scholarly journals Role of stress fibers and focal adhesions as a mediator for mechano-signal transduction in endothelial cells in situ

2008 ◽  
Vol Volume 4 ◽  
pp. 1273-1282 ◽  
Author(s):  
Kazuo Katoh
Keyword(s):  
Signal Transduction ◽  
Endothelial Cells ◽  
Focal Adhesions ◽  
Stress Fibers

Expression and spatial heterogeneity of dipeptidyl peptidases in endothelial cells of conduct vessels and capillaries

2011 ◽  
Vol 392 (3) ◽  
Author(s):  
Veerle Matheeussen ◽  
Lesley Baerts ◽  
Guido De Meyer ◽  
Gilles De Keulenaer ◽  
Pieter Van der Veken ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Spatial Heterogeneity ◽  
Serine Proteases ◽  
Published Data ◽  
Microvascular Endothelium ◽  
Dipeptidyl Peptidases ◽  
The Individual ◽  
Immunohistochemical Studies

AbstractDipeptidyl peptidase IV (DPPIV)/CD26 is by far the most extensively studied member of the prolyl oligopeptidase family of serine proteases. The discovery of the related enzymes DPP8 and DPP9 necessitates a (re-)evaluation of the DPPIV-like enzymatic activity in cells and organs. In this study, we aimed (1) to investigate the expression of the individual dipeptidyl peptidases in different types of endothelial cells (ECs) and (2) to reconsider published data in relation to our findings. Examination of DPP expression in rat primary ECs of aortic, endocardial and cardiac microvascular origin revealed the presence of DPPIV-like activity in all cell lysates. More than half of this activity could be attributed to DPP8/9. Western blot analysis revealed an abundance of the DPP8 protein as compared to DPP9. The expression of DPPIV and DPP8 was significantly higher in the cardiac microvascular endothelium than in the other ECs, suggesting a more pronounced role of these DPPs in the microvasculature.In situ, DPP activity in ventricular microvasculature was completely inhibited by sitagliptin, indicating that DPPIV is the predominant DPPIV-like enzyme in this organ. By contrast, immunohistochemical studies indicated DPP9 as the predominant DPP in human carotid artery ECs. In conclusion, our results support a highly regulated expression of individual DPPs in ECs, with a spatial heterogeneity in the cardiovascular tree.

Role of CPI-17 in the regulation of endothelial cytoskeleton

2004 ◽  
Vol 287 (5) ◽  
pp. L970-L980 ◽  
Author(s):  
Irina A. Kolosova ◽  
Shwu-Fan Ma ◽  
Djanybek M. Adyshev ◽  
Peyi Wang ◽  
Motoi Ohba ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Molecular Mechanisms ◽  
Rho Kinase ◽  
Focal Adhesions ◽  
Endothelial Permeability ◽  
Dominant Negative ◽  
Microvascular Endothelial Cell ◽  
Microvascular Endothelial ◽  
Lung Microvascular Endothelial Cell

We have previously shown that myosin light chain (MLC) phosphatase (MLCP) is critically involved in the regulation of agonist-mediated endothelial permeability and cytoskeletal organization (Verin AD, Patterson CE, Day MA, and Garcia JG. Am J Physiol Lung Cell Mol Physiol 269: L99–L108, 1995). The molecular mechanisms of endothelial MLCP regulation, however, are not completely understood. In this study we found that, similar to smooth muscle, lung microvascular endothelial cells expressed specific endogenous inhibitor of MLCP, CPI-17. To elucidate the role of CPI-17 in the regulation of endothelial cytoskeleton, full-length CPI-17 plasmid was transiently transfected into pulmonary artery endothelial cells, where the background of endogenous protein is low. CPI-17 had no effect on cytoskeleton under nonstimulating conditions. However, stimulation of transfected cells with direct PKC activator PMA caused a dramatic increase in F-actin stress fibers, focal adhesions, and MLC phosphorylation compared with untransfected cells. Inflammatory agonist histamine and, to a much lesser extent, thrombin were capable of activating CPI-17. Histamine caused stronger CPI-17 phosphorylation than thrombin. Inhibitory analysis revealed that PKC more significantly contributes to agonist-induced CPI-17 phosphorylation than Rho-kinase. Dominant-negative PKC-α abolished the effect of CPI-17 on actin cytoskeleton, suggesting that the PKC-α isoform is most likely responsible for CPI-17 activation in the endothelium. Depletion of endogenous CPI-17 in lung microvascular endothelial cell significantly attenuated histamine-induced increase in endothelial permeability. Together these data suggest the potential importance of PKC/CPI-17-mediated pathway in histamine-triggered cytoskeletal rearrangements leading to lung microvascular barrier compromise.

scholarly journals Activation of Rho-kinase and focal adhesion kinase regulates the organization of stress fibers and focal adhesions in the central part of fibroblasts

2017 ◽  
Author(s):  
Kazuo Katoh
Keyword(s):  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Adhesion Formation ◽  
Rho Kinase ◽  
Focal Adhesions ◽  
Fiber Formation ◽  
Stress Fibers ◽  
Focal Adhesion Formation ◽  
Specific Regulation

Specific regulation and activation of focal adhesion kinase (FAK) are thought to be important for focal adhesion formation, and activation of Rho-kinase has been suggested to play a role in determining the effects of FAK on the formation of stress fibers and focal adhesions. To clarify the role of FAK in stress fiber formation and focal adhesion organization, we examined the formation of new stress fibers and focal adhesions by activation of Rho-kinase in FAK knockout (FAK–/–) fibroblasts. FAK–/– cells were elliptical in shape, and showed reduced numbers of stress fibers and focal adhesions in the central part of the cells along with large focal adhesions in the peripheral regions. Activation of Rho-kinase in FAK–/– cells transiently increased the actin filaments in the cell center, but these did not form typical thick stress fibers. Moreover, only plaque-like structures as the origins of newly formed focal adhesions were observed in the center of the cell. Furthermore, introduction of an exogenous GFP-labeled FAK gene into FAK–/– cells resulted in increased numbers of stress fibers and focal adhesions in the center of the cells, which showed typical fibroblast morphology. These results indicated that FAK plays an important role in the formation of stress fibers and focal adhesions as well as in regulation of cell shape and morphology with the activation of Rho-kinase.

scholarly journals Distribution of Cytoskeletal Components in Endothelial Cells in the Guinea Pig Renal Artery

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Kazuo Katoh ◽  
Yasuko Noda
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Renal Artery ◽  
Laser Scanning ◽  
Fluid Shear Stress ◽  
Focal Adhesions ◽  
Laser Scanning Microscopy ◽  
Stress Fibers ◽  
Confocal Laser ◽  
Pulsatile Pressure

The cytoskeletal components of endothelial cells in the renal artery were examined by analysis of en face preparations under confocal laser scanning microscopy. Renal arterial endothelial cells were shown to be elongated along the direction of blood flow, while stress fibers ran perpendicular to the flow in the basal portion. Focal adhesions were observed along the stress fibers in dot-like configurations. On the other hand, stress fibers in the apical portion of cells ran along the direction of flow. The localizations of stress fibers and focal adhesions in endothelial cells in the renal artery differed from those of unperturbed aortic and venous endothelial cells. Tyrosine-phosphorylated proteins were mainly detected at the sites of cell-to-cell apposition, but not in focal adhesions. Pulsatile pressure and fluid shear stress applied over endothelial cells in the renal artery induce stress fiber organization and localization of focal adhesions. These observations suggest that the morphological alignment of endothelial cells along the direction of blood flow and the organization of cytoskeletal components are independently regulated.

scholarly journals Microvascular pericytes contain muscle and nonmuscle actins.

1985 ◽  
Vol 101 (1) ◽  
pp. 43-52 ◽  
Author(s):  
I M Herman ◽  
P A D'Amore
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Plasma Membrane ◽  
Fluorescence Microscopy ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Stress Fibers ◽  
Fiber Bundles

We have affinity-fractionated rabbit antiactin immunoglobulins (IgG) into classes that bind preferentially to either muscle or nonmuscle actins. The pools of muscle- and nonmuscle-specific actin antibodies were used in conjunction with fluorescence microscopy to characterize the actin in vascular pericytes, endothelial cells (EC), and smooth muscle cells (SMC) in vitro and in situ. Nonmuscle-specific antiactin IgG stained the stress fibers of cultured EC and pericytes but did not stain the stress fibers of cultured SMC, although the cortical cytoplasm associated with the plasma membrane of SMC did react with nonmuscle-specific antiactin. Whereas the muscle-specific antiactin IgG failed to stain EC stress fibers and only faintly stained their cortical cytoplasm, these antibodies reacted strongly with the fiber bundles of cultured SMC and pericytes. Similar results were obtained in situ. The muscle-specific antiactin reacted strongly with the vascular SMC of arteries and arterioles as well as with the perivascular cells (pericytes) associated with capillaries and post-capillary venules. The non-muscle-specific antiactin stained the endothelium and the pericytes but did not react with SMC. These findings indicate that pericytes in culture and in situ possess both muscle and nonmuscle isoactins and support the hypothesis that the pericyte may represent the capillary and venular correlate of the SMC.

Role of marginal stress fibers formed in the rat vascular endothelial cells

1993 ◽  
Vol 25 (6) ◽  
pp. 825-831 ◽  
Author(s):  
Keiji Sugimoto ◽  
Sachiko Fujii ◽  
Haruhiko Sago ◽  
Kazumi Yoshida ◽  
Tohru Takemasa ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Stress Fibers ◽  
Vascular Endothelial

Signal transduction in endothelial cells by the angiogenesis inhibitor histidine-rich glycoprotein targets focal adhesions

2006 ◽  
Vol 312 (13) ◽  
pp. 2547-2556 ◽  
Author(s):  
Chunsik Lee ◽  
Johan Dixelius ◽  
Åsa Thulin ◽  
Harukiyo Kawamura ◽  
Lena Claesson-Welsh ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Endothelial Cells ◽  
Angiogenesis Inhibitor ◽  
Focal Adhesions

scholarly journals Endothelial cell infection in vivo by equine infectious anaemia virus

1999 ◽  
Vol 80 (9) ◽  
pp. 2393-2397 ◽  
Author(s):  
J. Lindsay Oaks ◽  
Catherine Ulibarri ◽  
Timothy B. Crawford
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Infection ◽  
Tissue Macrophage ◽  
Cell Type Specific ◽  
Weakly Virulent ◽  
Equine Infectious Anaemia Virus

Equine infectious anaemia virus (EIAV) infection of horses is characterized clinically by recurrent episodes of fever, thrombocytopenia and anaemia. In vivo, the only site of virus replication that has been previously demonstrated for EIAV is the tissue macrophage. In this study, in situ hybridization for EIAV was combined with immunohistochemistry for cell-type-specific markers to identify infected endothelial cells. EIAV-infected endothelial cells and macrophages were detected in horses infected with either virulent wild-type or with weakly virulent tissue culture-adapted strains of EIAV. The role of endothelial cell infection in the pathogenesis of EIAV remains undefined, but could contribute to the development of thrombocytopenia. However, endothelial cell infection does not appear to be a determinant of virulence for EIAV.

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