title: Blood Brothers: Hemodynamics and Cell-Matrix Interactions in Endothelial Function.
abstract: Alterations in endothelial function contribute to a variety of vascular diseases. In pathological conditions, the endothelium shows a reduced ability to regulate vasodilation (endothelial dysfunction) and a conversion toward a proinflammatory and leaky phenotype (endothelial activation). At the interface between the vessel wall and blood, the endothelium exists in a complex microenvironment and must translate changes in these environmental signals to alterations in vessel function. Mechanical stimulation and endothelial cell interactions with the vascular matrix, as well as a host of soluble factors, coordinately contribute to this dynamic regulation.
  
  
  
  Blood hemodynamics play an established role in the regulation of endothelial function. However, a growing body of work suggests that subendothelial matrix composition similarly and coordinately regulates endothelial cell phenotype such that blood flow affects matrix remodeling, which affects the endothelial response to flow.
  
  
  
  Hemodynamics and soluble factors likely affect endothelial matrix remodeling through multiple mechanisms, including transforming growth factor β signaling and alterations in cell-matrix receptors, such as the integrins. Likewise, differential integrin signaling following matrix remodeling appears to regulate several key flow-induced responses, including nitric oxide production, regulation of oxidant stress, and activation of proinflammatory signaling and gene expression. Microvascular remodeling responses, such as angiogenesis and arteriogenesis, may also show coordinated regulation by flow and matrix.
  
  
  
  Identifying the mechanisms regulating the dynamic interplay between hemodynamics and matrix remodeling and their contribution to the pathogenesis of cardiovascular disease remains an important research area with therapeutic implications across a variety of conditions. Antioxid. Redox Signal. 25, 415-434.
authors.affiliation: 1 Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center-Shreveport , Shreveport, Louisiana.
authors.forename: Arif
authors.initials: A
authors.lastname: Yurdagul
authors.affiliation: 1 Department of Cell Biology and Anatomy, Louisiana State University Health Sciences Center-Shreveport , Shreveport, Louisiana.|2 Department of Pathology and Translational Pathobiology, Louisiana State University Health Sciences Center-Shreveport , Shreveport, Louisiana.
authors.forename: A Wayne
authors.initials: AW
authors.lastname: Orr
mesh_terms: D000818:Animals; D002448:Cell Adhesion; D002453:Cell Cycle; D004730:Endothelium, Vascular / Q000502:physiology*; D005109:Extracellular Matrix / Q000378:metabolism*; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D006439:Hemodynamics; D006801:Humans; D016023:Integrins / Q000378:metabolism; D040542:Mechanotransduction, Cellular; D018919:Neovascularization, Physiologic; D011485:Protein Binding; D033081:Shear Strength; D015398:Signal Transduction; D013314:Stress, Mechanical
chemical_list: D016326:Extracellular Matrix Proteins; D016023:Integrins