Effects of static and cyclic loading in regulating extracellular matrix synthesis by cardiovascular cells.
Extracellular matrix (ECM) provides several structural and functional characteristics to tissues including cell support, mechanical integrity and biological signaling. In cardiovascular tissues, cells produce various ECM components such as collagen, elastin, proteoglycans, matrix metalloproteinases, growth factors and signaling molecules. The cardiovascular cells (cardiac fibroblasts, cardiomyocytes, endothelial cells, and vascular smooth muscle cells) sense the changes in mechanical strains applied to them, through cell-surface receptors such as integrins and ion channels, and adjust their expression and synthesis of ECM molecules in order to adapt their environment to these changes. ECM changes due to altered mechanics are evident in numerous pathological situations including hypertension, cardiac hypertrophy, myocardial infarction, myxomatous heart valve disease, and atherosclerosis. In hypertrophic conditions, for example, increased mechanical loading is involved with enhanced collagen synthesis, whereas in myxomatous and atherosclerotic conditions reduced mechanical strains are accompanied by an accumulation of proteoglycans. Therefore, investigating the effects of various strain patterns on cardiovascular cells can enhance our understanding of ECM regulation and pathologies. This review focuses on the in vitro modulation of the synthesis of various ECM molecules through static or cyclic stretching of cardiovascular cells.
Gupta
Vishal
V
Department of Bioengineering, MS-142, Rice University, Houston, TX 77251-1892, USA.
Grande-Allen
K Jane
KJ
D000818:Animals; D002318:Cardiovascular Diseases / Q000378:metabolism / Q000473:pathology; D002319:Cardiovascular System / Q000166:cytology / Q000378:metabolism* / Q000473:pathology; D005109:Extracellular Matrix / Q000378:metabolism* / Q000648:ultrastructure; D016326:Extracellular Matrix Proteins / Q000096:biosynthesis*; D006801:Humans; D016023:Integrins / Q000378:metabolism; D007473:Ion Channels / Q000502:physiology; D008465:Mechanoreceptors / Q000378:metabolism*; D040542:Mechanotransduction, Cellular / Q000502:physiology
D016326:Extracellular Matrix Proteins; D016023:Integrins; D007473:Ion Channels