Increased plasma levels of cystatin C and transforming growth factor-beta 1 in patients with coronary artery ectasia: can there be a potential interaction between cystatin C and transforming growth factor-beta 1


Yetkin E., Acikgoz N., Sivri N., Tekin G. O., Yagmur J., Aksoy Y., ...Daha Fazla

CORONARY ARTERY DISEASE, cilt.18, sa.3, ss.211-214, 2007 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 18 Sayı: 3
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1097/mca.0b013e328087bd98
  • Dergi Adı: CORONARY ARTERY DISEASE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.211-214
  • İnönü Üniversitesi Adresli: Evet

Özet

Cystatin C, known as an inhibitor of the cathepsin family of cysteine proteases, has been evaluated in several cardiovascular disorders such as atherosclerosis and acute myocardial infarction. The potential interaction between transforming growth factor-beta 1 and cystatin C has also been demonstrated in some cell types. Accordingly, we aimed to compare the plasma levels of cystatin C and transforming growth factor-beta 1 in patients with coronary artery ectasia coexisting with coronary artery disease and those with coronary artery disease alone. Thirty-nine patients with coronary artery ectasia and coronary artery disease and 35 age and sex-matched patients with coronary artery disease alone were prospectively enrolled in the study. Blood samples of all patients and control participants for measuring plasma cystatin C and transforming growth factor-beta 1 levels were drawn >= 24 h after the coronary angiography. Cystatin C concentrations in plasma were measured by latex-enhanced reagent on a Behring Nephelometer II. Plasma levels of transforming growth factor-beta 1 were measured by using transforming growth factor-beta 1 enzyme-linked immunosorbent assay kit (BioSource International, Inc., Camarillo, California, USA). Plasma level of cystatin C was significantly higher in patients with coronary artery ectasia + coronary artery disease than in patients with coronary artery disease alone (1.05 0.30 mg/dl vs. 0.92 +/- 0.18 mg/mdl, P= 0.025, respectively). Transforming growth factor-beta 1 was also found to be significantly higher in patients with coronary artery ectasia +coronary artery disease compared with those with coronary artery disease (2.47 +/- 0.43 vs. 2.22 +/- 0.43 pg/ml, P=0.02, respectively). The plasma level of cystatin C was significantly but weakly correlated with that of transforming growth factor-beta 1 (r=0.217 P=0.02). We conclude that plasma levels of cystatin C and transforming growth factor-beta 1 are significantly higher in patients with combined coronary artery ectasia and coronary artery disease than in those with coronary artery disease. Correlation between transforming growth factor-beta 1 and cystatin C may also suggest that pathogenesis of coronary artery ectasia might have some different pathways from atherosclerosis with respect to the regulation of extracellular matrix remodeling. Therefore, the role of cystatin in the pathogenesis of coronary artery ectasia and its potential interaction with transforming growth factor-beta 1 should be evaluated in further studies. Coron Artery Dis 18:211-214 (C) 2007 Lippincott Williams & Wilkins.