scholarly journals SPONTANEOUS CONTRACTIONS OF THE HUMAN OVARY IN VITRO

Reproduction ◽  
1972 ◽  
Vol 28 (1) ◽  
pp. 113-115 ◽  
Author(s):  
Z. PALTI ◽  
M. FREUND
Keyword(s):  
Human Ovary ◽  
Spontaneous Contractions

scholarly journals FOS, a Critical Downstream Mediator of PGR and EGF Signaling Necessary for Ovulatory Prostaglandins in the Human Ovary

2018 ◽  
Vol 103 (11) ◽  
pp. 4241-4252 ◽  
Author(s):  
Yohan Choi ◽  
Katherine L Rosewell ◽  
Mats Brännström ◽  
James W Akin ◽  
Thomas E Curry ◽  
...  
Keyword(s):  
Target Genes ◽  
Activator Protein 1 ◽  
Egf Receptors ◽  
Human Ovary ◽  
Promoter Regions ◽  
Vitro Fertilization ◽  
Egf Signaling ◽  
Periovulatory Follicles

Abstract Context Fos null mice failed to ovulate and form a corpus luteum (CL) even when given exogenous gonadotropins, suggesting that ovarian Fos expression is critical for successful ovulation and CL formation. However, little is known about FOS in the human ovary. Objectives To determine the expression, regulation, and function of FOS in human periovulatory follicles. Design/Participants Timed periovulatory follicles were obtained from normally cycling women. Granulosa/lutein cells were collected from in vitro fertilization patients. Main Outcome Measures The in vivo expression after human chorionic gonadotropin (hCG) administration and in vitro regulation of FOS, JUN, JUNB, and JUND was evaluated at the mRNA and protein level. Binding of progesterone receptor (PGR) and FOS to their target genes was assessed by chromatin immunoprecipitation analyses. Prostaglandin E2 (PGE2) and progesterone were measured. Results The expression of FOS, JUNB, and JUND drastically increased in ovulatory follicles after hCG administration. In human granulosa/lutein cell cultures, hCG increased the expression of FOS and JUN proteins. Inhibitors of PGR and epidermal growth factor (EGF) receptors reduced hCG-induced increases in the expression and phosphorylation of FOS. PGR bound to the FOS gene. A selective FOS inhibitor blocked hCG-induced increases in PGE2 and the expression of prostaglandin (PG) synthases and transporters (PTGES, SLCO2A1, and ABCC1). FOS bound to the promoter regions of these genes. Conclusions The increase of FOS/activator protein 1 in human periovulatory follicles after hCG administration is mediated by collaborative actions of PGR and EGF signaling and critical for the upregulated expression of key ovulatory genes required for the rise in ovulatory PG in human granulosa cells.

271. Steroid metabolism and conjugation in the human ovary perfused in vitro

1974 ◽  
Vol 5 (4) ◽  
pp. 313 ◽  
Author(s):  
G. Sturm ◽  
E. Stähler ◽  
B. Grosch
Keyword(s):  
Steroid Metabolism ◽  
Human Ovary

scholarly journals Contractile activity is required for the expression of neonatal myosin heavy chain in embryonic chick pectoral muscle cultures.

1986 ◽  
Vol 103 (6) ◽  
pp. 2153-2161 ◽  
Author(s):  
L C Cerny ◽  
E Bandman
Keyword(s):  
Monoclonal Antibody ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Contractile Activity ◽  
Pectoral Muscle ◽  
Chicken Muscle ◽  
High K ◽  
Muscle Cultures ◽  
Spontaneous Contractions

The expression of neonatal myosin heavy chain (MHC) was examined in developing embryonic chicken muscle cultures using a monoclonal antibody (2E9) that has been shown to be specific for that isoform (Bandman, E., 1985, Science (Wash. DC), 227: 780-782). After 1 wk in vitro some myotubes could be stained with the antibody, and the number of cells that reacted with 2E9 increased with time in culture. All myotubes always stained with a second monoclonal antibody that reacted with all MHC isoforms (AG19) or with a third monoclonal antibody that reacted with the embryonic but not the neonatal MHC (EB165). Quantitation by ELISA of an extract from 2-wk cultures demonstrated that the neonatal MHC represented between 10 and 15% of the total myosin. The appearance of the neonatal isoform was inhibited by switching young cultures to medium with a higher [K+] which has been shown to block spontaneous contractions of myotubes in culture. Furthermore, if mature cultures that reacted with the neonatal antibody were placed into high [K+] medium, neonatal MHC disappeared from virtually all myotubes within 3 d. The effect of high [K+] medium was reversible. When cultures maintained in high [K+] medium for 2 wk were placed in standard medium, which permitted the resumption of contractile activity, within 24 h cells began to react with the neonatal specific antibody, and by 72 h many myotubes were strongly positive. Since similar results were also obtained by inhibiting spontaneous contractions with tetrodotoxin, we suggest that the development of contractile activity is not only associated with the maturation of myotubes in culture, but may also be the signal that induces the expression of the neonatal MHC.

scholarly journals Chemokine Ligand 20: A Signal for Leukocyte Recruitment During Human Ovulation?

Endocrinology ◽  
2015 ◽  
Vol 156 (9) ◽  
pp. 3358-3369 ◽  
Author(s):  
Linah Al-Alem ◽  
Muraly Puttabyatappa ◽  
Kathy Rosewell ◽  
Mats Brännström ◽  
James Akin ◽  
...  
Keyword(s):  
In Vitro Model ◽  
Leukocyte Migration ◽  
Human Ovary ◽  
Epithelial Growth Factor ◽  
Chemokine Ligand ◽  
Vitro Model ◽  
Ovulatory Process ◽  
Epithelial Growth

Ovulation is one of the cornerstones of female fertility. Disruption of the ovulatory process results in infertility, which affects approximately 10% of couples. Using a unique model in which the dominant follicle is collected across the periovulatory period in women, we have identified a leukocyte chemoattractant, chemokine ligand 20 (CCL20), in the human ovary. CCL20 mRNA is massively induced after an in vivo human chorionic gonadotropin (hCG) stimulus in granulosa (>10 000-fold) and theca (>4000-fold) cells collected during the early ovulatory (12–18 h) and late ovulatory (18–34 h) periods after hCG administration. Because the LH surge sets in motion an inflammatory reaction characterized by an influx of leukocytes and CCL20 is known to recruit leukocytes in other systems, the composition of ovarian leukocytes (CD45+) containing the CCL20 receptor CCR6 was determined immediately prior to ovulation. CD45+/CCR6+ cells were primarily natural killer cells (41%) along with B cells (12%), T cells (11%), neutrophils (10%), and monocytes (9%). Importantly, exogenous CCL20 stimulated ovarian leukocyte migration 59% within 90 minutes. Due to the difficulties in obtaining human follicles, an in vitro model was developed using granulosa-lutein cells to explore CCL20 regulation. CCL20 expression increased 40-fold within 6 hours after hCG, was regulated partially by the epithelial growth factor pathway, and was positively correlated with progesterone production. These results demonstrate that hCG dramatically increases CCL20 expression in the human ovary, that ovarian leukocytes contain the CCL20 receptor, and that CCL20 stimulates leukocyte migration. Our findings raise the prospect that CCL20 may aid in the final ovulatory events and contribute to fertility in women.

Seminal vesicle response to androgen with adrenaline, noradrenaline and acetylcholine

1960 ◽  
Vol 198 (1) ◽  
pp. 15-20 ◽  
Author(s):  
Jerome A. Grunt ◽  
James T. Higgins
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Seminal Vesicle ◽  
Testosterone Propionate ◽  
Water Soluble ◽  
Muscle System ◽  
Motor End Plate ◽  
Organ Response ◽  
Spontaneous Contractions

In a study of the end-organ response to androgen, use has been made of the seminal vesicle of the rat. Observations were made of the in vitro spontaneous contractions and responses to autonomic stimulating drugs. Vesicles of castrated rats contract spontaneously in vitro. Testosterone propionate given to the rat before sacrifice inhibits contractions, as does injection of water-soluble androgen into the in vitro chamber. Vesicles of castrates have lower thresholds to adrenaline and possibly to acetylcholine, but not to noradrenaline. The thresholds to acetylcholine but not to noradrenaline are elevated after injection of water-soluble androgen into the in vitro chamber. Several interpretations are discussed. Androgen and the autonomic nervous system probably interact at or near the cell membrane of the vesicle musculature. The three drugs tested most likely act at different loci along the nerve—motor end plate—muscle system, and noradrenaline is probably not a primary mediating agent of spontaneous contractions of the vesicle of the castrated rat.

Neural regulation of in vitro giant contractions in the rat colon

2001 ◽  
Vol 281 (1) ◽  
pp. G275-G282 ◽  
Author(s):  
Asensio Gonzalez ◽  
Sushil K. Sarna
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Sch 23390 ◽  
Circular Muscle ◽  
Electrical Field Stimulation ◽  
Muscle Cells ◽  
Enteric Neurons ◽  
Rat Colon ◽  
Spontaneous Contractions

The rat middle colon spontaneously generates regularly occurring giant contractions (GCs) in vitro. We investigated the neurohumoral and intracellular regulation of these contractions in a standard muscle bath. cGMP content was measured in strips and single smooth muscle cells. The circular muscle strips generated spontaneous GCs. Their amplitude and frequency were significantly increased by tetrodotoxin (TTX), ω-conotoxin, N ω-nitro-l-arginine (l-NNA), and the dopamine D1 receptor antagonist Sch-23390. The GCs were unaffected by hexamethonium, atropine, and antagonists of serotonergic (5-HT1–4), histaminergic (H1–2), and tachykininergic (NK1–2) receptors but enhanced by NK3receptor antagonism. The guanylate cyclase inhibitor 1H-[1,2,4]oxidiazolo[4,3-a]quinoxalin-1-one (ODQ) also enhanced GCs to the same extent as TTX and l-NNA, and each of the three agents prevented the effects of the others. GCs were abolished by electrical field stimulation, S-nitroso- N-acetyl-penicillamine, and 8-bromo-cGMP. BAY-K-8644 and apamin enhanced the GCs, but they were abolished by D-600. Basal cGMP content in strips was decreased by TTX,l-NNA, or ODQ, but these treatments had no effect on cGMP content of enzymatically dissociated single smooth muscle cells. We conclude that spontaneous contractions in the rat colonic muscle strips are not generated by cholinergic, serotonergic, or histaminergic input. Constitutive release of nitric oxide from enteric neurons sustains cGMP synthesis in the colonic smooth muscle to suppress spontaneous in vitro GCs.

Changes in spontaneous contractions of rat ileum by aflatoxin in vitro

2008 ◽  
Vol 46 (6) ◽  
pp. 2124-2127 ◽  
Author(s):  
Nevcihan Gursoy ◽  
Bulent Sarac ◽  
Nedim Durmus ◽  
Ahmet Parlak ◽  
Sahin Yildirim ◽  
...  
Keyword(s):  
Rat Ileum ◽  
Spontaneous Contractions

Sources and implications of basal nitric oxide in spontaneous contractions of guinea pig taenia caeci

2003 ◽  
Vol 285 (4) ◽  
pp. G747-G753 ◽  
Author(s):  
Catalina Caballero-Alomar ◽  
Carmen Santos ◽  
Diego Lopez ◽  
M. Teresa Mitjavila ◽  
Pere Puig-Parellada
Keyword(s):  
Nitric Oxide ◽  
Guinea Pig ◽  
Inhibitory Effect ◽  
No Production ◽  
Paramagnetic Resonance ◽  
Synthase Inhibitor ◽  
Spontaneous Contractions ◽  
Electron Paramagnetic

We examined in vitro the source and role of basal nitric oxide (NO) in proximal segments of guinea pig taenia caeci in nonadrenergic, noncholinergic (NANC) conditions. Using electron paramagnetic resonance (EPR), we measured the effect of the NO synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME, 10–4 M), the neuronal blocker tetrodotoxin (TTX, 10–6 M), or both on spontaneous contractions and on the production of basal NO. Both l-NAME and TTX, when tested alone, increased the amplitude and frequency of contractions. NO production was abolished by l-NAME and was inhibited by 38% by TTX. When tested together, l-NAME in the presence of TTX or TTX in the presence of l-NAME had no further effect on the amplitude or frequency of spontaneous contractions, and the NO production was inhibited. These findings suggest that basal NO consists of TTX-sensitive and TTX-resistant components. The TTX-sensitive NO has an inhibitory effect on spontaneous contractions; the role of TTX-resistant NO is unknown.

The α2-isoform of Na-K-ATPase mediates ouabain-induced hypertension in mice and increased vascular contractility in vitro

2005 ◽  
Vol 288 (2) ◽  
pp. H477-H485 ◽  
Author(s):  
Iva Dostanic ◽  
Richard J. Paul ◽  
John N. Lorenz ◽  
Steven Theriault ◽  
James W. Van Huysse ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Left Ventricular ◽  
Genetically Engineered ◽  
Wild Type ◽  
Vascular Contractility ◽  
Genetically Engineered Mice ◽  
Basal Tone ◽  
Induced Hypertension ◽  
Spontaneous Contractions

Although ouabain is known to induce hypertension, the mechanism of how this cardiac glycoside affects blood pressure is uncertain. The present study demonstrates that the α2-isoform of the Na-K-ATPase mediates the pressor effects of ouabain in mice. To accomplish this, we analyzed the effect of ouabain on blood pressure in wild-type mice, where the α2-isoform is sensitive to ouabain, and genetically engineered mice expressing a ouabain-insensitive α2-isoform of the Na-K-ATPase. Thus differences in the response to ouabain between these two genotypes can only be attributed to the α2-isoform of Na-K-ATPase. As the α1-isoform is naturally resistant to ouabain in rodents, it will not be inhibited by ouabain in either genotype. Whereas prolonged administration of ouabain increased levels of ouabain in serum from both wild-type and targeted animals, hypertension developed only in wild-type mice. In addition, bolus intravenous infusion of ouabain increased the systolic, mean arterial, and left ventricular blood pressure in only wild-type anesthetized mice. In vitro, ouabain increased vascular tone and thereby phenylephrine-induced contraction of the aorta in intact and endothelium-denuded wild-type mice but in α2-resistant mice. Ouabain also increased the magnitude of the spontaneous contractions of portal vein and the basal tone of the intact aorta from only wild-type mice. The increase in aortic basal tone was dependent on the presence of endothelium. Our studies also demonstrate that the α2-isoform of Na-K-ATPase mediates the ouabain-induced increase in vascular contractility. This could play a role in the development and maintenance of ouabain-induced hypertension.

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