Effects of Cyclic Peptide (Pro-Leu-Gly)2 on Calcium Signaling in Isolated Myometrial Cells from Pregnant Rat

2008 ◽  
Vol 89 (5) ◽  
pp. 277-280
Author(s):  
Yuji Kaneko ◽  
Hideki Shojo ◽  
Takanori Uchimura
Keyword(s):  
Calcium Signaling ◽  
Cyclic Peptide ◽  
Pregnant Rat ◽  
Myometrial Cells

Calcium channel current and its sensitivity to (+) isradipine in cultured pregnant rat myometrial cells

1989 ◽  
Vol 414 (4) ◽  
pp. 477-483 ◽  
Author(s):  
E. Honor� ◽  
T. Am�d�e ◽  
C. Martin ◽  
C. Dacquet ◽  
C. Mironneau ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Pregnant Rat ◽  
Myometrial Cells ◽  
Channel Current

Electrophysiological characterization of single pregnant rat myometrial cells in short-term primary culture

1986 ◽  
Vol 250 (1) ◽  
pp. C47-C54 ◽  
Author(s):  
P. Mollard ◽  
J. Mironneau ◽  
T. Amedee ◽  
C. Mironneau
Keyword(s):  
Action Potential ◽  
Primary Culture ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Short Term ◽  
Pregnant Rat ◽  
Myometrial Cells ◽  
The Mean ◽  
Electrophysiological Characterization ◽  
Specific Membrane

Smooth muscle cells were isolated from the longitudinal layer of pregnant rat myometrium (18-19 days) and studied either freshly dissociated or during short-term primary culture (until 30 h) using intracellular microelectrode techniques and direct microscopic observation. The isolated myometrial cells excluded trypan blue vital stain and could repetitively contract in response to various stimuli. Electrophysiological studies at 37 degrees C showed normal resting potential (-54.5 +/- 7.5 mV, n = 71). Action potentials with overshoot (+7.8 +/- 4.6 mV, n = 71) could be elicited by intracellular stimulation. Moreover, the membrane potential was largely dependent on the external K+ concentration. The action potential was suppressed in a Ca2+-free solution [with 0.1 mM ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid], and the overshoot amplitude was clearly Ca2+ dependent. The action potential was inhibited by Mn2+ ions (1 mM), Co2+ ions (1 mM), and D 600 (1 microM) but was unaffected by tetrodotoxin (2 microM) and external Na+ removal. Tetraethylammonium chloride (TEA, 10 mM) and 4-aminopyridine (4-AP, 10 mM) increased both overshoot amplitude and duration of the electrical responses. When the cell surface area was measured with light microscopy, the mean specific membrane resistance was 14.8 +/- 4.6 k omega . cm2 (n = 14), and the mean specific membrane capacitance was 2.3 +/- 0.7 microF/cm2 (n = 14). Outward-going rectification was consistently observed in all cells examined. This was either inhibited by TEA and 4-AP (10 mM each) or reduced in the presence of 1 mM Mn2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of estrogens on Ca channels in myometrial cells isolated from pregnant rats

1995 ◽  
Vol 268 (1) ◽  
pp. C64-C69 ◽  
Author(s):  
T. Yamamoto
Keyword(s):  
Steady State ◽  
Ca Channel ◽  
Ca Channels ◽  
Inhibitory Effects ◽  
Inactivation Curve ◽  
Pregnant Rat ◽  
Negative Direction ◽  
Myometrial Cells ◽  
Steady State Inactivation ◽  
Channel Currents

Whole cell patch-clamp techniques were applied to cultured smooth muscle cells isolated from the longitudinal layer of the late pregnant rat myometrium. Effects of estrogens on Ca channels were examined. Inhibitory effects of beta-estradiol (1 microM) on Ca channel currents were recognized. The inhibitory effects of beta-estradiol depended on holding potentials. beta-Estradiol shifted the steady-state inactivation curve in the negative direction by 7 mV at mid potential (n = 9). Diethylstilbestrol, a synthetic estrogen, gave similar effects on Ca channel currents at lower concentration (2 microM) to those of beta-estradiol. Strong inhibitory effects on Ca channel currents were obtained by higher concentration (20 microM). Diethylstilbestrol shifted the steady-state inactivation curve in the negative direction by 7 mV at mid potential (n = 5). The results indicate that estrogens influence the voltage dependency and the whole cell conductance of Ca channels of pregnant rat myometrial cells. The acute effect of estrogens may cause both electrical and mechanical depression of myometrium.

Functional expression of purinergic P2X7 receptors in pregnant rat myometrium

2010 ◽  
Vol 298 (4) ◽  
pp. R1117-R1124 ◽  
Author(s):  
Hiroshi Miyoshi ◽  
Kaoru Yamaoka ◽  
Satoshi Urabe ◽  
Miho Kodama ◽  
Yoshiki Kudo
Keyword(s):  
P2x7 Receptor ◽  
Uterine Contraction ◽  
Extracellular Atp ◽  
Receptor Expression ◽  
P2x Receptor ◽  
Receptor Subtype ◽  
P2x7 Receptors ◽  
Pregnant Rat ◽  
Myometrial Cells ◽  
Induced Currents

ATP has been reported to enhance the membrane conductance of myometrial cells and uterine contractility. Purinergic P2 receptor expression has been reported in the myometrium, using molecular biology, but the functional identity of the receptor subtype has not been determined. In this study, ATP-induced currents were recorded and characterized in single myometrial cells from pregnant rats using whole cell patch clamping. Extracellular ATP was applied in the range of 10 μM-1 mM and induced currents with an EC50 of 74 μM, with no desensitization, time dependency, or voltage dependency. The currents induced carried multiple monovalent cations, with conductances ranked as K+ > Cs+ > Li+ > Na+. They were activated by P2X receptor agonists, with their effectiveness ranked as 2′,3′- O-(4-benzoylbenzoyl)-ATP >> ATP > αβ-methylene-ATP > 2-methylthio ATP ≥ UTP ≥ GTP > ADP. These currents were blocked by the selective P2X7 receptor antagonist 3-[5-(2,3-dichlorophenyl)-1 H-tetrazol-1-yl]methyl pyridine (A-438079). We therefore concluded that ATP-induced currents in rat myometrial cells crossed cell membranes via P2X7 receptors. We further showed that the ATP-induced currents were blocked by extracellular Mg2+ (IC50 = 0.26 mM). Clinically, administering extracellular Mg2+ is known to inhibit uterine contraction. It therefore seems likely that uterine contraction may be induced by raised extracellular ATP and suppressed via Mg2+ inhibiting P2X7 receptors. Further research is needed into the P2X7 receptor as a therapeutic target in abnormal uterine contraction, as a possible treatment for premature labor.

Protein kinase C stimulates Ca2+ current in pregnant rat myometrial cells

1994 ◽  
Vol 72 (11) ◽  
pp. 1304-1307 ◽  
Author(s):  
Keiichi Shimamura ◽  
Masumi Kusaka ◽  
Nicholas Sperelakis
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Voltage Clamp ◽  
Cell Voltage ◽  
Pregnant Rat ◽  
Whole Cell ◽  
Myometrial Cells ◽  
Kinase C ◽  
Whole Cell Voltage Clamp ◽  
Voltage Dependent

The factors that regulate the voltage-dependent Ca2+ channels in pregnant uterine smooth muscle cells have not been elucidated, including any roles for protein kinase C (PKC). Therefore, the role of PKC in the regulation of the slow (L type) Ca2+ channels was examined in myometrial cells isolated from late pregnant (18–19 day) rat uterus, using the nystatin-perforated whole-cell voltage clamp. A PKC activator, phorbol 12, 13-dibutyrate (PDB), increased the L-type Ca2+ current (ICa(L)). Bath application of PDB (0.03 and 0.3 μM) increased the peak amplitude of ICa(L) by 21 ± 14% (n = 6) and 37 ± 8% (n = 9, p < 0.01), respectively. PDB did not change the holding current or shift the current–voltage relationship for ICa(L). The PKC inhibitors, H-7 (20 μM) or staurosporine (10 nM), reversed the effect of PDB. These results indicate that PKC may play a role in regulating Ca2+ channel function in pregnant rat myometrial cells and, therefore, may be involved in control of uterine contraction.Key words: protein kinase C, phorbol ester, calcium current, myometrial cell, nystatin-perforated patch, whole-cell voltage clamp.

scholarly journals Whole-Genome Uterine Artery Transcriptome Profiling and Alternative Splicing Analysis in Rat Pregnancy

2020 ◽  
Vol 21 (6) ◽  
pp. 2079 ◽  
Author(s):  
Kathirvel Gopalakrishnan ◽  
Sathish Kumar
Keyword(s):  
Smooth Muscle ◽  
Alternative Splicing ◽  
Vascular Smooth Muscle ◽  
Muscle Contraction ◽  
Calcium Signaling ◽  
Uterine Artery ◽  
Smooth Muscle Contraction ◽  
Differentially Expressed ◽  
Pregnant Rat ◽  
Vascular Smooth Muscle Contraction

During pregnancy, the uterine artery (UA) undergoes extensive remodeling to permit a 20–40 fold increase in blood flow with associated changes in the expression of a multitude of genes. This study used next-gen RNA sequencing technology to identify pathways and genes potentially involved in arterial adaptations in pregnant rat UA (gestation day 20) compared with non-pregnant rat UA (diestrus). A total of 2245 genes were differentially expressed, with 1257 up-regulated and 970 down-regulated in pregnant UA. Gene clustering analysis revealed a unique cluster of suppressed genes implicated in calcium signaling pathway and vascular smooth muscle contraction in pregnant UA. Transcription factor binding site motif scanning identified C2H2 ZF, AP-2 and CxxC as likely factors functional on the promoters of down-regulated genes involved in calcium signaling and vascular smooth muscle contraction. In addition, 1686 genes exhibited alternative splicing that were mainly implicated in microtubule organization and smooth muscle contraction. Cross-comparison analysis identified novel genes that were both differentially expressed and alternatively spliced; these were involved in leukocyte and B cell biology and lipid metabolism. In conclusion, this first comprehensive study provides a valuable resource for understanding the molecular mechanism underlying gestational uterine arterial adaptations during pregnancy.

Signal transduction in rat myometrial cells: comparison of the actions of endothelin-1, oxytocin and prostaglandin F2α

1995 ◽  
Vol 133 (4) ◽  
pp. 467-474 ◽  
Author(s):  
Miklós Molnár ◽  
Frank Hertelendy
Keyword(s):  
Signal Transduction ◽  
Phospholipase C ◽  
Inositol Phosphate ◽  
Rank Order ◽  
Prostaglandin F2α ◽  
Intact Cells ◽  
Pregnant Rat ◽  
Endothelin 1 ◽  
Myometrial Cells ◽  
Prostaglandin F

Molnár M, Hertelendy F. Signal transduction in rat myometrial cells: comparison of the actions of endothelin-1, oxytocin and prostaglandin F2α. Eur J Endocrinol 1995;133:467–74. ISSN 0804–4643 The objectives of this study were to evaluate and compare the actions of endothelin-1 (ET-1), oxytocin, prostaglandin F2α (PGF2α) and inositol 1,4,5-trisphosphate (IP3) on Ca2+ mobilization in permeabilized rat myometrial cells and to examine the activation of the inositol lipid cycle in intact myocytes. Cells were isolated from late pregnant rat myometrium and used as confluent monolayers after a single passage. All four agonists caused a biphasic release of45Ca2+ from non-mitochondrial pool(s), with the rank order of potency: oxytocin > PGF2α > ET-1 > IP3. Inhibitors of phospholipase C blocked ET-1-and oxytocin-promoted but not PGF2α-promoted 45Ca2+ efflux. Similarly, heparin, an IP3 receptor blocker, failed to inhibit PGF2α-induced Ca2+ release while inhibiting the action of the other agonists. Endothelin-1 and oxytocin stimulated inositol phosphate accumulation at concentrations similar to those that promoted 45Ca2+ efflux, whereas about 100 times higher concentrations of PGF2α were needed to activate this signaling pathway in intact cells. It is concluded that the primary action of PGF2α in myometrial cells is to enhance Ca2+ influx, whereas oxytocin and ET-1 receptors are coupled to phospholipase C, generating IP3 and raising the intracellular concentration of free Ca2+ from intracellular as well as extracellular sources. Frank Hertelendy, Dept. Ob/Gyn, St Loufis University Health Sciences Center, 3635 Vista Ave at Grand Blvd, St Louis, MO 63110-0250, USA

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