scholarly journals Mechanical transients of single toad stomach smooth muscle cells. Effects of lowering temperature and extracellular calcium.

1990 ◽  
Vol 95 (4) ◽  
pp. 697-715 ◽  
Author(s):  
M Yamakawa ◽  
D E Harris ◽  
F S Fay ◽  
D M Warshaw
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Dynamic Stiffness ◽  
Muscle Cells ◽  
Recovery Phase ◽  
Tension Transient ◽  
Crossbridge Cycle ◽  
Tension Recovery ◽  
Tension Transients

Smooth muscle's slow, economical contractions may relate to the kinetics of the crossbridge cycle. We characterized the crossbridge cycle in smooth muscle by studying tension recovery in response to a small, rapid length change (i.e., tension transients) in single smooth muscle cells from the toad stomach (Bufo marinus). To confirm that these tension transients reflect crossbridge kinetics, we examined the effect of lowering cell temperature on the tension transient time course. Once this was confirmed, cells were exposed to low extracellular calcium [( Ca2+]o) to determine whether modulation of the cell's shortening velocity by changes in [Ca2+]o reflected the calcium sensitivity of one or more steps in the crossbridge cycle. Single smooth muscle cells were tied between an ultrasensitive force transducer and length displacement device after equilibration in temperature-controlled physiological saline having either a low (0.18 mM) or normal (1.8 mM) calcium concentration. At the peak of isometric force, after electrical stimulation, small, rapid (less than or equal to 1.8% cell length in 3.6 ms) step stretches and releases were imposed. At room temperature (20 degrees C) in normal [Ca2+]o, tension recovery after the length step was described by the sum of two exponentials with rates of 40-90 s-1 for the fast phase and 2-4 s-1 for the slow phase. In normal [Ca2+]o but at low temperature (10 degrees C), the fast tension recovery phase slowed (apparent Q10 = 1.9) for both stretches and releases whereas the slow tension recovery phase for a release was only moderately affected (apparent Q10 = 1.4) while unaffected for a stretch. Dynamic stiffness was determined throughout the time course of the tension transient to help correlate the tension transient phases with specific step(s) in the crossbridge cycle. The dissociation of tension and stiffness, during the fast tension recovery phase after a release, was interpreted as evidence that this recovery phase resulted from both the transition of crossbridges from a low- to high-force producing state as well as a transient detachment of crossbridges. From the temperature studies and dynamic stiffness measurements, the slow tension recovery phase most likely reflects the overall rate of crossbridge cycling. From the tension transient studies, it appears that crossbridges cycle slower and have a longer duty cycle in smooth muscle. In low [Ca2+]o at 20 degrees C, little effect was observed on the form or time course of the tension transients.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Time-Course Analysis on the Differentiation of Bone Marrow-Derived Progenitor Cells Into Smooth Muscle Cells During Neointima Formation

2010 ◽  
Vol 30 (10) ◽  
pp. 1890-1896 ◽  
Author(s):  
Jan-Marcus Daniel ◽  
Wiebke Bielenberg ◽  
Philipp Stieger ◽  
Soenke Weinert ◽  
Harald Tillmanns ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Progenitor Cells ◽  
Time Course ◽  
Muscle Cells ◽  
Neointima Formation

Voltage-dependent calcium channel current in isolated gallbladder smooth muscle cells of guinea pig

1993 ◽  
Vol 264 (6) ◽  
pp. G1066-G1076 ◽  
Author(s):  
T. Shimada
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Reversal Potential ◽  
High Sensitivity ◽  
Muscle Cells ◽  
Patch Clamp Technique ◽  
Decay Component ◽  
Voltage Dependent

The voltage-dependent Ca2+ current was studied in enzymatically dispersed guinea pig gallbladder smooth muscle cells using the whole cell patch-clamp technique. Depolarizing voltage (V) steps induced an inward current (I) that was carried by Ca2+. The threshold potential was -40 to -30 mV, the maximal current was observed at +10 to +20 mV, and the reversal potential was around +80 mV. I-V curves obtained with holding potentials of -80 and -40 mV were not significantly different. This current had a high sensitivity to dihydropyridine drugs, and the Ba2+ or Sr2+ current was larger than the Ca2+ current. Activation was accelerated by increasing the membrane potential. In general, the time course of decay was well fitted by the sum of two exponentials, but consideration of a third (ultra-slow) decay component was also necessary when the current generated by a 2-s command pulse was analyzed. Superimposition of activation and inactivation curves showed the presence of a significant window current. Carbachol suppressed the Ca2+ current only when the pipette contained a low concentration of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid. These results show that the L-type Ca2+ current is dominant in gallbladder smooth muscle cells and may contribute to excitation-contraction coupling.

scholarly journals Changes in the components of extracellular matrix and in growth properties of cultured aortic smooth muscle cells upon ascorbate feeding.

1982 ◽  
Vol 92 (2) ◽  
pp. 462-470 ◽  
Author(s):  
E Schwartz ◽  
R S Bienkowski ◽  
B Coltoff-Schiller ◽  
S Goldfischer ◽  
O O Blumenfeld
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Cultured Cells ◽  
Growth Parameters ◽  
Muscle Cells ◽  
Cellular Protein ◽  
Collagen Accumulation ◽  
The Matrix

Culture conditions can modify the composition of the extracellular matrix of cultured calf aortas smooth muscle cells. In the absence of ascorbate the major components of the matrix are microfibrillar proteins; deposition of collagen occurs upon ascorbate supplementation and, with increased time of exposure of cells to ascorbate, collagen becomes the dominant protein of the extracellular matrix (greater than 80%). Collagen accumulation follows a sigmoidal time-course, suggesting that it is a cooperative phenomenon. Covalent crosslinks are not required for collagen accumulation in the matrix. Microfibrillar proteins and increased amounts of proteoglycans and fibronectin accumulate concurrently with collagen but elastin deposition was not observed either with or without ascorbate feeding. Addition of ascorbate leads to a general stimulation of incorporation of [14C]proline into cellular protein and to changes in cell growth parameters and morphology: cell-doubling time decreases from 62 to 47 h and plating efficiency increases approximately fourfold. We conclude that the composition of the extracellular matrix assembled by cultured cells is subject to experimental manipulation and that changes in endogenously deposited matrix may have significant effects on cellular functions.

Abstract P511: Targeting Il-1β Protects From Aortic Aneurysms Induced by Disrupted Tgfβ Signaling in Smooth Muscle Cells

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Daniela Carnevale ◽  
Raimondo Carnevale ◽  
Francesco Da Ros ◽  
Roberta Iacobucci ◽  
Manuel Casaburo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Molecular Mechanisms ◽  
Muscle Cells ◽  
Ascending Aorta ◽  
Aortic Aneurysms ◽  
Tgfβ Signaling ◽  
Aneurysm Formation ◽  
Aortic Pathology

Aortic aneurysms represent a life-threatening condition because of the current lack of effective treatments. Aneurysm formation is typically associated with extracellular matrix remodeling and persistent inflammation. Although the molecular mechanisms underlying aortic pathology remain largely unclear, TGFβ signaling is unquestionably implied and its downstream target Smad4 showed protective functions for maintenance of aortic walls’ integrity. Using mice with smooth muscle cells (SMCs) specific deletion of Smad4 in the adult ( Smad4 -SMC iko ), developing spontaneous aneurysms (Ascending Aorta Diameter: Smad4 -SMC iko 2.15±0.03; Smad4 -SMC wt 1.7±0.03;***p< 0.001), we investigated the molecular mechanisms activated by dysregulation of TGFβ signaling. Structural disarrangement of ascending aorta in Smad4 -SMC iko mice was clearly appreciated early after Smad4 deletion as discrete breaks of elastic lamellae (breaks/section: Smad4 -SMC iko 2.05±0.5; Smad4 -SMC wt 0.83±0.4;***p< 0.001). Interestingly, the islands of damage in the aorta of Smad4 -SMC iko were enriched of immune infiltrate, mainly monocytes/macrophages, as indicated by FACS and immunofluorescence. We then analyzed several pathways downstream to Smad4 inhibition, finding a selective activation of NF-kB/IL-1β in SMCs. To test the relevance of this pathway in the formation of aneurysms, we deleted Smad4 in SMCs of mice with Il1r1 null background ( Smad4 -SMC iko ; Il1r1 -/- ). Ultrasonographic analyses revealed that ablation of IL1 receptor1 protected Smad4 -SMC iko mice from the progression of pathology and improved their overall survival. In the end, to test the translational potential of our findings, we neutralized IL-1β signaling with the clinically relevant murine version of the FDA-approved clinical drug canakinumab. During a time course of 16 weeks, while a weekly administration of control immunoglobulins did not change aneurysm progression in Smad4 -SMC iko mice, treatment with anti-IL-1β antibody significantly hampered aneurysm formation in the aorta ( Smad4 -SMC iko +anti- IL-1β 1.85±0.02; Smad4 -SMC iko +anti-IgG 2.09±0.03; ***p< 0.001) These findings identify a mechanistic target for controlling aneurysms progression induced by disrupted TGFβ signaling.

Time Course of Changes in Concentration of Intracellular Free Calcium in Cultured Cerebrovascular Smooth Muscle Cells Exposed to Oxyhemoglobin

Neurosurgery ◽  
1992 ◽  
Vol 30 (3) ◽  
pp. 346-350 ◽  
Author(s):  
Yoshihiro Takanashi ◽  
Bryce K. A. Weir ◽  
Bozena Vollrath ◽  
Hidetoshi Kasuya ◽  
R. Loch Macdonald ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Muscle Cells ◽  
Intracellular Free Calcium ◽  
Free Calcium ◽  
Cerebrovascular Smooth Muscle Cells

scholarly journals Glycyrrhetinic derivatives inhibit hyperpolarization in endothelial cells of guinea pig and rat arteries

2002 ◽  
Vol 282 (1) ◽  
pp. H335-H341 ◽  
Author(s):  
Marianne Tare ◽  
H. A. Coleman ◽  
Helena C. Parkington
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Endothelial Cell ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Time Course ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Resting Membrane Potential ◽  
Variable Effect

Glycyrrhetinic acid (GA) derivatives have been used to implicate gap junctions in vasorelaxation attributed to endothelium-derived hyperpolarizing factor (EDHF). The aim of this study was to assess whether GA compounds affect endothelial cell hyperpolarization. Membrane potentials were recorded from dye-identified endothelial and smooth muscle cells of guinea pig coronary and rat mesenteric arteries. GA derivatives had varied effects on the resting membrane potential: depolarization, hyperpolarization, or no effect, depending on the artery. 18α-GA (50 μM) had a small variable effect on ACh-induced hyperpolarizations in endothelial cells. 18β-GA (30 μM) and carbenoxolone (100 μM) significantly reduced ACh-induced hyperpolarizations in both endothelial and smooth muscle cells. Smooth muscle action potentials in rat tail arteries were smaller and slower in the presence of 18β-GA. Nerve-induced excitatory junction potentials were inhibited by 18β-GA and carbenoxolone, whereas the time course of their decay initially increased and then decreased. In conclusion, the GA compounds had a range of effects. Their inhibition of the EDHF hyperpolarization and relaxation in the smooth muscle may stem from the inhibition of endothelial cell hyperpolarization.

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