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NotificationsNotify me of updates to Stressed Out and Actin Up: Stress-Activated Protein Kinase Regulation of Actin Remodeling Directs Endothelial Cell Morphology and Migration pp. 177-205
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Stressed Out and Actin Up: Stress-Activated Protein Kinase Regulation of Actin Remodeling Directs Endothelial Cell Morphology and Migration pp. 177-205 $0.00
Authors:  (Meron Mengistu, Joshua B. Slee, Linda J. Lowe-Krentz, Department of Biological Sciences, Lehigh University, Bethlehem, Pennyslvania, USA)
Abstract:
Actin remodeling in the vascular system is central for functions such as vascular
remodeling and contractility. Endothelial cells (EC) that form a monolayer lining the
vasculature undergo remodeling of their actin cytoskeleton in order to (1) change their
polarity, which gives them contractility that allows them to reduce their height in order to
decrease the magnitude of the strain they experience from the blood flow, (2) migrate
during vascular remodeling, and (3) maintain cell-cell contacts for endothelial integrity
and barrier function. Dysfunction in ECs is the first step of atherogenesis, where cell
morphology, migration, and barrier integrity are affected. Atherosclerosis is a
geometrically focal disorder where endothelial dysfunction and subsequent plaque
formation occur in areas of blood re-circulation, such as the outer wall of vessel
bifurcations and areas near vascular branching points. Blood flow exerts different
magnitudes of fluid shear stress (FSS) on endothelial cells, playing a crucial role in the
localization of atherosclerotic lesions. ECs found in regions of arterial curvatures and
bifurcations experience lower FSS conditions and are pre-disposed to atherosclerotic
lesions, while ECs lining the straight parts of arteries are exposed to higher FSS
conditions and are atheroprotected. FSS is an important regulator of EC morphology and
migration. Under low FSS, ECs are polygonal in shape and experience high turnover,
while they are elongated with their longer axes that align in the direction of flow when
exposed to higher FSS conditions. Such morphological change is driven by FSSstimulated
fiber formation and alignment of these fibers in the direction of flow. Cell-cell
integrity is also compromised during atherogenesis, where breaks in the monolayer of
ECs provide openings for monocytes and low-density lipoprotein (LDL) to enter the wall
of the artery and contribute to plaque formation. After atherosclerotic lesions have
formed, one of the treatment options is angioplasty where the blocked or narrowed
arteries are opened using stents. Endothelialization of stents, which requires EC
migration, is important to control vascular tone and prevent restenosis, the re-narrowing
of the artery. In order to remodel the actin cytoskeleton for morphology changes,
migration and maintenance of the barrier function, FSS and other stimuli need to be
translated into chemical signals. The signaling activities of Stress-Activated Protein
Kinases (SAPKs) JNK and p38 are involved in actin remodeling events that regulate
actin dynamics. Both JNK and p38 activities are transiently activated by the higher FSS
treatments, and required to achieve actin alignment in the direction of flow. Other stimuli
that alter actin remodeling and barrier changes also induce activation of stress kinases.
JNK activity is detected in association with stress fibers and cortical actin, and its activity
is required in EC morphology adaptation. p38 activity seems to play a role in actin
remodeling near focal adhesions, where it is detected at the ends of stress fibers. In this
chapter, we review the role of these SAPKs in actin remodeling that leads to EC
alignment in the direction of flow, migration, and maintenance of cell-cell integrity. 


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Stressed Out and Actin Up: Stress-Activated Protein Kinase Regulation of Actin Remodeling Directs Endothelial Cell Morphology and Migration pp. 177-205