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.

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.

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.

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.

scholarly journals Contribution of Kv7.5 potassium channels inhibition and TRPC6 non‐selective channels activation in AVP induced calcium oscillations in A7r5 smooth muscle cells

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Bharath Kumar Mani ◽  
Lioubov I. Brueggemann ◽  
Leanne L. Cribbs ◽  
Kenneth L. Byron
Keyword(s):  
Smooth Muscle ◽  
Potassium Channels ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Calcium Oscillations

scholarly journals Localization of Ca2+-Activated K+ Channel, SK3, in Fibroblast-Like Cells Forming Gap Junctions With Smooth Muscle Cells in the Mouse Small Intestine

2003 ◽  
Vol 92 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Akikazu Fujita ◽  
Tadayoshi Takeuchi ◽  
Hanai Jun ◽  
Fumiaki Hata
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Muscle Cells ◽  
K Channel ◽  
Mouse Small Intestine

Macrophages influence gap junctional intercellular communication between smooth muscle cells in a co-culture model

1998 ◽  
Vol 5 (3) ◽  
pp. 197-203 ◽  
Author(s):  
Anne Mensink ◽  
Frederik P.J Mul ◽  
Thea van der Wijk ◽  
Abraham Brouwer ◽  
Jan H Koeman
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Intercellular Communication ◽  
Muscle Cells ◽  
Gap Junctional Intercellular Communication ◽  
Culture Model ◽  
Gap Junctional
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