Journals / Turkish Journal of Biology / 2014 / Cilt: 38 - Sayı: 2

A preliminary proteomic evaluation of smooth muscle cells in thoracic aortic aneurysms

Pages
238–252
Publication Date
2014-05-16
DOI
—
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AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Here we have attempted to shed light on the cellular mechanisms of TAAs.

📌 3 Key Takeaways

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Objective & Hypothesis:Aortic aneurysm is characterized as localized degeneration of the aorta leading to advanced weakening and widening of the vessel.
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Key Findings & Data:Label-free nano LC-MS/MS analysis of cell extracts resulted in the identification of 256 proteins, 26 of which were differentially regulated by >=1.4-fold.
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Conclusion & Impact:Here we have attempted to shed light on the cellular mechanisms of TAAs.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Key words: Label-free proteomics · thoracic aortic aneurysm · smooth muscle cell

Abstract

Aortic aneurysm is characterized as localized degeneration of the aorta leading to advanced weakening and widening of the vessel. While the exact mechanisms have yet to be determined, current studies indicate that the degradation of extracellular matrix (ECM) proteins and apoptosis of vascular smooth muscle cells (SMCs) may result in extendibility, dilation, and rupture of the vessel. Within the aortic wall, SMCs are implicated as key components involved in disease development, as numerous molecular changes have been reported to occur. Most current studies involve either investigation of proteins constituting a group or pathway in SMCs, or analyses of the whole aortic tissue. In order to determine which proteins are important in the development of thoracic aortic aneurysms (TAAs), we performed comparative proteomic analyses using cultured SMCs from TAAs versus controls. Label-free nano LC-MS/MS analysis of cell extracts resulted in the identification of 256 proteins, 26 of which were differentially regulated by >=1.4-fold. Both previously described and new proteins were identified that were involved in oxidative stress, ECM formation, energy metabolism, or the 14-3-3 pathway. Among these, differential expression of SerpinH1, a protease inhibitor for collagenases, was further verified via immunoblotting. Here we have attempted to shed light on the cellular mechanisms of TAAs.

Özet

Aortic aneurysm is characterized as localized degeneration of the aorta leading to advanced weakening and widening of the vessel. While the exact mechanisms have yet to be determined, current studies indicate that the degradation of extracellular matrix (ECM) proteins and apoptosis of vascular smooth muscle cells (SMCs) may result in extendibility, dilation, and rupture of the vessel. Within the aortic wall, SMCs are implicated as key components involved in disease development, as numerous molecular changes have been reported to occur. Most current studies involve either investigation of proteins constituting a group or pathway in SMCs, or analyses of the whole aortic tissue. In order to determine which proteins are important in the development of thoracic aortic aneurysms (TAAs), we performed comparative proteomic analyses using cultured SMCs from TAAs versus controls. Label-free nano LC-MS/MS analysis of cell extracts resulted in the identification of 256 proteins, 26 of which were differentially regulated by >=1.4-fold. Both previously described and new proteins were identified that were involved in oxidative stress, ECM formation, energy metabolism, or the 14-3-3 pathway. Among these, differential expression of SerpinH1, a protease inhibitor for collagenases, was further verified via immunoblotting. Here we have attempted to shed light on the cellular mechanisms of TAAs.

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Cite This Article

AYHAN, C. A., BAYKAL, B., SERHATLI, M. (2014). A preliminary proteomic evaluation of smooth muscle cells in thoracic aortic aneurysms. Turkish Journal of Biology, Cilt: 38 - Sayı: 2, 238–252. https://ajindex.com/articles/182220

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References (10)

  1. Abdulkareem N, Skroblin P, Jahangiri M, Mayr M (2013). Proteomics in aortic aneurysm—what have we learnt so far? Proteom Clin Appl 7: 504–515.
  2. Alenghat FJ, Ingber DE (2002). Mechanotransduction: all signals point to cytoskeleton, matrix, and integrins. Sci STKE 2002: pe6. Baykal AT, Baykal B, Serhatlı M, Adıgüzel Z, Tunçer MA, Kaçar Ö, Baysal K, Açılan Ayhan C (2013). Proteomic evidence for the plasticity of cultured vascular smooth muscle cells. Turk J Biol 37: 414–425.
  3. Berrier AL, Yamada KM (2007). Cell-matrix adhesion. J Cell Physiol 213: 565–573.
  4. Blunder S, Messner B, Aschacher T, Zeller I, Türkcan A, Wiedemann D, Andreas M, Bluschke G, Laufer G, Schachner T et al. (2011). Characteristics of TAV- and BAV-associated thoracic aortic aneurysms—smooth muscle cell biology, expression profiling, and histological analyses. Atherosclerosis 220: 355–361.
  5. Boddy AM, Lenk GM, Lillvis JH, Nischan J, Kyo Y, Kuivaniemi H (2008). Basic research studies to understand aneurysm disease. Drug News Perspect 21: 142–148.
  6. Booher AM, Eagle KA (2011). Diagnosis and management issues in thoracic aortic aneurysm. Am Heart J 162: 38–46.e1. Christiansen HE, Schwarze U, Pyott SM, Al-Swaid A, Al Balwi M, Alrasheed S, Pepin MG, Weis MA, Eyre DR, Byers PH (2010). Homozygosity for a missense mutation in SERPINH1, which encodes the collagen chaperone protein HSP47, results in severe recessive osteogenesis imperfecta. Am J Hum Genet 86: 389– 3 D’Aguanno S, D’Alessandro A, Pieroni L, Roveri A, Zaccarin M, Marzano V, De Canio M, Bernardini S, Federici G, Urbani A (2010). New insights into neuroblastoma cisplatin resistance: a comparative proteomic and meta-mining investigation. J Proteome Res 10: 416–428.
  7. Drogemuller C, Becker D, Brunner A, Haase B, Kircher P, Seeliger F, Fehr M, Baumann U, Lindblad-Toh K, Leeb T (2009). A missense mutation in the SERPINH1 gene in Dachshunds with osteogenesis imperfecta. PLoS Genet 5: e1000579. El-Hamamsy I, Yacoub MH (2009). Cellular and molecular mechanisms of thoracic aortic aneurysms. Nat Rev Cardiol 6: 771–786.
  8. Freeman AK, Morrison DK (2011). 14-3-3 Proteins: diverse functions in cell proliferation and cancer progression. Semin Cell Dev Biol 7: 681–687.
  9. Gardino AK, Yaffe MB (2011). 14-3-3 proteins as signaling integration points for cell cycle control and apoptosis. Semin Cell Dev Biol 7: 688–695.
  10. Guo DC, Pannu H, Tran-Fadulu V, Papke CL, Yu RK, Avidan N, Bourgeois S, Estrera AL, Safi HJ, Sparks E et al. (2007). Mutations in smooth muscle alpha-actin