SCIRP Mobile Website
Paper Submission

Why Us? >>

  • - Open Access
  • - Peer-reviewed
  • - Rapid publication
  • - Lifetime hosting
  • - Free indexing service
  • - Free promotion service
  • - More citations
  • - Search engine friendly

Free SCIRP Newsletters>>

Add your e-mail address to receive free newsletters from SCIRP.

 

Contact Us >>

WhatsApp  +86 18163351462(WhatsApp)
   
Paper Publishing WeChat
Book Publishing WeChat
(or Email:book@scirp.org)

Article citations

More>>

Bot, I., de Jager, S.C., Zernecke, A., Lindstedt, K.A., van Berkel, T.J., Weber, C. and Biessen, E.A. (2007) Perivascular mast cells promote atherogenesis and induce plaque destabilization in apolipoprotein E-deficient mice. Circulation, 115, 2516-2525. doi:10.1161/01.ATV.14.9.1480

has been cited by the following article:

  • TITLE: Anti eotaxin-2 antibodies attenuate the initiation and progression of experimental atherosclerosis

    AUTHORS: Adi Mor, Arnon Afek, Michal Entin-Meer, Gad Keren, Jacob George

    KEYWORDS: Atherosclerosis; Vulnerable Plaque; Inflammation; Eotaxin-2; Chemokines

    JOURNAL NAME: World Journal of Cardiovascular Diseases, Vol.3 No.4, July 18, 2013

    ABSTRACT: Background: The chemokine eotaxin-2 is a potent chemoattractant for inflammatory cells, the predominants of which are eosinophils. Human and murine atherosclerotic plaques are known to exhibit inflammatory phenotypes where a complex interaction of cytokine and chemokines plays a role. We tested the hypothesis that eotaxin-2 (eo-2) plays a causative role in the initiation and progression of experimental atherosclerosis. Methods and Results: Sera collected from atherosclerotic ApoE knockout (KO) mice, exhibited significantly higher levels of eo-2 compared to sera collected from their background age matched C57BL/6 litters by ELISA. Moreover, levels of eo-2 were higher in old atherosclerotic ApoE KO mice than in young animals. Similarly, the expression level of the eo-2 receptor, CCR3, was increased in splenocytes of old ApoE compared to the young littermates. Administration of polyclonal blocking antibodies to eotaxin-2 resulted in a significant reduction of early atherosclerotic plaques in ApoE KO mice whereas prolonged treatment of mice with advanced plaques led to atheroma stabilization. A monoclonal antibody (D8) prepared against eo-2 attenuated adhesion of lymphocytes to fibronectin and potently inhibited their migration towards VEGF. Monoclonal blocking antibodies to eo-2 also significantly reduced atherosclerotic plaques in ApoE KO mice. Conclusion: Eo-2 serum levels are elevated in sera of ApoE KO mice with experimental atherosclerosis and its blockade is associated with reduced fatty streak accumulation and increased plaque stabilization.