Increased flow and shear stress enhance in vivo transforming growth factor-beta1 after experimental arterial injury
| Autor: | Hisham S. Bassiouny, Seymour Glagov, Hrachya Kocharyan, Ruo H. Song, John E. Fortunato |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Male
medicine.medical_specialty Intimal hyperplasia Vascular smooth muscle Carotid Artery Common Hemodynamics Blood Pressure Muscle Smooth Vascular Catheterization Transforming Growth Factor beta Internal medicine medicine Animals RNA Messenger Lagomorpha biology Vascular disease Chemistry Anatomy Blood flow Hyperplasia medicine.disease biology.organism_classification Endocrinology Blood pressure Hemorheology Endothelium Vascular Rabbits Cardiology and Cardiovascular Medicine Carotid Artery Injuries Blood Flow Velocity |
| Zdroj: | Arteriosclerosis, thrombosis, and vascular biology. 20(4) |
| ISSN: | 1079-5642 |
| Popis: | Abstract —We have previously demonstrated that high-flow (HF) conditions inhibit experimental intimal hyperplasia. We hypothesized that such flow conditions may alter transforming growth factor-β1 (TGF-β1) after mural injury. The right common carotid artery (CCA) was balloon-injured in 54 New Zealand White male rabbits. Flow was thereafter preserved (normal flow [NF]), reduced by partial outflow occlusion (low flow [LF]), or increased by ligation of the left CCA (HF). Four sham-operated animals served as uninjured controls. Mean blood flow and pressure in the right CCA were measured before and after flow modulation and before euthanasia (3, 7, and 14 days). TGF-β1 mRNA and protein levels in the right CCA were determined by Northern and ELISA analyses at each time point. At 7 and 14 days, intimal hyperplasia was quantified, and the transmural localization of TGF-β1 was determined by immunohistochemical analysis. Mean flow was reduced from 22±1 to 10±3 mL/min in the LF group and increased to 34±2 mL/min in the HF group ( P 2 and increased in the HF group to 63±6 dyne/cm 2 at 7 days compared with values in uninjured controls (39±2 dyne/cm 2 , P 2 , P P |
| Databáze: | OpenAIRE |
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