scholarly journals Intercellular communication controls agonist-induced calcium oscillations independently of gap junctions in smooth muscle cells

2019 ◽  
Author(s):  
S.E. Stasiak ◽  
R.R. Jamieson ◽  
J. Bouffard ◽  
E.J. Cram ◽  
H. Parameswaran
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Intercellular Communication ◽  
Muscle Cells ◽  
Calcium Oscillations ◽  
Isolated Cells ◽  
Mechanical Signaling ◽  
Frequency Modulate ◽  
The Individual

AbstractWe report the existence of a unique mode of communication among human smooth muscle cells (SMCs) where they use force to frequency modulate long-range calcium waves. An important consequence of this mechanical signaling is that changes in stiffness of the underlying extracellular matrix can interfere with the frequency modulation of Ca2+ waves causing healthy SMCs to falsely perceive a much higher agonist dose than they actually received. This distorted sensing of contractile agonist dose on stiffer matrices is absent in isolated SMCs, even though the isolated cells can sense matrix rigidity. We show that intercellular communication that enables this collective Ca2+ response does not involve transport across gap junctions or extracellular diffusion of signaling molecules. The aberrant communication between cells that distorts the individual cell's perception of contractile stimulus can explain the sudden, exaggerated narrowing of the lumen when exposed to low dose of inhaled agonists in diseases like asthma.

scholarly journals Intercellular communication controls agonist-induced calcium oscillations independently of gap junctions in smooth muscle cells

2020 ◽  
Vol 6 (32) ◽  
pp. eaba1149
Author(s):  
S. E. Stasiak ◽  
R. R. Jamieson ◽  
J. Bouffard ◽  
E. J. Cram ◽  
H. Parameswaran
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Intercellular Communication ◽  
Muscle Cells ◽  
Calcium Oscillations ◽  
Isolated Cells ◽  
Healthy Human ◽  
Mechanical Signaling ◽  
Frequency Modulate

In this study, we report the existence of a communication system among human smooth muscle cells that uses mechanical forces to frequency modulate long-range calcium waves. An important consequence of this mechanical signaling is that changes in stiffness of the underlying extracellular matrix can interfere with the frequency modulation of Ca2+ waves, causing smooth muscle cells from healthy human donors to falsely perceive a much higher agonist dose than they actually received. This aberrant sensing of contractile agonist dose on stiffer matrices is completely absent in isolated smooth muscle cells, although the isolated cells can sense matrix rigidity. We show that the intercellular communication that enables this collective Ca2+ response in smooth muscle cells does not involve transport across gap junctions or extracellular diffusion of signaling molecules. Instead, our data support a collective model in which mechanical signaling among smooth muscle cells regulates their response to contractile agonists.

Gap junctions and direct intercellular communication between rat uterine smooth muscle cells

1985 ◽  
Vol 249 (1) ◽  
pp. C20-C31 ◽  
Author(s):  
W. C. Cole ◽  
R. E. Garfield ◽  
J. S. Kirkaldy
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Intercellular Communication ◽  
Contractile Activity ◽  
Muscle Cells ◽  
Uterine Wall ◽  
Longitudinal Distribution ◽  
Uterine Smooth Muscle ◽  
Apparent Diffusion

We have tested the hypothesis that an increase in direct intercellular communication accompanies the development of gap junctions (GJs) between rat uterine smooth muscle cells at parturition. Intercellular communication in these tissues was studied by exposing one portion of small strips of myometrium to 2-[3H]deoxy-D-glucose (2-DG) and determining the longitudinal distribution of tracer after a 5-h period of diffusion. The distribution of 2-DG was greater in parturient compared with ante- and postpartum tissues. Similarly, the apparent diffusion coefficient of 2-DG was almost 10-fold greater in delivering tissues (1.86 X 10(-6) cm2/s) than before (0.199 X 10(-6) cm2/s) or after (0.296 X 10(-6) cm2/s) parturition. Control experiments indicated that the redistribution of 2-DG was dependent on the presence of GJs and was the result of intracellular and direct cell-to-cell diffusion. The appearance of GJs is the myometrium at term facilitates direct intercellular communication between uterine smooth muscle cells during labor. This improved communication may be responsible for synchronizing and coordinating electrical, metabolic, and contractile activity in the uterine wall and, hence, the effective expulsion of fetuses.

Activation of a cGMP-sensitive calcium-dependent chloride channel may cause transition from calcium waves to whole cell oscillations in smooth muscle cells

2007 ◽  
Vol 293 (1) ◽  
pp. H215-H228 ◽  
Author(s):  
Jens Christian Brings Jacobsen ◽  
Christian Aalkjær ◽  
Holger Nilsson ◽  
Vladimir V. Matchkov ◽  
Jacob Freiberg ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Chloride Channel ◽  
Muscle Cells ◽  
Calcium Oscillations ◽  
Calcium Waves ◽  
Whole Cell ◽  
Calcium Dependent ◽  
The Individual

In vitro, α-adrenoreceptor stimulation of rat mesenteric small arteries often leads to a rhythmic change in wall tension, i.e., vasomotion. Within the individual smooth muscle cells of the vascular wall, vasomotion is often preceded by a period of asynchronous calcium waves. Abruptly, these low-frequency waves may transform into high-frequency whole cell calcium oscillations. Simultaneously, multiple cells synchronize, leading to rhythmic generation of tension. We present a mathematical model of vascular smooth muscle cells that aims at characterizing this sudden transition. Simulations show calcium waves sweeping through the cytoplasm when the sarcoplasmic reticulum (SR) is stimulated to release calcium. A rise in cGMP leads to the experimentally observed transition from waves to whole cell calcium oscillations. At the same time, membrane potential starts to oscillate and the frequency approximately doubles. In this transition, the simulated results point to a key role for a recently discovered cGMP-sensitive calcium-dependent chloride channel. This channel depolarizes the membrane in response to calcium released from the SR. In turn, depolarization causes a uniform opening of L-type calcium channels on the cell surface, stimulating a synchronized release of SR calcium and inducing the shift from waves to whole cell oscillations. The effect of the channel is therefore to couple the processes of the SR with those of the membrane. We hypothesize that the shift in oscillatory mode and the associated onset of oscillations in membrane potential within the individual cell may underlie sudden intercellular synchronization and the appearance of vasomotion.

Characterization and confocal imaging of calponin in gastrointestinal smooth muscle

1993 ◽  
Vol 265 (5) ◽  
pp. C1371-C1378 ◽  
Author(s):  
M. P. Walsh ◽  
J. D. Carmichael ◽  
G. J. Kargacin
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Thin Filament ◽  
Muscle Cells ◽  
Biochemical Properties ◽  
Confocal Imaging ◽  
Isolated Cells ◽  
Independent Manner

Calponin isolated from chicken gizzard smooth muscle binds in vitro to actin in a Ca(2+)-independent manner and thereby inhibits the actin-activated Mg(2+)-adenosinetriphosphatase of smooth muscle myosin. This inhibition is relieved when calponin is phosphorylated by protein kinase C or Ca2+/calmodulin-dependent protein kinase II, suggesting that calponin is involved in thin filament-associated regulation of smooth muscle contraction. To further examine this possibility, calponin was isolated from toad stomach smooth muscle, characterized biochemically, and localized in intact isolated cells. Toad stomach calponin had the same basic biochemical properties as calponin from other sources. Confocal immunofluorescence microscopy revealed that calponin in intact smooth muscle cells was localized to long filamentous structures that were colabeled by antibodies to actin or tropomyosin. Preservation of the basic biochemical properties of calponin from species to species suggests that these properties are relevant for its in vivo function. Its colocalization with actin and tropomyosin indicates that calponin is associated with the thin filament in intact smooth muscle cells.

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