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      EPAC in Vascular Smooth Muscle Cells

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          Abstract

          Vascular smooth muscle cells (VSMCs) are major components of blood vessels. They regulate physiological functions, such as vascular tone and blood flow. Under pathological conditions, VSMCs undergo a remodeling process known as phenotypic switching. During this process, VSMCs lose their contractility and acquire a synthetic phenotype, where they over-proliferate and migrate from the tunica media to the tunica interna, contributing to the occlusion of blood vessels. Since their discovery as effector proteins of cyclic adenosine 3′,5′-monophosphate (cAMP), exchange proteins activated by cAMP (EPACs) have been shown to play vital roles in a plethora of pathways in different cell systems. While extensive research to identify the role of EPAC in the vasculature has been conducted, much remains to be explored to resolve the reported discordance in EPAC’s effects. In this paper, we review the role of EPAC in VSMCs, namely its regulation of the vascular tone and phenotypic switching, with the likely involvement of reactive oxygen species (ROS) in the interplay between EPAC and its targets/effectors.

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          Most cited references 74

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          Paxillin and focal adhesion signalling.

          To facilitate a rapid response to environmental change, cells use scaffolding - or adaptor - proteins to recruit key components of their signal-transduction machinery to specific subcellular locations. Paxillin is a multi-domain adaptor found at the interface between the plasma membrane and the actin cytoskeleton. Here it provides a platform for the integration and processing of adhesion- and growth factor-related signals.
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            Mitochondrial fission mediates high glucose-induced cell death through elevated production of reactive oxygen species.

            One of the main causes of cardiovascular complications in diabetes is the hyperglycaemia-induced cell injury, and mitochondrial fission has been implicated in the apoptotic process. We investigated the role of mitochondrial fission in high glucose-induced cardiovascular cell injury. We used several types of cultured mouse, rat, and bovine cells from the cardiovascular system, and evaluated mitochondrial morphology, reactive oxygen species (ROS) levels, and apoptotic parameters in sustained high glucose incubation. Adenoviral infection was used for the inhibition of the fission protein DLP1. We found that mitochondria were short and fragmented in cells incubated in sustained high glucose conditions. Under the same conditions, cellular ROS levels were high and cell death was increased. We demonstrated that the increased level of ROS causes mitochondrial permeability transition (MPT), phosphatidylserine exposure, cytochrome c release, and caspase activation in prolonged high glucose conditions. Importantly, maintaining tubular mitochondria by inhibiting mitochondrial fission in sustained high glucose conditions normalized cellular ROS levels and prevented the MPT and subsequent cell death. These results demonstrate that mitochondrial fragmentation is an upstream factor for ROS overproduction and cell death in prolonged high glucose conditions. These findings indicate that the fission-mediated fragmentation of mitochondrial tubules is causally associated with enhanced production of mitochondrial ROS and cardiovascular cell injury in hyperglycaemic conditions.
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              Vascular smooth muscle cells in atherosclerosis

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                Author and article information

                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                21 July 2020
                July 2020
                : 21
                : 14
                Affiliations
                [1 ]Department of Biology, American University of Beirut, P.O. Box 11-0236, Beirut, Lebanon; nww04@ 123456mail.aub.edu (N.W.); eliasbay@ 123456aub.edu.lb (E.B.)
                [2 ]Department of Pharmacology and Therapeutics, Beirut Arab University, P.O. Box 11-5020, Beirut, Lebanon; san413@ 123456bau.edu.lb
                [3 ]Department of Biology, United Arab Emirates University, P.O. Box 15551, Al-Ain, UAE; yusra.aldhaheri@ 123456uaeu.ac.ae (Y.A.-D.); r_iratni@ 123456uaeu.ac.ae (R.I.)
                [4 ]Department of Clinical and Experimental Medicine, University of Messina, 98125 Messina, Italy; abitto@ 123456unime.it
                [5 ]Department of Pharmacology and Toxicology, American University of Beirut, P.O. Box 11-0236, Beirut, Lebanon; ae88@ 123456aub.edu.lb
                [6 ]Department of Pharmacology and Toxicology, Alexandria University, 21526 Alexandria, Egypt
                [7 ]Department of Nutrition, University of Petra, P.O. Box 961343, Amman 11196, Jordan; abadran@ 123456uop.edu.jo
                [8 ]Department of Biochemistry and Molecular Genetics, American University of Beirut, P.O. Box 11-0236, Beirut, Lebanon; firasko@ 123456gmail.com
                [9 ]Department of Biomedical Sciences, Qatar University, P.O. Box 2713, Doha, Qatar
                Author notes
                [* ]Correspondence: ae81@ 123456aub.edu.lb ; Tel.: +961-1-350000 (ext. 4891)
                Article
                ijms-21-05160
                10.3390/ijms21145160
                7404248
                32708284
                ca78324c-4e88-44e4-a1d9-04a4456c35b3
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                Categories
                Review

                Molecular biology

                epac, vascular smooth muscle cells, ros, camp, phenotypic switch, cardiovascular disease

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