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Cameron Lab

Jian FuScott James Cameron, Ph.D, M.D.

Assistant Professor, Department of Medicine, Aab Cardiovascular Research Institute, Department of Surgery, Cardiac

2009 | M.D. | Medicine | SUNY Upstate Medical University

2003 | Ph.D. | Pharmacology | University of Rochester School of Medicine & Dentistry                                                                 Cameron profile

Research Overview

Our laboratory studies signal transduction pathways in the cardiovascular system as they relate to thrombotic and ischemic diseases. Our research focus is mostly basic and translational in nature. We are particularly interested in identifying existing and novel platelet signaling pathways in myocardial ischemia and in peripheral vascular disorders such as advanced peripheral artery disease (PAD), chronic venous insufficiency (CVI), and aortic aneurysmal disease. An overarching theme of our laboratory is personalized medicine where we aim to better define platelet function in disease states, paying close attention to post-receptor signal transduction pathways. 

Platelets are small anucleate blood particles which play an important role in thrombosis, hemostasis, and inflammation. When patients are treated with anti-platelet drugs, some do not derive expected benefits or they experience off-target adverse events. We have initiated several lines of investigation that show the megakaryocyte-derived platelet phenotype may be fundamentally different in various diseases.

Project 1: Using a murine model of myocardial infarction, we have shown that platelet RNA and the platelet proteome as well as platelet agonist responsiveness are different in the post-myocardial infarct environment. A career-development grant was awarded to study the role of ERK5 and related protein kinases in changing platelet function in ischemic disease. We began enrolling patients with ST-segment elevation myocardial infarction (STEMI) and non ST-segment elevation myocardial infarction (NSTEMI) in July of 2016 to study this phenomenon immediately when the patient arrives in the emergency department at Strong Memorial Hospital.

Project 2: Using a murine model of abdominal aortic aneurysm (AAA) and, along with our colleagues in vascular surgery and cardiac surgery at the University of Rochester, we are studying platelet function both as a consequence of aortic disease and in promoting aortic disease progression. We use genetic approaches to identify platelet targets useful in modulating vascular disease.

Project 3: Using a murine model of critical limb ischemia (CLI) and various models mimicking the human condition of hypoxia, we have identified two important signal transduction mechanisms which lead to dysregulated platelet behavior. This may in part explain why patients with PAD are predisposed to heart attack and stroke. We recently extended our studies to human platelets from PAD patients with our colleagues in vascular surgery at the University of Rochester and in the Department of Pathology at the Johns Hopkins Hospital.

Project 4: It is well-documented that patients who are exposed to inhaled pollutants are predisposed to adverse cardiovascular events. Using platelets taken from patients with acute myocardial infarction, we are working with our colleagues in environmental medicine and public health at the University of Rochester to study the role of particulate matter and environmental pollutants in changing platelet function and promoting thrombosis. These studies may reveal protective mechanisms that could be employed to prevent adverse cardiac events caused by pollutants.

Project 5: Using our existing database of patients with venous thromboembolism (VTE), we are studying various clinical and translational aspect of high risk pulmonary embolism locally and as part of the National Pulmonary Embolism Response Team (PERT) consortium.

We utilize contemporary cell biology, biochemistry, molecular biology, and animal models to address these questions. Our overall goal is to evaluate gaps in clinical care, identify viable signaling pathways in human tissue for drug intervention, and then finally to utilize animal models to test the working hypothesis. We are a friendly, collaborative laboratory with a keen interest in the career development of all laboratory members.

Recent Publications

  1. Schmidt R, Morrell CN, Ling FS, Simlote P, Fernandez G, Rich DQ, Adler D, Gervase J, Cameron SJ. "The Platelet Phenotype in Patients with ST-segment Elevation Myocardial Infarction is Different from Non ST-segment Elevation Myocardial Infarction". Translational Research. 2018; 105: 1-12.

  2. Parsons, MR; Stoner, MC; Doyle, A; Mix, D; Cameron, SJ. "Lights Out: An Unusual Case of Amaurosis Fugax". American Journal of Medicine. 2018; 131(2)(2): e39-e42.

  3. Davis HE, Lu M, Cameron SJ, Bodkin R. "Asymptomatic Hypotension in a Patient with Catheter-related Right Atrial Thrombus". Western Journal of Emergency Medicine. 2018; 2(1).

  4. Ayman Elbadawi, Colin Wright, MD Dhwani Patel, Yu Lin Chen, Justin Mazzillo, Pamela Cameron, Geoffrey D. Barnes, and Scott J. Cameron. "The Impact of a Multi-Specialty Team for High Risk Pulmonary Embolism on Resident and Fellow Education". Vascular Medicine. 2018.

  5. Conrad Gleber, Ayhan Yoruk, M.D, Luke Eastburg, Bruce I. Goldman, and Scott J. Cameron. "Conduction Dysfunction Then It's Expunction: Giant Cell Myocarditis Manifesting as Arrhythmias and Heart Block". American Journal of Medicine. 2018.

  6. Cameron SJ, Mix D, Ture S, Schmidt R, Mohan A, Pariser D, Stoner M, Shah P, Chen L, Zhang H, Field DJ, Modjeski KL, Toth S, Morrell CN. "Hypoxia and Ischemia Promote a Maladaptive Platelet Phenotype". Atherosclerosis Thrombosis and Vascular Biology. 2018.

  7. Daniel Patrick Croft, Robert Block,Scott Cameron, Kristin Evans, Charles Lowenstein, Frederick Ling, Wojciech Zareba, Philip Hopke, Mark Utell, Sally Thurston, Kelly Thevenet-Morrison, David Rich. "Do elevated blood levels of omega-3 fatty acids modify effects of particulate air pollutants on fibrinogen?". Air Quality, Atmosphere & Health. 2018.

More papers:PubMed