scholarly journals Heterogeneous expression of transient outward currents in smooth muscle cells of the mouse small intestine

2002 ◽  
Vol 544 (1) ◽  
pp. 19-27 ◽  
Author(s):  
Jonathan C. F. Lee ◽  
Carlos Barajas‐López ◽  
Jan D. Huizinga
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Outward Currents ◽  
Mouse Small Intestine ◽  
Heterogeneous Expression

Immunoelectron microscopic localization of fibronectin in the smooth muscle layer of mouse small intestine.

1987 ◽  
Vol 35 (4) ◽  
pp. 411-417 ◽  
Author(s):  
K Kurisu ◽  
Y Ohsaki ◽  
K Nagata ◽  
T Kukita ◽  
H Yoshikawa ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Small Intestine ◽  
Smooth Muscle Cells ◽  
Basal Lamina ◽  
Muscle Cells ◽  
Muscle Layer ◽  
Secretory Vesicle ◽  
Smooth Muscle Layer ◽  
Mouse Small Intestine

We studied the ultrastructural distribution of fibronectin in the smooth muscle layer of mouse small intestine with affinity-purified antibodies using the immunogold technique. Fibronectin was present over the pericellular area extending from the cell membrane to the extracellular matrix beyond the basal lamina. Distribution of the glycoprotein over the pericellular area was heterogeneous, i.e., it was localized more abundantly in the narrow space between smooth muscle cells, the gaps having a width of 60-80 nm where the two dense bands in adjacent cells matched each other. Such localization suggests that fibronectin contributes to cell adhesion. Within the basement membrane, gold label was localized both in lamina lucida and lamina densa, more densely in the latter than in the former. Fibronectin was also co-distributed with collagen fibers in the extracellular matrix. Within smooth muscle cells, gold particles were observed on rough endoplasmic reticulum and secretory vesicle-like structures. These results suggest that smooth muscle cells synthesize fibronectin and secrete it as a component of the basal lamina and extracellular matrix.

scholarly journals Characterization of Muscarinic Receptor-Mediated Cationic Currents in Longitudinal Smooth Muscle Cells of Mouse Small Intestine

2006 ◽  
Vol 100 (3) ◽  
pp. 215-226 ◽  
Author(s):  
Takashi Sakamoto ◽  
Toshihiro Unno ◽  
Hayato Matsuyama ◽  
Mai Uchiyama ◽  
Mitsunobu Hattori ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Smooth Muscle Cells ◽  
Muscarinic Receptor ◽  
Muscle Cells ◽  
Longitudinal Smooth Muscle ◽  
Mouse Small Intestine

Isolation of plasma membranes of smooth muscle cells of the rabbit small intestine

1984 ◽  
Vol 97 (1) ◽  
pp. 134-136 ◽  
Author(s):  
V. K. Rybal'chenko ◽  
P. V. Pogrebnoi ◽  
T. G. Gruzina ◽  
V. I. Karamushka
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Smooth Muscle Cells ◽  
Plasma Membranes ◽  
Muscle Cells ◽  
Rabbit Small Intestine

scholarly journals TREK-1 currents in smooth muscle cells from pregnant human myometrium

2013 ◽  
Vol 305 (6) ◽  
pp. C632-C642 ◽  
Author(s):  
Nathanael S. Heyman ◽  
Chad L. Cowles ◽  
Scott D. Barnett ◽  
Yi-Ying Wu ◽  
Charles Cullison ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Human Myometrium ◽  
Regulation Of Expression ◽  
Hek 293 ◽  
Myometrial Cells ◽  
Outward Currents ◽  
293 Cells ◽  
Interfering Rna

The mechanisms governing maintenance of quiescence during pregnancy remain largely unknown. The current study characterizes a stretch-activated, tetraethylammonium-insensitive K+ current in smooth muscle cells isolated from pregnant human myometrium. This study hypothesizes that these K+ currents can be attributed to TREK-1 and that upregulation of this channel during pregnancy assists with the maintenance of a negative cell membrane potential, conceivably contributing to uterine quiescence until full term. The results of this study demonstrate that, in pregnant human myometrial cells, outward currents at 80 mV increased from 4.8 ± 1.5 to 19.4 ± 7.5 pA/pF and from 3.0 ± 0.8 to 11.8 ± 2.7 pA/pF with application of arachidonic acid (AA) and NaHCO3, respectively, causing intracellular acidification. Similarly, outward currents were inhibited following application of 10 μM fluphenazine by 51.2 ± 9.8% after activation by AA and by 73.9 ± 4.2% after activation by NaHCO3. In human embryonic kidney (HEK-293) cells stably expressing TREK-1, outward currents at 80 mV increased from 91.0 ± 23.8 to 247.5 ± 73.3 pA/pF and from 34.8 ± 8.9 to 218.6 ± 45.0 pA/pF with application of AA and NaHCO3, respectively. Correspondingly, outward currents were inhibited 89.5 ± 2.3% by 10 μM fluphenazine following activation by AA and by 91.6 ± 3.4% following activation by NaHCO3. Moreover, currents in human myometrial cells were activated by stretch and were reduced by transfection with small interfering RNA or extracellular acidification. Understanding gestational regulation of expression and gating of TREK-1 channels could be important in determining appropriate maintenance of uterine quiescence during pregnancy.

scholarly journals The Influence of Sarcoplasmic Reticulum Ca2+ Concentration on Ca2+ Sparks and Spontaneous Transient Outward Currents in Single Smooth Muscle Cells

1999 ◽  
Vol 113 (2) ◽  
pp. 215-228 ◽  
Author(s):  
Ronghua ZhuGe ◽  
Richard A. Tuft ◽  
Kevin E. Fogarty ◽  
Karl Bellve ◽  
Fredric S. Fay ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Potassium Channels ◽  
Smooth Muscle Cells ◽  
High Speed ◽  
Muscle Cells ◽  
Wide Field ◽  
Outward Currents ◽  
The Relationship ◽  
Spontaneous Transient Outward Currents

Localized, transient elevations in cytosolic Ca2+, known as Ca2+ sparks, caused by Ca2+ release from sarcoplasmic reticulum, are thought to trigger the opening of large conductance Ca2+-activated potassium channels in the plasma membrane resulting in spontaneous transient outward currents (STOCs) in smooth muscle cells. But the precise relationships between Ca2+ concentration within the sarcoplasmic reticulum and a Ca2+ spark and that between a Ca2+ spark and a STOC are not well defined or fully understood. To address these problems, we have employed two approaches using single patch-clamped smooth muscle cells freshly dissociated from toad stomach: a high speed, wide-field imaging system to simultaneously record Ca2+ sparks and STOCs, and a method to simultaneously measure free global Ca2+ concentration in the sarcoplasmic reticulum ([Ca2+]SR) and in the cytosol ([Ca2+]CYTO) along with STOCs. At a holding potential of 0 mV, cells displayed Ca2+ sparks and STOCs. Ca2+ sparks were associated with STOCs; the onset of the sparks coincided with the upstroke of STOCs, and both had approximately the same decay time. The mean increase in [Ca2+]CYTO at the time and location of the spark peak was ∼100 nM above a resting concentration of ∼100 nM. The frequency and amplitude of spontaneous Ca2+ sparks recorded at −80 mV were unchanged for a period of 10 min after removal of extracellular Ca2+ (nominally Ca2+-free solution with 50 μM EGTA), indicating that Ca2+ influx is not necessary for Ca2+sparks. A brief pulse of caffeine (20 mM) elicited a rapid decrease in [Ca2+]SR in association with a surge in [Ca2+]CYTO and a fusion of STOCs, followed by a fast restoration of [Ca2+]CYTO and a gradual recovery of [Ca2+]SR and STOCs. The return of global [Ca2+]CYTO to rest was an order of magnitude faster than the refilling of the sarcoplasmic reticulum with Ca2+. After the global [Ca2+]CYTO was fully restored, recovery of STOC frequency and amplitude were correlated with the level of [Ca2+]SR, even though the time for refilling varied greatly. STOC frequency did not recover substantially until the [Ca2+]SR was restored to 60% or more of resting levels. At [Ca2+]SR levels above 80% of rest, there was a steep relationship between [Ca2+]SR and STOC frequency. In contrast, the relationship between [Ca2+]SR and STOC amplitude was linear. The relationship between [Ca2+]SR and the frequency and amplitude was the same for Ca2+ sparks as it was for STOCs. The results of this study suggest that the regulation of [Ca2+]SR might provide one mechanism whereby agents could govern Ca2+ sparks and STOCs. The relationship between Ca2+ sparks and STOCs also implies a close association between a sarcoplasmic reticulum Ca2+ release site and the Ca2+-activated potassium channels responsible for a STOC.

Oxygen-induced fetal pulmonary vasodilation is mediated by intracellular calcium activation of KCa channels

2001 ◽  
Vol 281 (6) ◽  
pp. L1379-L1385 ◽  
Author(s):  
Valerie A. Porter ◽  
Michael T. Rhodes ◽  
Helen L. Reeve ◽  
David N. Cornfield
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Intracellular Calcium ◽  
Muscle Cells ◽  
Pulmonary Vasodilation ◽  
Outward Currents ◽  
Acute Increase ◽  
Pulmonary Artery Smooth Muscle ◽  
Spontaneous Transient Outward Currents

O2 sensing in fetal pulmonary artery smooth muscle is critically important in the successful transition to air breathing at birth. However, the mechanism by which the fetal pulmonary vasculature senses and responds to an acute increase in O2tension is not known. Isolated fetal pulmonary artery smooth muscle cells were kept in primary culture for 5–14 days in a hypoxic environment (20–30 mmHg). These cells showed a 25.1 ± 1.7% decrease in intracellular calcium in response to an acute increase in O2 tension. Low concentrations of caffeine (0.5 mM) and diltiazem also decreased intracellular calcium. The decrease in intracellular calcium concentration in response to increasing O2 was inhibited by iberiotoxin and ryanodine. Freshly isolated fetal pulmonary artery smooth muscle cells exhibited “spontaneous transient outward currents,” indicative of intracellular calcium spark activation of calcium-sensitive potassium channels. The frequency of spontaneous transient outward currents increased when O2 tension was increased to normoxic levels. Increasing fetal pulmonary O2 tension in acutely instrumented fetal sheep increased fetal pulmonary blood flow. Ryanodine attenuated O2-induced pulmonary vasodilation. This study demonstrates that fetal pulmonary vascular smooth muscle cells are capable of responding to an acute increase in O2tension and that this O2 response is mediated by intracellular calcium activation of calcium-sensitive potassium channels.

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