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Results: 71 to 80 of 89

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Integrins and the cytoskeleton: focal adhesion kinase and paxillin.
Yasuda T, Kondo S, Owada S, Ishida M, Harris RC
(1999) Nephrol Dial Transplant 14 Suppl 1: 58-60
MeSH Terms: Animals, Cell Adhesion Molecules, Cells, Cultured, Cytoskeletal Proteins, Cytoskeleton, Focal Adhesion Kinase 1, Focal Adhesion Protein-Tyrosine Kinases, Glomerular Mesangium, Integrins, Paxillin, Phosphoproteins, Phosphorylation, Protein-Tyrosine Kinases, Rats, Stress, Mechanical, Tyrosine
Added January 28, 2014
1 Communities
1 Members
0 Resources
16 MeSH Terms
A 7-amino-acid insert in the heavy chain nucleotide binding loop alters the kinetics of smooth muscle myosin in the laser trap.
Lauzon AM, Tyska MJ, Rovner AS, Freyzon Y, Warshaw DM, Trybus KM
(1998) J Muscle Res Cell Motil 19: 825-37
MeSH Terms: Actins, Adenosine Triphosphate, Amino Acid Sequence, Animals, Chickens, Kinetics, Lasers, Molecular Motor Proteins, Muscle Contraction, Muscle, Smooth, Myosin Heavy Chains, Photochemistry, Protein Structure, Tertiary, Stress, Mechanical
Show Abstract · Added May 19, 2014
Two smooth muscle myosin heavy chain isoforms differ by a 7-amino-acid insert in a flexible surface loop located near the nucleotide binding site. The non-inserted isoform is predominantly found in tonic muscle, while the inserted isoform is mainly found in phasic muscle. The inserted isoform has twice the actin-activated ATPase activity and actin filament velocity in the in vitro motility assay as the non-inserted isoform. We used the laser trap to characterize the molecular mechanics and kinetics of the inserted isoform ((+)insert) and of a mutant lacking the insert ((-)insert), analogous to the isoform found in tonic muscle. The constructs were expressed as heavy meromyosin using the baculovirus/insect cell system. Unitary displacement (d) was similar for both constructs (approximately 10 nm) but the attachment time (t(on) for the (-)insert was twice as long as for the (+)insert regardless of the [MgATP]. Both the relative average isometric force (Favg(-insert)/Favg(+insert) = 1.1 +/- 0.2 (mean +/- SE) using the in vitro motility mixture assay, and the unitary force (F approximately 1 pN) using the laser trap, showed no difference between the two constructs. However, as under unloaded conditions, t(on) under loaded conditions was longer for the (-)insert compared with the (+)insert construct at limiting [MgATP]. These data suggest that the insert in this surface loop does not affect the mechanics but rather the kinetics of the cross-bridge cycle. Through comparisons of t(on) from d measurements to various [MgATP], we conclude that the insert affects two specific steps in the cross-bridge cycle, that is, MgADP release and MgATP binding.
1 Communities
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14 MeSH Terms
Mechanical stretch/relaxation stimulates a cellular renin-angiotensin system in cultured rat mesangial cells.
Becker BN, Yasuda T, Kondo S, Vaikunth S, Homma T, Harris RC
(1998) Exp Nephrol 6: 57-66
MeSH Terms: Angiotensin II, Angiotensinogen, Animals, Biomechanical Phenomena, Blotting, Northern, Blotting, Southern, Cells, Cultured, Glomerular Mesangium, Mechanoreceptors, Peptidyl-Dipeptidase A, Phosphatidylinositols, Polymerase Chain Reaction, Pressure, RNA, Messenger, Rats, Receptors, Angiotensin, Renin, Renin-Angiotensin System, Stress, Mechanical
Show Abstract · Added August 19, 2013
Angiotensin II (Ang II) may play a significant role mediating intraglomerular hypertension and glomerular sclerosis. Therefore, we investigated whether a model of pressure-induced stress, mechanical stretch/relaxation, affected the renin-angiotensin system (RAS) in cultured rat mesangial cells. Type 1 Ang II receptor (AT1R) expression was assessed by 125I-Ang II binding and quantitative reverse-transcription polymerase chain reaction. Stretch/relaxation increased steady-state AT1R mRNA levels as well as specific [125I]Ang II binding. Increased AT1R expression was associated with altered AT1R signaling. Ang II (100 nM) increased total phosphoinositide hydrolysis in control cells (186 +/- 25%, n = 6; p < 0.025 vs. no treatment). However, stretch/relaxation for 48 h further augmented AT1R-mediated PI hydrolysis (293 +/- 38%, n = 6; p < 0.025 vs. Ang II treatment alone). We examined other RAS components in mesangial cells subjected to stretch/relaxation. Angiotensinogen, determined by radioimmunoassay of Ang I generation in conditioned media, increased with stretch/relaxation, and reverse-transcription polymerase chain reaction demonstrated increased angiotensinogen gene expression in stretch/relaxation-treated cells. However, renin activity and angiotensin-converting-enzyme-like activity were unaffected by stretch/relaxation. Thus, mesangial cells maintain a local RAS similar to those described in other tissues, and AT1R expression and angiotensinogen production in this cellular RAS are increased by stretch/relaxation. It is likely that mesangial cells in vivo, exposed to variations in intraglomerular pressure, may regulate their responses via a local RAS.
1 Communities
1 Members
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19 MeSH Terms
Mechanical stress-cell function relationships in renal cells.
Harris RC, Kondo S, Yasuda T
(1997) Exp Nephrol 5: 263-70
MeSH Terms: Animals, Endothelium, Vascular, Extracellular Matrix Proteins, Glomerular Mesangium, Humans, Kidney, Muscle, Smooth, Muscle, Smooth, Vascular, Renal Artery, Renal Circulation, Stress, Mechanical
Added January 28, 2014
1 Communities
1 Members
0 Resources
11 MeSH Terms
Alteration of cellular function in rat mesangial cells in response to mechanical stretch relaxation.
Yasuda T, Akai Y, Kondo S, Becker BN, Homma T, Owada S, Ishida M, Harris RC
(1996) Contrib Nephrol 118: 222-8
MeSH Terms: Animals, Cells, Cultured, Gelatinases, Glomerular Mesangium, Matrix Metalloproteinase 2, Metalloendopeptidases, Prostaglandins, Protein Kinase C, Proto-Oncogenes, Rats, Stress, Mechanical, Transforming Growth Factor beta
Added January 28, 2014
1 Communities
1 Members
0 Resources
12 MeSH Terms
Regulation of endothelial cell nitric oxide synthase mRNA expression by shear stress.
Uematsu M, Ohara Y, Navas JP, Nishida K, Murphy TJ, Alexander RW, Nerem RM, Harrison DG
(1995) Am J Physiol 269: C1371-8
MeSH Terms: Animals, Cattle, Cells, Cultured, Dactinomycin, Endothelium, Vascular, Humans, Nitric Oxide Synthase, Nitrites, Potassium Channel Blockers, RNA, Messenger, Stress, Mechanical, Transcription, Genetic
Show Abstract · Added December 10, 2013
Shear stress enhances expression of Ca(2+)-calmodulin-sensitive endothelial cell nitric oxide synthase (ecNOS) mRNA and protein in bovine aortic endothelial cells (BAEC). The present studies were performed to investigate mechanisms responsible for regulation of ecNOS mRNA expression by shear stress and to determine if this induction of ecNOS mRNA is accompanied by an enhanced nitric oxide (NO) production. Shear stresses of 15 dyn/cm2 for 3-24 h resulted in a two- to threefold increase of ecNOS mRNA content quantified by Northern analysis in BAEC. Shear stresses (1.2-15 dyn/cm2) for 3 h resulted in an induction of ecNOS mRNA in a dose-dependent manner. In human aortic endothelial cells, shear stresses of 15 dyn/cm2 for 3 h also resulted in ecNOS mRNA induction. In BAEC, this induction in ecNOS mRNA was prevented by coincubation with actinomycin D (10 micrograms/ml). The K+ channel antagonist tetraethylammonium chloride (3 mM) prevented increase in ecNOS mRNA in response to shear stress. The ecNOS promotor contains putative binding domains for AP-1 complexes, potentially responsive to activation of protein kinase C (PKC). However, selective PKC inhibitor calphostin C (100 nM) did not inhibit ecNOS induction by shear stress. Finally, production of nitrogen oxides under both basal conditions and in response to the calcium ionophore A-23187 (1 microM) by BAEC exposed to shear stress was increased approximately twofold compared with cells not exposed to shear stress. These data suggest that ecNOS mRNA expression is regulated by K+ channel opening, but not by activation of PKC, and that shear not only enhances ecNOS mRNA expression but increases capacity of endothelial cells to release NO.
1 Communities
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0 Resources
12 MeSH Terms
Geometric properties and the predicted mechanical behavior of adult human clavicles.
Harrington MA, Keller TS, Seiler JG, Weikert DR, Moeljanto E, Schwartz HS
(1993) J Biomech 26: 417-26
MeSH Terms: Acromion, Adult, Aged, Biomechanical Phenomena, Clavicle, Elasticity, Female, Forecasting, Humans, Image Processing, Computer-Assisted, Male, Middle Aged, Porosity, Rotation, Sternum, Stress, Mechanical
Show Abstract · Added March 5, 2014
An image processing system was used to examine histomorphometric properties of 15 adult male and female human clavicles. Variations in porosity, cross-sectional area, anatomic and principal moments of inertia were assessed at 2.5-5.0% increments along the length of the clavicles. The clavicle's biomechanical behavior (axial, flexural, and torsional rigidities and the critical force for buckling) was modeled from these data using beam theory. Over threefold variations in porosity and moments of inertia were found along the length of the s-shaped clavicle--the greatest porosity and moments of inertia were located in the variably shaped sternal and acromial thirds of the bone in contrast to the denser and smaller, more circulatory shaped central third of the bone. Clavicle orientation, as indicated by the direction of greatest resistance to bending (maximum principal moment of inertia), was found to rotate from a primarily cranio-caudal orientation at the sternum to a primarily anterior-posterior orientation at the acromion. Based on cross-sectional geometry, section moduli, and estimates of flexural and torsional rigidity, the clavicle was found to be weakest in the central third of its length. These data concur with the fracture location most commonly reported clinically. Analysis of Euler buckling predicted a minimum critical force for buckling during axial loading of approximately two to three body weights for an average adult. Thus, buckling, or a combination of axial loading and bending or torsional loading, must be considered as possible failure mechanisms for this commonly injured bone.
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16 MeSH Terms
Shear-induced platelet activation measured by flow cytometry.
Purvis NB, Giorgio TD, Stelzer GT, Shults KE
(1994) Ann N Y Acad Sci 714: 309-11
MeSH Terms: Antibodies, Monoclonal, Blood Platelets, Cell Membrane, Flow Cytometry, Humans, Platelet Activation, Platelet Aggregation, Platelet Membrane Glycoproteins, Stress, Mechanical
Added March 20, 2014
0 Communities
1 Members
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9 MeSH Terms
The effect of bilayer composition on calcium ion transport facilitated by fluid shear stress.
Giorgio TD, Yek SH
(1995) Biochim Biophys Acta 1239: 39-44
MeSH Terms: Calcium, Cholesterol, Diffusion, Ion Transport, Lipid Bilayers, Liposomes, Permeability, Phosphatidylcholines, Phospholipids, Stress, Mechanical, Viscosity
Show Abstract · Added March 20, 2014
Passive calcium ion permeability across liposome bilayers is increased during exposure to fluid shear forces attainable in the mammalian vasculature. In this study, liposomes prepared from three different lipid mixtures (phosphatidylcholine alone; phosphatidylcholine and cholesterol; a mixture of anionic and cationic phospholipids plus cholesterol) are exposed to uniform shear stress in a rotational viscometer. Liposome permeability to calcium ion is estimated from continuous measurement of free intraliposome calcium ion concentration using a fluorescence technique. Calcium ion permeability in the absence of fluid force and susceptibility to shear-induced permeability modulation are positively correlated with estimated bilayer compressibility. Fluid shear forces are presumed to influence bilayer packing and modulate defect formation in proportion to bilayer compressibility. Bilayer defects produced by fluid forces may increase liposome permeability.
0 Communities
1 Members
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11 MeSH Terms
A note on the use of Quin2 in studying shear-induced platelet aggregation.
Giorgio TD, Hellums JD
(1986) Thromb Res 41: 353-9
MeSH Terms: Adenosine Diphosphate, Aminoquinolines, Blood Platelets, Calcium, Collagen, Humans, In Vitro Techniques, Platelet Aggregation, Stress, Mechanical, Thrombin
Show Abstract · Added March 20, 2014
Quin2, a calcium ion chelator which can penetrate plasma membranes, was used to study the role of intracellular calcium ion concentration in mediating shear-induced platelet activation. Washed platelet suspensions were subjected to various levels of uniform, known shear stress in a cone and plate viscometer in the absence of added agonists. Additional samples were aggregated in response to chemical platelet agonists in a conventional aggregometer. The aggregometer response of Quin2-containing platelets to collagen, thrombin and ADP exhibited increased lag time and reduced maximum rate of aggregation in comparison to controls. However, the extent of aggregation of the Quin2-containing platelets eventually reached the same level as that of the controls. Very different results were obtained for aggregation by shear stress in the viscometer. Shear-induced aggregation was significantly suppressed by Quin2 treatment at both short (30 seconds) and long (300 seconds) times of exposure to the shear field. Shear-induced dense granular release and cellular lysis were unaltered by Quin2 treatment at 30 second exposure times, but both were significantly increased by Quin2 treatment at 300 second exposure times. These results suggest that intracellular calcium ion mobilization is an important early step in shear-induced platelet activation. Additionally, Quin2 appears to have effects resulting in increased platelet fragility. Thus, the findings raise questions on the suitability of Quin2 as an intracellular calcium ion probe in studies in shear fields.
0 Communities
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10 MeSH Terms