مورد إلكتروني
Vascular remodeling in the internal mammary artery graft and association with in situ endothelin-1 and receptor expression
| العنوان: | Vascular remodeling in the internal mammary artery graft and association with in situ endothelin-1 and receptor expression |
|---|---|
| المصدر: | Circulation |
| بيانات النشر: | Lippincott Williams and Wilkins 2006 |
| تفاصيل مُضافة: | Sutherland, Allison Nataatmadja, Maria Walker, Philip Cuttle, Leila Garlick, Bruce West, Malcom |
| نوع الوثيقة: | Electronic Resource |
| مستخلص: | BACKGROUND: The vasoconstricting peptide endothelin-1 (ET-1) has been associated with atherosclerotic cardiovascular disease, vascular smooth muscle cell (VSMC) growth stimulation, and intimal thickening. ET-1 binds 2 receptor subtypes, endothelin A and B, and the ETA receptor mediates vasoconstriction and VSMC growth. This study aims to quantitatively assess arterial remodeling variables and compare them with changes in ET-1, ETA, and ETB expression in the internal mammary artery (IMA). METHODS AND RESULTS: Specimens from 55 coronary artery disease (CAD) patients (45 men, 10 women; mean age 65 years) and 14 control IMA specimens (from 7 men and 7 women; mean age 45 years) were collected. IMA cross sections were assessed by histochemical and immunohistochemical staining methods to quantify the levels of medionecrosis, fibrosis, VSMC growth, ET-1, ETA, ETB, and macrophage infiltration. The percentage area of medionecrosis in the patients was almost double that in the controls (31.85+/-14.52% versus 17.10+/-9.96%, P=0.0006). Total and type 1 collagen was significantly increased compared with controls (65.8+/-18.3% versus 33.7+/-13.7%, P=0.07, and 14.2+/-10.0% versus 4.8+/-2.8%, P=0.01, respectively). Despite ACE and/or statin therapy, ET-1 expression and cell cycling were significantly elevated in the patient IMAs relative to the controls (46.27+/-18.46 versus 8.56+/-8.42, P=0.0001, and 37.29+/-12.88 versus 11.06+/-8.18, P=0.0001, respectively). ETA and ETB staining was elevated in the patient vessels (46.88+/-11.52% versus 18.58+/-7.65%, P=0.0001, and 42.98+/-7.08% versus 34.73+/-5.20%, P=0.0067, respectively). A mild presence of macrophages was noted in all sections. CONCLUSIONS: Elevated distribution of collagen indicative of fibrosis coupled with increased cell cycling and high levels of ET-1 and ETA expression in the absence of chronic inflammation suggests altered IMA VSMC regulation is fundamental to the remodeling process. |
| مصطلحات الفهرس: | Aged, Case-Control Studies, Endothelin/analysis, Female, Fibrosis/pathology, Mammary Arteries/chemistry/*pathology, Middle Aged, Necrosis, Receptor, Receptors, Contribution to Journal |
| URL: | doi:10.1161/CIRCULATIONAHA.105.582890 Sutherland, Allison, Nataatmadja, Maria, Walker, Philip, Cuttle, Leila, Garlick, Bruce, & West, Malcom (2006) Vascular remodeling in the internal mammary artery graft and association with in situ endothelin-1 and receptor expression. Circulation, 113(9), pp. 1180-1188. |
| الإتاحة: | Open access content. Open access content free_to_read Copyright 2006 American Heart Association, Inc. This work is covered by copyright. Unless the document is being made available under a Creative Commons Licence, you must assume that re-use is limited to personal use and that permission from the copyright owner must be obtained for all other uses. If the document is available under a Creative Commons License (or other specified license) then refer to the Licence for details of permitted re-use. It is a condition of access that users recognise and abide by the legal requirements associated with these rights. If you believe that this work infringes copyright please provide details by email to qut.copyright@qut.edu.au |
| ملاحظة: | application/pdf |
| أرقام أخرى: | ATUTQ oai:eprints.qut.edu.au:67217 Faculty of Health; Institute of Health and Biomedical Innovation; School of Biomedical Sciences 871405508 |
| المصدر المساهم: | QUEENSLAND UNIV OF TECH From OAIster®, provided by the OCLC Cooperative. |
| رقم الأكسشن: | edsoai.ocn871405508 |
| قاعدة البيانات: | OAIster |
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