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ANRIL Proposal

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ANRIL Proposal
Azam Khorshidi

Dissecting the role of ANRIL in modulating endothelial cells function and atherosclerosis

Name: Azam (Anna) Khorshidi
Department: Laboratory Medicine & Pathobiology
Program: PhD
Supervisor: Dr. Burton Yang
Topic of graduate study: Role of miR-17 in the breast cancer initiation and progression
Key words: Atherosclerosis, Plaque formation, lncRNA, Endothelia dysfunction
Email: anna.khorshidi@mail.utoronto.ca

1

Azam Khorshidi

Impact:
Endothelial dysfunction is considered a key event in the evolution of atherosclerotic plaques.
This study will seek to uncover the role of a recently discovered long non-coding RNA
(LncRNA) in controlling the integrity of endothelial cells (ECs) of the arterial wall and its possible role in preventing senescence.
1. Introduction
1.1 Atherosclerosis is a leading cause of death worldwide. Atherosclerosis is the primary cause of heart disease and stroke and, thus, the most common cause of morbidity and mortality worldwide [1]-[2]. In western societies, it is the underlying cause of about 50% of all deaths.
Epidemiological studies have revealed several important environmental and genetic risk factors associated with atherosclerosis. Progress in defining the cellular and molecular interactions involved, however, has been hindered by the disease’s complexity [3-4]. Several risk factors for atherosclerosis have been identified such as tobacco use, obesity and hyperlipidemia.
1.2 Different stages of atheromatous plaque development. Atherogenesis refers to the development of plaques in the inner lining of the arteries. Arterial endothelial cells, which normally resist attachment of the white blood cells streaming past them, express adhesion molecules that capture leukocytes on their surfaces when subjected to irritative stimuli (such as dyslipidaemia, hypertension or pro-inflammatory mediators). Parallel changes in endothelial permeability and the composition of the extracellular matrix



References: Lusis AJ. Atherosclerosis. Nature 2000; 407(6801):233-41. interferon-gamma signalling response. Nature 2011; 470(7333):264-8.

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