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SirT1 regulates vascular smooth muscle cell plasticity : implications for age-related cardiovascular disease / by Anne Marie Thompson.

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Author	Thompson, Annemarie.
Title	SirT1 regulates vascular smooth muscle cell plasticity : implications for age-related cardiovascular disease / by Anne Marie Thompson.
Date	2014
Abstract	Loss of vascular smooth muscle cell function is a hallmark of vascular disease. Vascular smooth muscle cells become increasingly resistant to phenotypic modulation, apoptotic and senescent. Sirtuin 1 (SirT1) is a deactylase that regulates substrates associated with stress mitigation, metabolism and aging. We investigated the role of SirT1 in cellular aging and the function this protein plays in the context of phenotypic modulation, cellular response to stress and cellular senescence. We utilized isolated human smooth muscle cells from patients ranging in age from 12-82 years. We made the novel finding that SirT1, upon stimulation, induced vascular smooth muscle cell differentiation through activation of AKT2. Furthermore, we demonstrate that endogenous SirT1 levels are significantly reduced as a product of age. Age-related loss of SirT1 correlated in functional deficits; diminished stress response, reduced capacity for migration and proliferation and increased cellular senescence. Manipulation of SirT1 levels in young cells resulted in loss of migration and proliferation capability. These data, at least in part, explain one of the molecular changes that occur in the aged vasculature, which predisposes the population to increased risk of cardiovascular disease
Description	xv, 114 leaves : ill. (some col.)
Format	application/pdf
College	Dartmouth College. Experimental and Molecular Medicine Program. NhDDartmouth Medical School.
Issuing Body	Dartmouth Dissertations are made available through the Dartmouth Digital Library.
Degree	Thesis (Ph.D.)--Dartmouth College.
Copyright	All rights reserved. No part of this book may be reproduced in any form by any electronic or mechanical means without permission in writing from the author.
DOI	http://dx.doi.org/10.1349/ddlp.1211

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