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Adventitial fibroblast abormality in thoracic aortic aneurysms and aortic dissections
Jong Hui Suh1, Jeong-Seob Yoon, Hwan Wook Kim
1Department of Thoracic and Cardiovascular Surgery, Incheon St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Korea.
The Korean Journal of Thoracic and Cardiovascular Surgery
|February 11, 2012
Summary
Adventitial fibroblasts from patients with thoracic aortic aneurysms and dissections (TAAD) show impaired extracellular matrix production and smooth muscle cell transformation. Restoring fibroblast function may offer a new treatment strategy for TAAD.
Area of Science:
- Cardiovascular Biology
- Vascular Cell Biology
- Aortic Disease Pathogenesis
Background:
- Thoracic aortic aneurysms and dissections (TAAD) result from wall tension and defective repair mechanisms involving aortic wall cells.
- Adventitial fibroblasts are crucial for extracellular matrix (ECM) production and smooth muscle cell (SMC) transformation during aortic remodeling.
- This study investigates potential defects in ECM production and SMC transformation in adventitial fibroblasts from TAAD patients.
Purpose of the Study:
- To investigate the functional capacity of adventitial fibroblasts in patients with TAAD.
- To assess ECM production and SMC transformation in TAAD-derived fibroblasts.
- To explore potential therapeutic targets for TAAD.
Main Methods:
- Adventitial fibroblasts were isolated from TAAD patients and control organ donors.
- ECM production was assessed by analyzing MMP-3 expression after TNF-α stimulation.
- SMC transformation capacity was evaluated by measuring SMC marker expression (SM α-actin, SM-MHC, Ki-67, SM calponin) after TGF-β1 treatment.
Main Results:
- TAAD fibroblasts exhibited significantly lower MMP-3 expression compared to controls.
- TGF-β1-stimulated TAAD fibroblasts showed reduced expression of SM α-actin, SM-MHC, and Ki-67.
- Fibroblast-to-SMC transformation was notably delayed in TAAD fibroblasts.
Conclusions:
- Adventitial fibroblasts from TAAD patients have compromised ECM production and SMC transformation capabilities.
- These cellular defects contribute to the pathogenesis of TAAD.
- Functional restoration of adventitial fibroblasts presents a potential novel therapeutic strategy for TAAD prevention and treatment.
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