THE RELATIONSHIP BETWEEN THE CALCIUM CONTENT OF DEPOLARIZED MAMMALIAN SMOOTH MUSCLE AND ITS CONTRACTILITY IN RESPONSE TO ACETYLCHOLINE

1968 ◽  
Vol 46 (4) ◽  
pp. 435-446 ◽  
Author(s):  
Julia M Potter ◽  
MP Sparrow
Keyword(s):  
Smooth Muscle ◽  
Calcium Content ◽  
The Relationship

scholarly journals The Role and Mechanism ofα-Klotho in the Calcification of Rat Aortic Vascular Smooth Muscle Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Tianlei Chen ◽  
Huijuan Mao ◽  
Cheng Chen ◽  
Lin Wu ◽  
Ningning Wang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Signaling Pathway ◽  
Vascular Smooth Muscle Cells ◽  
Calcium Content ◽  
Alizarin Red S ◽  
Alizarin Red ◽  
Calcium Deposits

Objective. To investigate the role and possible mechanism ofα-Klotho in the calcification and the osteogenic transition of cultured VSMCs.Methods. VSMCs were culturedin vitroand divided into 5 groups, each using a different medium: (1) control; (2)β-GP; (3)β-GP + Klotho; (4)β-GP + LiCl; (5)β-GP + Klotho + LiCl. Calcium deposits were visualized using Alizarin Red S staining. The calcium concentrations were determined by the o-cresolphthalein complexone method. BMP2, Runx2 andβ-catenin levels were estimated by western blotting, and the level ofα-SMA was determined by using immunofluorescence at day 12.Results.β-GP induced an increase in the expression of BMP2, Runx2, andβ-catenin. The calcium content increased, and the expression ofα-SMA decreased. Alizarin Red S staining was positive under the high phosphorus conditions. BMP2, Runx2, andβ-catenin levels and the calcium content decreased when the cells were cultured with rmKlotho; however, the levels of each were upregulated after treatment with the LiCl.Conclusions. Klotho can ameliorate the calcification and osteogenic transition of VSMCs induced byβ-GP. The mechanism of Klotho in preventing calcification in VSMCs may be partially mediated by the inhibition of the Wnt/β-catenin signaling pathway.

scholarly journals The relationship between lymphangion chain length and maximum pressure generation established through in vivo imaging and computational modeling

2017 ◽  
Vol 313 (6) ◽  
pp. H1249-H1260 ◽  
Author(s):  
Mohammad S. Razavi ◽  
Tyler S. Nelson ◽  
Zhanna Nepiyushchikh ◽  
Rudolph L. Gleason ◽  
J. Brandon Dixon
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Minimally Invasive ◽  
Chain Length ◽  
Maximum Pressure ◽  
Computational Simulations ◽  
A Chain ◽  
Lymphatic Pumping ◽  
The Relationship

The intrinsic contraction of collecting lymphatic vessels serves as a pumping system to propel lymph against hydrostatic pressure gradients as it returns interstitial fluid to the venous circulation. In the present study, we proposed and validated that the maximum opposing outflow pressure along a chain of lymphangions at which flow can be achieved increases with the length of chain. Using minimally invasive near-infrared imaging to measure the effective pumping pressure at various locations in the rat tail, we demonstrated increases in pumping pressure along the length of the tail. Computational simulations based on a microstructurally motivated model of a chain of lymphangions informed from biaxial testing of isolated vessels was used to provide insights into the pumping mechanisms responsible for the pressure increases observed in vivo. These models suggest that the number of lymphangions in the chain and smooth muscle cell force generation play a significant role in determining the maximum outflow pressure, whereas the frequency of contraction has no effect. In vivo administration of nitric oxide attenuated lymphatic contraction, subsequently lowering the effective pumping pressure. Computational simulations suggest that the reduction in contractile strength of smooth muscle cells in the presence of nitric oxide can account for the reductions in outflow pressure observed along the lymphangion chain in vivo. Thus, combining modeling with multiple measurements of lymphatic pumping pressure provides a method for approximating intrinsic lymphatic muscle activity noninvasively in vivo while also providing insights into factors that determine the extent that a lymphangion chain can transport fluid against an adverse pressure gradient. NEW & NOTEWORTHY Here, we report the first minimally invasive in vivo measurements of the relationship between lymphangion chain length and lymphatic pumping pressure. We also provide the first in vivo validation of lumped parameter models of lymphangion chains previously developed through data obtained from isolated vessel testing.

scholarly journals MiR-365-3p is Involved in IL17-Mediated Asthma in Mouse Model

2020 ◽  
Author(s):  
Weijia Wang ◽  
Ying Li ◽  
Xiaoyan Qu ◽  
Dong Shang ◽  
Qiaohong Qin ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Target Gene ◽  
Alveolar Epithelial Cells ◽  
Mouse Lung ◽  
Collagen Deposition ◽  
Wild Type ◽  
Sterile Saline ◽  
The Relationship

Abstract BACKGROUND The IL-17 superfamily, which mediates cross-talk between the adaptive and innate immune systems, has been associated with severity of asthma. The role of miRNAs in the disease has been paid much attention. To explore the roles of IL-17 in asthma and the relationship between IL-17 and miRNAs, we used a model of severe asthma driven by chronic respiratory exposure to house dust mite (HDM) exposure in wild type and IL-17KO mice, followed with miRNA profiling assays and analysis.METHODS Male and female C57BL/6 mice (6-8 weeks old) and IL-17KO mice (C57BL/6 background) were exposed to purified HDM extract intranasally for 5 days/week for 5 consecutive weeks. Sterile saline was used as the control. The parameters including airway responsiveness, inflammatory cells in bronchoalveolar lavage fluid (BALF), airway smooth muscle bundle, collagen deposition, and cytokine levels in BALF were examined. The miRNA profile of mouse lung tissue was analyzed by microarray assays. The dysregulation of miRNA related to IL-17 and asthma was validated by qRT-PCR. The in vitro cell culture experiment was performed to confirm the relationship between IL-17 and selected miRNA. The regulation of miRNA on predicted target gene was validated by administration of miRNA mimics. RESULTS The expression of IL-17A significantly increased in wild type (WT) mice with HDM exposure compared to the control mice. IL-17 deficiency did not reduce airway hyper responsiveness (AHR) induced by HDM exposure. In comparison to HDM-exposed WT mice, BALF neutrophils in IL-17KO mice were significantly decreased. In WT mice, HDM exposure led to increased expression of IL-4 and KC, which was significantly decreased in IL-17KO mice. Furthermore, under HDM exposure, significantly less airway smooth muscle mass and collagen deposition was found in IL-17KO mice compared to WT mice. In the dysregulated miRNAs, the decreased expression of miR-365-3p in HDM-exposed WT mice was validated, and its expression recovered in IL-17KO mice. Furthermore, miR-365-3p was decreased in mouse alveolar epithelial cells by IL-17 treatment. The transfection of miR-365-3p mimics decreased the expression of predicted target gene ARRB2.

Cooperative attachment of cross bridges predicts regulation of smooth muscle force by myosin phosphorylation

2004 ◽  
Vol 287 (3) ◽  
pp. C594-C602 ◽  
Author(s):  
Christopher M. Rembold ◽  
Robert L. Wardle ◽  
Christopher J. Wingard ◽  
Timothy W. Batts ◽  
Elaine F. Etter ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Time Course ◽  
Muscle Force ◽  
Regulatory System ◽  
Force Development ◽  
Cross Bridge ◽  
Cross Bridges ◽  
The Relationship ◽  
Cooperative Activation

Serine 19 phosphorylation of the myosin regulatory light chain (MRLC) appears to be the primary determinant of smooth muscle force development. The relationship between MRLC phosphorylation and force is nonlinear, showing that phosphorylation is not a simple switch regulating the number of cycling cross bridges. We reexamined the MRLC phosphorylation-force relationship in slow, tonic swine carotid media; fast, phasic rabbit urinary bladder detrusor; and very fast, tonic rat anococcygeus. We found a sigmoidal dependence of force on MRLC phosphorylation in all three tissues with a threshold for force development of ∼0.15 mol Pi/mol MRLC. This behavior suggests that force is regulated in a highly cooperative manner. We then determined whether a model that employs both the latch-bridge hypothesis and cooperative activation could reproduce the relationship between Ser19-MRLC phosphorylation and force without the need for a second regulatory system. We based this model on skeletal muscle in which attached cross bridges cooperatively activate thin filaments to facilitate cross-bridge attachment. We found that such a model describes both the steady-state and time-course relationship between Ser19-MRLC phosphorylation and force. The model required both cooperative activation and latch-bridge formation to predict force. The best fit of the model occurred when binding of a cross bridge cooperatively activated seven myosin binding sites on the thin filament. This result suggests cooperative mechanisms analogous to skeletal muscle that will require testing.

Regulation of shortening velocity by cross-bridge phosphorylation in smooth muscle

1988 ◽  
Vol 255 (1) ◽  
pp. C86-C94 ◽  
Author(s):  
C. M. Hai ◽  
R. A. Murphy
Keyword(s):  
Smooth Muscle ◽  
Shortening Velocity ◽  
Internal Load ◽  
Cross Bridge ◽  
Bridge Model ◽  
The Family ◽  
Cross Bridges ◽  
Latch State ◽  
The Relationship ◽  
State Stress

We have proposed a model that incorporates a dephosphorylated "latch bridge" to explain the mechanics and energetics of smooth muscle. Cross-bridge phosphorylation is proposed as a prerequisite for cross-bridge attachment and rapid cycling. Features of the model are 1) myosin light chain kinase and phosphatase can act on both free and attached cross bridges, 2) dephosphorylation of an attached phosphorylated cross bridge produces a noncycling "latch bridge," and 3) latch bridges have a slow detachment rate. This model quantitatively predicts the latch state: stress maintenance with reduced phosphorylation, cross-bridge cycling rates, and ATP consumption. In this study, we adapted A. F. Huxley's formulation of crossbridge cycling (A. F. Huxley, Progr. Biophys. Mol. Biol. 7: 255-318, 1957) to the latch-bridge model to predict the relationship between isotonic shortening velocity and phosphorylation. The model successfully predicted the linear dependence of maximum shortening velocity at zero external load (V0) on phosphorylation, as well as the family of stress-velocity curves determined at different times during a contraction when phosphorylation values varied. The model implies that it is unnecessary to invoke an internal load or multiple regulatory mechanisms to explain regulation of V0 in smooth muscle.

Time course of airway hyperresponsiveness and remodeling induced by hyperoxia in rats

1995 ◽  
Vol 269 (2) ◽  
pp. L227-L233 ◽  
Author(s):  
J. L. Szarek ◽  
H. L. Ramsay ◽  
A. Andringa ◽  
M. L. Miller
Keyword(s):  
Smooth Muscle ◽  
Airway Hyperresponsiveness ◽  
Time Course ◽  
Electrical Field Stimulation ◽  
Maximal Response ◽  
Sprague Dawley ◽  
Electrical Field ◽  
Muscle Area ◽  
Sprague Dawley Rats ◽  
The Relationship

The purpose of this study was to answer two questions concerning hyperoxia-induced airway hyperresponsiveness: 1) What is the time course of the development of airway hyperresponsiveness? 2) What is the relationship between the increase in responsiveness and smooth muscle area? Segments of intrapulmonary bronchi were isolated from male Sprague-Dawley rats that had been exposed to 80-85% O2 for a period of 1, 3, 5, or 7 days and from aged-matched control animals that breathed room air. Hyperoxia increased the sensitivity (log concentration or frequency that elicited a half-maximal response) and reactivity (maximum tension developed) of the airways to electrical field stimulation (EFS) after 3, 5, and 7 days; sensitivity to acetylcholine was not affected, but reactivity was increased after 7 days. Hyperoxia increased smooth muscle area beginning 5 days after commencing the exposure. After normalizing tension responses to smooth muscle area, reactivity of the airways to the stimuli was not different between the two groups, but sensitivity to EFS was still increased. The increase in reactivity observed after 5 and 7 days of exposure can be explained by an increase in smooth muscle area that occurred at these time points. The fact that the sensitivity of the airways to EFS remained increased after normalization, together with the fact that the increase in airway responsiveness after 3 days of exposure occurred at a time when smooth muscle area was not different from control, suggests that mechanisms other than increased smooth muscle area contribute to the development of hyperoxia-induced airway hyperresponsiveness.

scholarly journals Water Loss during Contracture of Muscle

1962 ◽  
Vol 46 (1) ◽  
pp. 131-142 ◽  
Author(s):  
Benjamin Kaminer
Keyword(s):  
Smooth Muscle ◽  
Water Loss ◽  
Significant Loss ◽  
Frog Muscle ◽  
Tetanic Stimulation ◽  
Force Of Contraction ◽  
Freezing And Thawing ◽  
Microscopic Studies ◽  
Relationship Of ◽  
The Relationship

The relationship of contracture and exudation of water in frozenthawed frog muscle was studied. With maximum shortening, there was a water loss of 35 per cent of the weight of muscle. By restricting the contraction, it was demonstrated that the amount of water loss was proportional to the degree of shortening, there being no significant loss with isometric contraction. Muscle already shortened by tetanic stimulation also exuded water on subsequent freezing and thawing. The force of contraction could be reduced by depleting the muscle of calcium and it was shown that the amount of water exuded was also proportional to the tensile ability of the muscle. In a smooth muscle (anterior byssus retractor of Mytilus) which did not contract vigorously only a little water exuded. Contracture produced by caffeine was similarly associated with a loss of water. Microscopic studies revealed a disruption of the sarcomeres of the frozen-thawed muscle which contracted; glycerol-extracted and calcium-depleted muscles, which did not contract on freeze-thawing, did not show such disruption. Freezing and thawing of actomyosin caused a reversible syneresis of the protein. It is concluded that the exudation of the water is not merely due to the freezing and thawing but is also dependent on the contractile events.

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