Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll Molecular basis of endothelial cell morphogenesis in three-dimensional extracellular matrices Davis GE; Bayless KJ; Mavila AAnat Rec 2002[Nov]; 268 (3): 252-75Although many studies have focused on blood vessel development and new blood vessel formation associated with disease processes, the question of how endothelial cells (ECs) assemble into tubes in three dimensions (i.e., EC morphogenesis) remains unanswered. EC morphogenesis is particularly dependent on a signaling axis involving the extracellular matrix (ECM), integrins, and the cytoskeleton, which regulates EC shape changes and signals the pathways necessary for tube formation. Recent studies reveal that genes regulating this matrix-integrin-cytoskeletal (MIC) signaling axis are differentially expressed during EC morphogenesis. The Rho GTPases represent an important class of molecules involved in these events. Cdc42 and Rac1 are required for the process of EC intracellular vacuole formation and coalescence that regulates EC lumen formation in three-dimensional (3D) extracellular matrices, while RhoA appears to stabilize capillary tube networks. Once EC tube networks are established, supporting cells, such as pericytes, are recruited to further stabilize these networks, perhaps by regulating EC basement membrane matrix assembly. Furthermore, we consider recent work showing that EC morphogenesis is balanced by a tendency for newly formed tubes to regress. This morphogenesis-regression balance is controlled by differential gene expression of such molecules as VEGF, angiopoietin-2, and PAI-1, as well as a plasmin- and matrix metalloproteinase-dependent mechanism that induces tube regression through degradation of ECM scaffolds that support EC-lined tubes. It is our hope that this review will stimulate increased interest and effort focused on the basic mechanisms regulating capillary tube formation and regression in 3D extracellular matrices.|*Gene Expression Regulation[MESH]|*Models, Cardiovascular[MESH]|Capillaries/*embryology/ultrastructure[MESH]|Cytoskeleton/physiology[MESH]|Endothelial Growth Factors/physiology[MESH]|Endothelium, Vascular/*embryology[MESH]|Extracellular Matrix[MESH]|Integrins/physiology[MESH]|Intercellular Signaling Peptides and Proteins/physiology[MESH]|Lymphokines/physiology[MESH]|Morphogenesis/genetics[MESH]|Neovascularization, Physiologic/physiology[MESH]|Signal Transduction/physiology[MESH]|Vascular Endothelial Growth Factor A[MESH]|Vascular Endothelial Growth Factors[MESH]|rho GTP-Binding Proteins/physiology[MESH] |