Novel Model of Inflammatory Neointima Formation Reveals a Potential Role of Myeloperoxidase in Neointimal Hyperplasia.
From: Vascular Biology Center and Dept. of Surgery, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
American journal of physiology. Heart and circulatory physiology
- Publish Date: Dec 2006
- ISSN: 0363-6135
- Volume: 291
- Issue: 6
- Pages: H3087-93
- Medium: Print
- Language: English
- Citation (JAMA): Yang Jian, Cheng Yunhui, Ji Ruirui, et al. Novel Model of Inflammatory Neointima Formation Reveals a Potential Role of Myeloperoxidase in Neointimal Hyperplasia.. Am. J. Physiol. Heart Circ. Physiol. Dec 2006;291:H3087-93
Abstract
Atherosclerosis, which is characterized by neointima formation, is an inflammatory disease. However, there is no inflammatory product-elicited neointimal model to support the causal role of inflammation in atherogenesis. We reported previously that leukocyte-derived MPO induces vascular injury responses such as endothelial dysfunction. We now test the role of MPO in inflammatory neointima formation. We infused temporarily isolated rat common carotid arteries with MPO (200 nM) and incubated for 1 h. We found that although MPO itself did not induce any neointima formation 2 wk after treatment, in the presence of its substrate, hydrogen peroxide, MPO was able to elicit neointimal hyperplasia. We further confirmed that MPO-induced neointimal hyperplasia is mediated by its product, hypochlorous acid (HOCl). HOCl elicited apoptosis both in intima and media followed by vascular proliferative response and resulted in neointima formation with a heterogeneous cell population. Both histological and functional features of HOCl-treated vessels are similar to those in atherosclerotic lesions. To our knowledge, this is the first direct in vivo demonstration of neointimal formation induced by a product of the inflammatory cascade. The results suggest that MPO may be a mediator for pathological neointima growth. This novel neointimal model could be useful for studying inflammation and atherosclerosis.
Mesh Headings (Keywords): Animals, Apoptosis, Atherosclerosis, Carotid Arteries, Cell Proliferation, Disease Models, Animal, Dose-Response Relationship, Drug, Endothelium, Vascular, Hyperplasia, Hypochlorous Acid, Peroxidase, Rats, Rats, Sprague-Dawley, Time Factors, Tunica Intima, Tunica Media
Check for Full Text / PubMed Unique Identifier (PMID): 16844918
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.