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Please use this identifier to cite or link to this item: http://hdl.handle.net/1807/25625

Title: Calcium-sensitive Mmechanisms in Vascular Smooth Muscle Cell Cycle Progression as Targets for Therapy
Authors: Hui, Sonya
Advisor: Husain, Mansoor
Department: Physiology
Keywords: Calcium
Cell Cycle
Vascular smooth muscle cell
Issue Date: 1-Jan-2011
Abstract: Increased intracellular calcium (Ca2+) is required for vascular smooth muscle cell (VSMC) proliferation through mechanisms that are not well-known. Preventing calmodulin (CaM)-cyclin E interaction with a synthetic peptide inhibits VSMC proliferation in a cyclin E-dependent manner, without increasing de-differentiation or cell death, or affecting re-endothelialization or collagen deposition. Moreover, in situ Ca2+-sensitive phosphorylation and degradation of the cell cycle inhibitor p27Kip1 (p27) in VSMC is specific to G1 and dependent on camodulin kinase-II (CaMK-II) and the proteasome, but not MEK. Lastly, IQGAP1 binding to CaM increases during G1 with no change in total IQGAP1 expression across the cell cycle. Therefore, we determined the clinical potential of an established mechanism (CaM/cyclin E), the existence of a putative mechanism (CaMK-II/p27), and a target novel mechanism (CaM-IQGAP1). Characterization of calcium-sensitive mechanisms of VSMC cycle control could form the basis for new drug-eluting stent agents that have increased selectivity for rapidly dividing VSMC.
URI: http://hdl.handle.net/1807/25625
Appears in Collections:Master
Department of Physiology - Master theses

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