Mechanotransduction and arterial smooth muscle cells: new insight into hypertension and atherosclerosis

Vascular cells depend on multiple stimuli to maintain a biomechanically and biologically stable environment. Mechanical stresses contribute significantly to multiple cellular processes that regulate vascular structure and function. For example, fluid shear stresses control endothelial cell molecular responses. Less attention has focused on responses of the smooth muscle cell, the ‘other’ major vascular cell, to mechanical stimuli, in part because of the experimental difficulties in applying precisely controlled deformation. With the advent of new bioengineered devices, combined with modem technologies for studying molecular expression, we are beginning to understand how the smooth muscle cell responds to and controls the biomechanical environment. These studies will help us to understand vascular diseases where vascular mechanics plays a prominent role, such as hypertension, aneurysm formation and atherosclerotic plaque rupture.

[1]  T. Yamakawa,et al.  Mechanotransduction of rat aortic vascular smooth muscle cells requires RhoA and intact actin filaments. , 1999, Circulation research.

[2]  K. Burridge,et al.  Bidirectional signaling between the cytoskeleton and integrins. , 1999, Current opinion in cell biology.

[3]  L A Hillger,et al.  Moderate dose, three-drug therapy with niacin, lovastatin, and colestipol to reduce low-density lipoprotein cholesterol <100 mg/dl in patients with hyperlipidemia and coronary artery disease. , 1997, The American journal of cardiology.

[4]  F. Luscinskas,et al.  Fluid Flow Modulates Vascular Endothelial Cytosolic Calcium Responses to Adenine Nucleotides , 1994, Microcirculation.

[5]  T D Brown,et al.  Techniques for mechanical stimulation of cells in vitro: a review. , 2000, Journal of biomechanics.

[6]  A. Grodzinsky,et al.  Structure‐Dependent Dynamic Mechanical Behavior of Fibrous Caps From Human Atherosclerotic Plaques , 1991, Circulation.

[7]  B. Berk,et al.  Laminar shear stress: mechanisms by which endothelial cells transduce an atheroprotective force. , 1998, Arteriosclerosis, thrombosis, and vascular biology.

[8]  G. Osol Mechanotransduction by vascular smooth muscle. , 1995, Journal of vascular research.

[9]  A. Barakat,et al.  Spatial relationships in early signaling events of flow-mediated endothelial mechanotransduction. , 1997, Annual review of physiology.

[10]  D E Ingber,et al.  Mechanotransduction across the cell surface and through the cytoskeleton. , 1993, Science.

[11]  A. Chiavegato,et al.  Myosin gene expression and cell phenotypes in vascular smooth muscle during development, in experimental models, and in vascular disease. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[12]  M. Glogauer,et al.  Regulation of stretch-activated intracellular calcium transients by actin filaments. , 1999, Biochemical and biophysical research communications.

[13]  K. Jacobson,et al.  Regulation of cell movement is mediated by stretch-activated calcium channels , 1999, Nature.

[14]  J. Ricotta,et al.  Effect of pressure on cultured smooth muscle cells. , 1997, Life sciences.

[15]  R. Kamm,et al.  Distribution of Circumferential Stress in Ruptured and Stable Atherosclerotic Lesions A Structural Analysis With Histopathological Correlation , 1993, Circulation.

[16]  Van C. Mow,et al.  Cell Mechanics and Cellular Engineering , 2011, Springer New York.

[17]  N. Boudreau,et al.  Extracellular matrix and integrin signalling: the shape of things to come. , 1999, The Biochemical journal.

[18]  P. Libby,et al.  Mechanical strain tightly controls fibroblast growth factor-2 release from cultured human vascular smooth muscle cells. , 1997, Circulation research.

[19]  R. Nemenoff,et al.  Activation of JNK/SAPK and ERK by mechanical strain in vascular smooth muscle cells depends on extracellular matrix composition. , 1997, Biochemical and biophysical research communications.

[20]  P. Libby,et al.  Transcriptional profile of mechanically induced genes in human vascular smooth muscle cells. , 1999, Circulation research.

[21]  P. Libby,et al.  Small Mechanical Strains Selectively Suppress Matrix Metalloproteinase-1 Expression by Human Vascular Smooth Muscle Cells* , 1998, Journal of Biological Chemistry.

[22]  P. Davies,et al.  Flow-mediated endothelial mechanotransduction. , 1995, Physiological reviews.

[23]  M. Gimbrone,et al.  Biomechanical activation: an emerging paradigm in endothelial adhesion biology. , 1997, The Journal of clinical investigation.

[24]  S Glagov,et al.  Cyclic stretching stimulates synthesis of matrix components by arterial smooth muscle cells in vitro. , 2003, Science.

[25]  P. Ganz,et al.  Role of endothelial dysfunction in coronary artery disease and implications for therapy. , 1997, The American journal of cardiology.