scholarly journals Ligation of α 5 β 1 ‐ integrins triggers Ca 2+ sparks in renal vascular smooth muscle cells

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Lavanya Balasubramanian ◽  
C.‐M. Lo ◽  
C.S. Landon ◽  
J.S.K. Sham ◽  
K.‐P. Yip
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Renal Vascular

EGF and TGF-beta regulate neutral endopeptidase expression in renal vascular smooth muscle cells

1997 ◽  
Vol 272 (6) ◽  
pp. C1836-C1843 ◽  
Author(s):  
P. L. Tharaux ◽  
A. Stefanski ◽  
S. Ledoux ◽  
J. M. Soleilhac ◽  
R. Ardaillou ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Transforming Growth Factor ◽  
Muscle Cells ◽  
Neutral Endopeptidase ◽  
Tgf Beta ◽  
Renal Vascular

We recently reported that neutral endopeptidase (NEP) expression on renal vascular smooth muscle cells (VSMC) was downregulated in the presence of serum. Here we examine the role of epidermal growth factor (EGF) and transforming growth factor-beta 1 (TGF-beta) in this downregulation and the consequences of the changes in NEP activity on their mitogenic effects. EGF inhibited NEP activity, whereas TGF-beta was stimulatory. Expression of the enzyme was studied by measuring the binding of [125I]RB-104, a specific NEP inhibitor, and the fluorescence intensity of NEP-labeled cells. Both parameters were decreased by EGF and were increased by TGF-beta. NEP mRNA expression in EGF-treated cells was reduced after 48 h. In contrast, it was increased in TGF-beta-treated cells. Interestingly, NEP inhibition influenced the mitogenic effect of EGF. Indeed, thiorphan, an NEP inhibitor, and an anti-NEP antibody decreased EGF-dependent [3H]thymidine incorporation and cell proliferation by approximately 50%. TGF-beta had no effect on VSMC growth. These results indicate that EGF but not TGF-beta participates in the downregulatory potency of serum on NEP expression in VSMC. They also demonstrate that the full effect of EGF on VSMC proliferation depends on intact NEP activity.

scholarly journals Remanent cell traction force in renal vascular smooth muscle cells induced by integrin-mediated mechanotransduction

2013 ◽  
Vol 304 (4) ◽  
pp. C382-C391 ◽  
Author(s):  
Lavanya Balasubramanian ◽  
Chun-Min Lo ◽  
James S. K. Sham ◽  
Kay-Pong Yip
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Resistance ◽  
Vascular Smooth Muscle Cells ◽  
Traction Force ◽  
Muscle Cells ◽  
Myogenic Response ◽  
Cell Traction ◽  
Renal Vascular

It was previously demonstrated in isolated renal vascular smooth muscle cells (VSMCs) that integrin-mediated mechanotransduction triggers intracellular Ca2+ mobilization, which is the hallmark of myogenic response in VSMCs. To test directly whether integrin-mediated mechanotransduction results in the myogenic response-like behavior in renal VSMCs, cell traction force microscopy was used to monitor cell traction force when the cells were pulled with fibronectin-coated or low density lipoprotein (LDL)-coated paramagnetic beads. LDL-coated beads were used as a control for nonintegrin-mediated mechanotransduction. Pulling with LDL-coated beads increased the cell traction force by 61 ± 12% (9 cells), which returned to the prepull level after the pulling process was terminated. Pulling with noncoated beads had a minimal increase in the cell traction force (12 ± 9%, 8 cells). Pulling with fibronectin-coated beads increased the cell traction force by 56 ± 20% (7 cells). However, the cell traction force was still elevated by 23 ± 14% after the pulling process was terminated. This behavior is analogous to the changes of vascular resistance in pressure-induced myogenic response, in which vascular resistance remains elevated after myogenic constriction. Fibronectin is a native ligand for α5β1-integrins in VSMCs. Similar remanent cell traction force was found when cells were pulled with beads coated with β1-integrin antibody (Ha2/5). Activation of β1-integrin with soluble antibody also triggered variations of cell traction force and Ca2+ mobilization, which were abolished by the Src inhibitor. In conclusion, mechanical force transduced by α5β1-integrins triggered a myogenic response-like behavior in isolated renal VSMCs.

Integrin mobilizes intracellular Ca2+ in renal vascular smooth muscle cells

2001 ◽  
Vol 280 (3) ◽  
pp. C593-C603 ◽  
Author(s):  
Wah-Lun Chan ◽  
N.-H. Holstein-Rathlou ◽  
Kay-Pong Yip
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Initial Response ◽  
Rgd Peptides ◽  
Intracellular Ca ◽  
Functional Blocking ◽  
Renal Vascular

Peptides with the Arg-Gly-Asp (RGD) motif induce vasoconstriction in rat afferent arterioles by increasing the intracellular Ca2+ concentration ([Ca2+]i) in vascular smooth muscle cells (VSMC). This finding suggests that occupancy of integrins on the plasma membrane of VSMC might affect vascular tone. The purpose of this study was to determine whether occupancy of integrins by exogenous RGD peptides initiates intracellular Ca2+ signaling in cultured renal VSMC. When smooth muscle cells were exposed to 0.1 mM hexapeptide GRGDSP, [Ca2+]i rapidly increased from 91 ± 4 to 287 ± 37 nM and then returned to the baseline within 20 s (P < 0.05, 34 cells/5 coverslips). In controls, the hexapeptide GRGESP did not trigger Ca2+mobilization. Local application of the GRGDSP induced a regional increase of cytoplasmic [Ca2+]i, which propagated as Ca2+ waves traveling across the cell and induced a rapid elevation of nuclear [Ca2+]i. Spontaneous recurrence of smaller-amplitude Ca2+ waves were found in 20% of cells examined after the initial response to RGD-containing peptides. Blocking dihydropyridine-sensitive Ca2+ channels with nifedipine or removal of extracellular Ca2+ did not inhibit the RGD-induced Ca2+mobilization. However, pretreatment of 20 μM ryanodine completely eliminated the RGD-induced Ca2+ mobilization. Anti-β1 and anti-β3-integrin antibodies with functional blocking capability simulate the effects of GRGDSP in [Ca2+]i. Incubation with anti-β1- or β3-integrin antibodies inhibited the increase in [Ca2+]i induced by GRGDSP. We conclude that exogenous RGD-containing peptides induce release of Ca2+ from ryanodine-sensitive Ca2+stores in renal VSMC via integrins, which can trigger cytoplasmic Ca2+ waves propagating throughout the cell.

Ischemia induces alterations in actin filaments in renal vascular smooth muscle cells

2002 ◽  
Vol 282 (6) ◽  
pp. F1012-F1019 ◽  
Author(s):  
Osun Kwon ◽  
Carrie L. Phillips ◽  
Bruce A. Molitoris
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Vascular Reactivity ◽  
Ischemia Reperfusion ◽  
Muscle Cells ◽  
Renal Vasculature ◽  
Significant Damage ◽  
Renal Vascular

Although altered renal vascular reactivity is known to occur after ischemia, the structural basis explaining the phenomenon has not been clarified. To evaluate for structural damage to the renal vasculature in ischemic acute renal failure (ARF), F-actin in the renal vasculature of rat kidneys and cultured vascular smooth muscle cells was examined using confocal fluorescence microscopy. The left renal artery was clamped for 15 or 45 min in Sprague-Dawley rats. In other experimental groups, 45 min of renal arterial clamping was followed by 1 or 3 h of reperfusion. Control kidneys were procured without any preceding interventional procedure. F-actin was labeled with either fluorescein or Texas red-conjugated phalloidin. Serial optical sections were collected by confocal microscopy, and image volumes were rendered three dimensionally. The degree of cytoskeletal damage in the vasculature was assessed by semiquantitative scoring of the staining for F-actin. Disorganization/disarray of F-actin, reflected by disruption and clumping of the actin filaments, was observed in arteries, arterioles, and the vasa rectae of the kidney after ischemia or ischemia-reperfusion. Smooth muscle cells from arteries and arterioles showed significant damage to F-actin after either 15 or 45 min of ischemia in a duration-dependent manner. The actin cytoskeleton tended to recover from damage from 45 min of ischemia 1 and 3 h after reperfusion. The vasa rectae did not demonstrate significant damage to F-actin after 15- or 45-min ischemia. However, significant damage to the vasa rectae was manifest 3 h after the reperfusion following 45 min of ischemia. In summary, disorganization/disarray of F-actin in vascular smooth muscle cells of the kidney was observed after ischemia or ischemia-reperfusion. A similar finding was observed in cultured vascular smooth muscle cells. We suggest that this disorganization of the actin cytoskeleton may play a contributory role in the loss of autoregulation of renal blood flow and the aberrant vascular reactivity in postischemic ARF.

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