Kibbe, Faculty Advisor, Melina

Rossi, \u2707, Nicholas

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Illinois Wesleyan UniversityDigital Commons @ IWUJohn Wesley Powell Student ResearchConference 2007, 18th Annual JWP ConferenceApr 14th, 9:00 AM - 10:00 AMThe Role of Antioxidants in Nitric-Oxide InducedApoptosis in Vascular Smooth Muscle CellsNicholas Rossi, '07Illinois Wesleyan UniversityMelina Kibbe, Faculty AdvisorIllinois Wesleyan UniversityFollow this and additional works at: http://digitalcommons.iwu.edu/jwprcThis Event is brought to you for free and open access by The Ames Library, the Andrew W. Mellon Center for Curricular and FacultyDevelopment, the Office of the Provost and the Office of the President. It has been accepted for inclusion in Digital Commons @ IWU bythe faculty at Illinois Wesleyan University. For more information, please contact digitalcommons@iwu.edu.©Copyright is owned by the author of this document.Nicholas Rossi, '07 and Melina Kibbe, Faculty Advisor, "The Role of Antioxidants in Nitric-Oxide Induced Apoptosis inVascular Smooth Muscle Cells" (April 14, 2007). John Wesley Powell Student Research Conference. Paper 22.http://digitalcommons.iwu.edu/jwprc/2007/posters/22THE JOHN WESLEY POWELL S TUDENT RESEARCH CONFERENCE - APRIL 2007 Poster Presentation P69 THE ROLE OF ANTIOXIDANTS IN NITRIC-OXIDE INDUCED APOPTOSIS IN VASCULAR SMOOTH MUSCLE CELLS Nicholas Rossi and Melina Kibbe* Biology Department, Illinois Wesleyan University Northwestern University Apoptosis of vascular smooth muscle cel ls (VSMC) has been identified as having an important role in the prevention of neointimal hyperplasia. This is due to the ability of NO to induce programmed cell death, or apoptosis, of VSMC following injury. While the regulation of VSMC apoptosis i s  complex and not fully understood, it has been shown that upon VSMC stimulation with NO there i s  upregulation of the tumor suppressor gene p53 .  Previous studies indicate that down-regulation of p53 results in an increase in cellular ROS. Since p53 is a transcription factor known to affect the transcription of antioxidant proteins, it has been speculated that increased ROS levels are a result of the absence of p53 transcribed antioxidant proteins. ROS levels in VSMC were measured using flow cytometry both at baseline and following NO exposure. At baseline, ROS levels were significantly higher in p53-1- than p53+1+ VSMC. In response to NO treatment, the ROS increase was more pronounced in p53-1- than p53+1+ VSMC. Western blot analysis was performed to identify which pro- and anti-oxidant proteins were affected. The antioxidant protein most differentially expressed between p53-1- and p53+1+ VSMC was peroxiredoxin (PRX)-III. Appropriately, PRX-III is a mitochondrion specific H202 scavenging enzyme and has been cited as a critical regulator of mitochondrial H202. The prospect of PRX­III providing a p53 mediated protective effect in p53+1+ VSMC matches well with the current understanding of PRX-III ' s  role in mitochondria as well  as the model of NO-induced apoptosis. 

The Role of Antioxidants in Nitric-Oxide Induced Apoptosis in Vascular Smooth Muscle Cells

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The Role of Antioxidants in Nitric-Oxide Induced Apoptosis in Vascular Smooth Muscle Cells

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