Facility, Harvard Medical School, Boston, Massachusetts
e Department of Biology, Biomolecular Research Center, Boise State University, Boise, Idaho
f Department of Cardiothoracic Surgery, St. Luke's – Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, New York
g Department of Cardiothoracic Surgery, Attikon University Hospital, National and Kapodistrian University of Athens, Athens, Greece
h Division of Cardiothoracic Surgery, Cardiovascular Center at the Ronald Reagan UCLA Medical Center, Los Angeles, California
i Department of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, California

Accepted for publication April 9, 2009.

* Address correspondence to Dr McCully, Division of Cardiothoracic Surgery, Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, 77 Avenue Louis Pasteur, Room 144, Boston, MA 02115 (Email: james_mccully{at}hms.harvard.edu).

Background: The molecular mechanisms leading to ascending thoracic aortic aneurysms (ATAAs) remain unknown. We hypothesized that alterations in expression levels of specific fibrillar collagens occur during the aneurysmal process.

Methods: Surgical samples from ascending aortas from patients with degenerative ATAAs were subdivided by aneurysm diameter: small, 5 to 6 cm; medium, 6 to 7 cm; and large, greater than 7 cm; and compared with nonaneurysmal aortas (mean diameter, 2.3 cm).

Results: Histology, immunofluorescence, and electron microscopy demonstrated greater disorganization of extracellular matrix constituents in ATAAs as compared with control with an increase in collagen {alpha}1(XI) within regions of cystic medial degenerative lesions. Real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) showed collagens type V and {alpha}1(XI) were significantly and linearly increased in ATAAs as compared with control (p < 0.001). There was no change in the messenger ribonucleic acid (mRNA) expression levels of collagens type I and III. Western blot analysis showed collagens type I and III were significantly decreased and collagens {alpha}1(XI) and V were significantly increased and were linearly correlated with the size of the aneurysm (p < 0.001 for both).

Conclusions: These results demonstrate that increased collagen {alpha}1(XI) and collagen V mRNA and protein levels are linearly correlated with the size of the aneurysm and provide a potential mechanism for the generation and progression of aneurysmal enlargement.


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