Effect of oxytocin on estrogen-induced uterine luminal fluid accumulation in ovariectomized rats and the role of prostaglandins

1978 ◽  
Vol 56 (6) ◽  
pp. 908-914 ◽  
Author(s):  
T. G. Kennedy
Keyword(s):  
Acute Effect ◽  
Ovariectomized Rats ◽  
Fluid Accumulation ◽  
Indirect Measure ◽  
Uterine Contractions ◽  
Dose Dependent Fashion ◽  
Fluid Formation ◽  
17Β Estradiol ◽  
Dose Dependent

In estrogen-treated ovariectomized rats, uterine luminal fluid accumulation has been used as an indirect measure of cervical tone, with loss of luminal fluid being interpreted as indicating reduced tone. Since the recently reported ability of analogues of prostaglandins E2 and F2α to cause loss of luminal fluid might have resulted, not from reduced cervical tone, but from uterine contractions forcing fluid through constricted cervices, the effects of oxytocin, also a stimulator of myometrial activity, on luminal fluid accumulation were investigated. When ovariectomized rats, implanted 72 h previously with a Silastic capsule containing 17β-estradiol, were given a single injection of oxytocin and killed 1–2 h later, oxytocin, in a dose-dependent fashion, reduced uterine luminal fluid accumulation. For a supramaximal dose of oxytocin, this effect was seen within 15 min. In rats in which one uterine horn was ligated at the cervical end, fluid accumulation in the ligated horns did not differ significantly in control and treated rats, whereas in nonligated horns, oxytocin reduced the fluid accumulation, suggesting that loss of fluid occurred through the cervix rather than by reabsorption. Given twice daily for 3 days commencing immediately after the insertion of the estrogen-containing capsule, oxytocin had no effect on luminal fluid accumulation in horns ligated at the cervical end, indicating that oxytocin did not inhibit luminal fluid formation. Prostaglandin biosynthesis did not appear to be essential for the acute effect of oxytocin since treatment of rats with indomethacin, although reducing uterine and cervical prostaglandin levels, did not inhibit the effect of oxytocin. However, loss of fluid occurred slightly sooner following oxytocin administration in controls than in indomethacin-treated animals. In addition, for animals autopsied 10 min after oxytocin injection, the dose–response relationship between oxytocin and uterine luminal fluid was affected by indomethacin treatment. These data suggest that prostaglandins act synergistically with oxytocin to bring about loss of uterine luminal fluid accumulation. However, the validity of the use of luminal fluid accumulation as an indicator of cervical tone remains to be resolved.

Induction of cell—cell adhesion by monovalent antibodies in a germ cell culture

Development ◽  
1985 ◽  
Vol 90 (1) ◽  
pp. 211-222
Author(s):  
Wai Chang Ho ◽  
Kathleen B. Bechtol
Keyword(s):  
Monoclonal Antibodies ◽  
Cell Adhesion ◽  
Germ Cell ◽  
Germ Cells ◽  
Antigen Expression ◽  
Fab Fragment ◽  
Cell Age ◽  
Dose Dependent Fashion ◽  
Dose Dependent

Four monoclonal antibodies, XT-I, MT-23, MT-24 and MT-29, that bind the XT-1-differentiation-antigen of male germ cells have been used to investigate the biological role of the XT-1-molecule of germ cells in short-term primary culture. Cultures from 10 days postpartum mice demonstrate increasing numbers of antigen-positive germ cells and increased antigen expression per cell with succeeding days of culture. Treatment of the antigen-positive cultures with three of the monoclonal antibodies, XT-I, MT-23 and MT-24, increases germ cell-germ cell adhesion in a dose-dependent fashion. Treatment with the fourth monoclonal antibody, MT-29, does not induce cell adhesion. The monovalent, Fab fragment of XT-I-antibody also elicits tight cell adhesion, thus ruling out antibody cross linking of molecules or cells. Saturating or near saturating amounts of the positive antibodies are required to produce adhesion, a result consistent with perturbation of a function that is performed by the sum of action of many of the XT-1-molecules on the cell. The ability of germ cells to undergo antibody-elicited tight adhesion is dependent on germ cell age and/or XT-1-antigen concentration. We hypothesize that the XT- 1-molecule is involved in regulation of cell adhesion, an event which must occur in normal development.

cAMP-stimulated rise of [Ca2+]i in rabbit connecting tubules: role of peritubular Ca

1990 ◽  
Vol 258 (3) ◽  
pp. F751-F755 ◽  
Author(s):  
J. E. Bourdeau ◽  
B. K. Eby
Keyword(s):  
Parathyroid Hormone ◽  
Ethylene Glycol ◽  
Cell Activation ◽  
Proximal Tubules ◽  
Tetraacetic Acid ◽  
Luminal Membrane ◽  
Dose Dependent Fashion ◽  
Dose Dependent

Parathyroid hormone (PTH) increases cytosolic free Ca concentration ([ Ca2+]i) by mechanisms that depend on extracellular Ca in both cultured renal proximal tubules and isolated rabbit connecting tubules (CNTs). In CNTs 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP) mimics this action, implicating cAMP as a second messenger, and part of the rise, due to increased luminal membrane Ca entry, is likely related to Ca absorption. In cultured proximal tubules the rise in [Ca2+]i, presumably mediated by increased Ca entry across the basolateral plasmalemma, activates gluconeogenesis and shortens microvilli. In the present study we examined cAMP-mediated Ca entry across the basolateral membranes of CNT cells, an effect potentially related to cell activation. Single CNTs were dissected from rabbit kidneys and loaded with fura-2. [Ca2+]i was measured by dual-wavelength excitation during perfusion of isolated segments in vitro. With 1.8 or 2.0 mM Ca in the lumen and the bath, suffusate 8-BrcAMP increased [Ca2+]i within minutes in a dose-dependent fashion. The increase persisted as long as 8-BrcAMP was present and reversed on its withdrawal. With 0.1 microM Ca in the lumen and the bath, 8-BrcAMP, but not ionomycin, failed to increase [Ca2+]i, implying that extracellular Ca is the major source. In tubules perfused with 2 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid to eliminate luminal Ca, but suffused with 1.8 or 2.0 mM Ca, 8-BrcAMP increased [Ca2+]i (though less so than with Ca in the lumen), implying Ca entry across basolateral cell membranes. This rise in [Ca2+]i was attenuated markedly by the presence of 50 microM LaCl3 in the bath.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence for a potential role of glucagon during eye growth regulation in chicks

2002 ◽  
Vol 19 (6) ◽  
pp. 755-766 ◽  
Author(s):  
MARITA P. FELDKAEMPER ◽  
FRANK SCHAEFFEL
Keyword(s):  
Visual Processing ◽  
Growth Regulation ◽  
Amacrine Cells ◽  
Early Gene ◽  
Eye Growth ◽  
Dose Dependent Fashion ◽  
High Concentrations ◽  
Dose Dependent ◽  
Glucagon Antagonist

Eye growth and refraction are regulated by visual processing in the retina. Until now, the messengers released by the retina to induce these changes are largely unknown. Previously, it was found that glucagon amacrine cells respond to defocus in the retinal image and even to its sign. The expression of the immediate-early gene product ZENK increased in this cell population in eyes wearing plus lenses and decreased in minus lens-treated chicks. Moreover, it was shown that the amount of retinal glucagon mRNA increased during treatment with positive lenses. Therefore, it seems likely that these cells contribute to the visual regulation of ocular growth and that glucagon may act as a stop signal for eye growth. The purpose of the present study was to accumulate further evidence for a role of glucagon in the visual control of eye growth. Chicks were treated with plus and minus lenses after injection of different amounts of the glucagon antagonist des-His1-Glu9-glucagon-amide or the agonist Lys17,18,Glu21-glucagon, respectively. Refractive development and eye growth were recorded by automated infrared photorefraction and A-scan ultrasound, respectively. The glucagon antagonist inhibited hyperopia development, albeit only in a narrow concentration range, and at most by 50%, but not myopia development. In contrast, the agonist inhibited myopia development in a dose-dependent fashion. At high concentrations, it also prevented hyperopia development.

Chorioamnionitis reduces placental endocrine functions: the role of bacterial lipopolysaccharide and superoxide anion

1997 ◽  
Vol 155 (3) ◽  
pp. 401-410 ◽  
Author(s):  
T Okada ◽  
N Matsuzaki ◽  
K Sawai ◽  
T Nobunaga ◽  
K Shimoya ◽  
...  
Keyword(s):  
Manganese Superoxide Dismutase ◽  
Northern Blot Analysis ◽  
Inflammatory Responses ◽  
Placental Lactogen ◽  
Manganese Superoxide ◽  
Histologic Chorioamnionitis ◽  
Dose Dependent Fashion ◽  
Dose Dependent ◽  
Stimulation Of

Chorioamnionitis has been shown to be one of the most important factors in inducing preterm delivery. The present study was undertaken to examine the effects of chorioamnionitis on placental endocrine functions. Preterm placentas with histologic chorioamnionitis produced smaller amounts of human chorionic gonadotropin (hCG) and human placental lactogen (hPL) than those without chorioamnionitis (P < 0.001). To examine the mechanism involved in the suppression of placental endocrine functions induced by chorioamnionitis, we initially confirmed the expression of lipopolysaccharide (LPS) receptor, i.e. the CD14 molecule, on trophoblasts by Northern blot analysis and immunohistochemistry. We then stimulated purified trophoblasts with LPS, which is the major agent which induces inflammatory responses in the host via the LPS receptor. The trophoblasts stimulated with LPS produced reduced amounts of hCG, hPL, and progesterone in a time- and dose-dependent fashion in spite of the induced manganese-superoxide dismutase (SOD) synthesis. Stimulation of trophoblasts with hypoxanthine and xanthine oxidase resulted in suppressed hCG production, while the simultaneous addition of SOD into the culture medium reversed the suppression of hCG production. LPS in the placenta with chorioamnionitis might directly stimulate trophoblasts through the LPS receptor (CD14), thus reducing placental endocrine functions. Superoxide anions which exogenously act on trophoblasts might be generated by simultaneous stimulation of neutrophils and monocytes at the feto-maternal interface by LPS, and additively reduce placental endocrine functions.

scholarly journals Identification of a new metalloproteinase inhibitor that forms tight-binding complexes with collagenase

1990 ◽  
Vol 269 (1) ◽  
pp. 183-187 ◽  
Author(s):  
T E Cawston ◽  
V A Curry ◽  
I M Clark ◽  
B L Hazleman
Keyword(s):  
Connective Tissue ◽  
Culture Media ◽  
Tight Binding ◽  
Gel Filtration ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Metalloproteinase Inhibitor ◽  
Dose Dependent Fashion ◽  
Dose Dependent ◽  
Extracellular Activity

Connective-tissue cells produce a family of metalloproteinases which, once activated, can degrade all the components of the extracellular matrix. These potent enzymes are all inhibited by the tissue inhibitor of metalloproteinases (TIMP), and it was thought that the levels of this inhibitor controlled the extracellular activity of these enzymes. We recently detected a new metalloproteinase inhibitor present in culture media of WI-38 fibroblasts. The inhibitor, named ‘large inhibitor of metalloproteinases’ (LIMP), can be separated from TIMP by gel filtration on Ultrogel AcA 44, where it is eluted with an apparent Mr of 76,000. A portion of this inhibitor-containing peak binds to concanavalin A-Sepharose, indicating that at least some of the inhibitor contains carbohydrate. LIMP inhibits collagenase (MMP-1), stromelysin (MMP-3) and gelatinase (MMP-2) in a dose-dependent fashion. Collagenase forms tight-binding complexes with LIMP, which can be separated from free collagenase on gel-filtration columns. The complex is eluted with Mr 81,600 (AcA 44) or Mr 60,000 (Superose 12). This complex is larger than that formed between collagenase and TIMP, which has Mr 52,800 (Aca 44) or 41,000 (Superose 12). Polyclonal antibody to TIMP does not recognize LIMP by immunoblotting, and will not block the inhibition of collagenase by LIMP, showing that LIMP is not a multimeric form of TIMP. The role of this new inhibitor in connective-tissue breakdown studies and its relationship to previously described inhibitors of metalloproteinases is discussed.

Role of nitric oxide and superoxide anion in spontaneous lung chemiluminescence

1997 ◽  
Vol 272 (2) ◽  
pp. L262-L267 ◽  
Author(s):  
M. L. Barnard ◽  
B. Robertson ◽  
B. P. Watts ◽  
J. F. Turrens
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Light Emission ◽  
No Synthase ◽  
O2 Concentration ◽  
Dose Dependent Fashion ◽  
Spontaneous Chemiluminescence ◽  
Oxidant Production ◽  
Dose Dependent

Inhibition of nitric oxide (.NO) synthase by nitro-L-arginine (NLA) decreased baseline chemiluminescence in a dose-dependent fashion up to 78% at 300 microM NLA. This inhibition was prevented by pretreatment with 1 mM arginine. Similarly, addition of superoxide dismutase (SOD; 200 U/ml) to the perfusion buffer inhibited spontaneous light emission by 57%. Addition of NLA after SOD or vice versa did not inhibit light emission any further, suggesting that both .NO and O2.- were precursors of the same oxidant. Production of additional extracellular O2.- by neutrophils activated with phorbol 12-myristate 13-acetate increased light emission by >200%, but this increase was insensitive to NLA. Increasing the intracellular steady-state O2.- concentration by perfusion of control lungs with the Cu and Zn-containing SOD inhibitor diethyldithiocarbamate (1 mM) stimulated light emission up to fourfold, but this spontaneous chemiluminescence was also insensitive to NLA. In experiments using cultured endothelial cells supplemented with extracellular bovine serum albumin (BSA), 5 microM of the Ca2+ ionophore A-23187 (a stimulant of .NO synthase) stimulated chemiluminescence by 40%. This increase was again SOD and NLA sensitive. Addition of NLA after SOD or vice versa did not change light emission. These results suggest that the background chemiluminescence of isolated-perfused intact lungs may result from the constant release of small amounts of O2.- and .NO by endothelial cells into the capillary lumen, which in turn react with BSA in the perfusion buffer.

Thrombopoietin in thrombocytopenic mice: evidence against regulation at the mRNA level and for a direct regulatory role of platelets

Blood ◽  
1996 ◽  
Vol 87 (2) ◽  
pp. 567-573 ◽  
Author(s):  
R Stoffel ◽  
A Wiestner ◽  
RC Skoda
Keyword(s):  
Mrna Level ◽  
Rnase Protection Assay ◽  
Chain Reaction ◽  
Rnase Protection ◽  
Dose Dependent Fashion ◽  
Liver And Kidney ◽  
Polymerase Chain ◽  
Dose Dependent ◽  
Posttranscriptional Level

Thrombopoietin (TPO), originally described as an activity in the serum of thrombocytopenic animals that leads to increased production of platelets, has recently been isolated and cloned. Its closest relative in the cytokine superfamily, erythropoietin (EPO), is transcriptionally regulated during anemia, and it was expected that TPO would similarly be regulated during thrombocytopenia. We induced thrombocytopenia in mice and confirmed that TPO activity was upregulated, as determined by a bioassay. Liver and kidney were found to be the major sources of TPO mRNA. Surprisingly, TPO mRNA in these tissues was not upregulated in thrombocytopenic mice. Using a sensitive RNase protection assay that can distinguish between TPO isoforms, we found no change in the profile of mRNA for these isoforms. A semiquantitative reverse transcription- polymerase chain reaction assay also did not demonstrate upregulation of TPO mRNA in the spleen. Thus, the increase of TPO activity during thrombocytopenia is not caused by regulation at the level of TPO mRNA. Furthermore, isolated mouse platelets absorbed high amounts of bioactive TPO out of TPO-conditioned medium in a dose-dependent fashion. Our results are consistent with TPO protein being regulated at a posttranscriptional level and/or directly through absorption and metabolism by platelets.

Gastrin regulates the human histidine decarboxylase promoter through an AP-1-dependent mechanism

1997 ◽  
Vol 272 (4) ◽  
pp. G822-G830 ◽  
Author(s):  
M. Hocker ◽  
Z. Zhang ◽  
J. L. Merchant ◽  
T. C. Wang
Keyword(s):  
B Cells ◽  
Histidine Decarboxylase ◽  
Dominant Negative ◽  
Response Element ◽  
F9 Cells ◽  
Cis Acting ◽  
Dose Dependent Fashion ◽  
F9 Embryonal Carcinoma Cells ◽  
Dose Dependent

The histidine decarboxylase (HDC) gene is regulated transcriptionally by gastrin and phorbol 12-myristate 13-acetate (PMA) through a protein kinase C (PKC)-related pathway. To determine the role of AP-1 (fos/jun) in the regulation of the HDC promoter, gastric cancer (AGS-B) cells stably expressing the cholecystokinin-B/ gastrin receptor and the 1.8-kb human (h) HDC-luciferase (luc) construct were cotransfected with constructs expressing c-fos and c-jun. Overexpression of c-fos and c-jun activated the HDC promoter in a dose-dependent fashion in 1.8-kb hHDC-luc/AGS-B cells as well as in transfected F9 embryonal carcinoma cells, which lack endogenous AP-1 activity. PMA was unable to activate the HDC promoter in F9 cells, which were not transfected with c-fos and c-jun. Gastrin stimulation increased c-fos and c-jun mRNA abundance and AP-1-dependent transcriptional activity, as assessed by a reporter construct in which the CAT reporter gene is under the control of a 12-O-tetradecanoylphorbol-13-acetate response element multimer. Gastrin-stimulated HDC promoter activity was blocked by transfection of c-fos antisense and dominant negative c-jun expression constructs. Finally, overexpression of c-fos and c-jun activated the hHDC promoter through a downstream cis-acting element (gastrin response element), which does not bind AP-1. In conclusion, activation of AP-1 is essential for gastrin-stimulated HDC transcription, but the mechanism appears to be indirect.

scholarly journals MicroRNA-19b-3p promotes cell proliferation and osteogenic differentiation of BMSCs by interacting with lncRNA H19

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Gan Xiaoling ◽  
Liu Shuaibin ◽  
Liang Kailu
Keyword(s):  
Cell Proliferation ◽  
Protein Expression ◽  
Postmenopausal Osteoporosis ◽  
Critical Role ◽  
Dependent Manner ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
17Β Estradiol ◽  
Dose Dependent

Abstract Background To investigated the role of miR-19b-3p in regulating bone marrow mesenchymal stem cell (BMSC) proliferation and osteoblast differentiation. Methods The expression of miR-19b-3p and lncRNA H19 were measured in postmenopausal osteoporosis patients and BMP-22 induced BMSCs using qRT-PCR. MiR-19b-3p mimic or inhibitor was transfected into BMP-2 induced BMSCs. Cell proliferation was measured by BrdU method. Protein expression of RUNX2 and COL1A1 were measured by western blot. PcDNA3.1-lncRNA H19 with or without miR-19b-3p mimic was transfected into BMP-2 induced BMSCs. Results The expression of miR-19b-3p was significantly up-regulated in postmenopausal osteoporosis patients and BMP-2 induced BMSCs. MiR-19b-3p overexpression dramatically elevated, while miR-19b-3p inhibition decreased cell proliferation of BMSCs. Additionally, protein expression levels of RUNX2 and COL1A1, as well as ALP activity were significantly promoted by miR-19b-3p mimic transfection and inhibited by miR-19b-3p inhibitor transfection. LncRNA H19 was obviously down-regulated in postmenopausal osteoporosis patients. H19 overexpression significantly decreased cell proliferation and differentiation by down-regulating miR-19b-3p. Moreover, the expression of miR-19b-3p was inhibited, while H19 elvated in 17β-estradiol (E2) treated BMSCs in a dose-dependent manner. Conclusion These data were the first to reveal the critical role of H19/miR-19b-3p in postmenopausal osteoporosis, and provided a new therapeutic target for OP.

scholarly journals Potential role of hypothalamic microRNAs in regulation of FOS and FTO expression in response to hypoglycemia

2019 ◽  
Vol 69 (6) ◽  
pp. 981-991 ◽  
Author(s):  
Bashair M. Mussa ◽  
Jalal Taneera ◽  
Abdul Khader Mohammed ◽  
Ankita Srivastava ◽  
Debasmita Mukhopadhyay ◽  
...  
Keyword(s):  
Nervous System ◽  
Potential Role ◽  
Autonomic Failure ◽  
Regulatory Proteins ◽  
Molecular Signature ◽  
Regulatory Mechanisms ◽  
Dose Dependent Fashion ◽  
Sympathetic Nervous ◽  
Dose Dependent

AbstractHypoglycemia-associated autonomic failure (HAAF) is a serious complication of diabetes which is associated with the absence of physiological homeostatic counter-regulatory mechanisms that are controlled by the hypothalamus and sympathetic nervous system. Identification of biomarkers for early detection of HAAF requires an advanced understanding of molecular signature of hypoglycemia which is yet to be identified. The outcomes of the present study have shown that the viability and the apoptotic rate of the hypothalamic neurons (mHypoE-N39) were decreased significantly due to hypoglycemia in a dose-dependent fashion (p < 0.05). Although there are more than 1000 miRNAs differentially expressed in hypothalamus, only twelve miRNAs (miR-7a, miR-7b, miR-9, miR-29b, miR-29c, miR-30a, miR-30b, miR-30c, miR-101b-3p, miR-181a-5p, miR-378-3p and miR-873-5p) were correlated to two main hypothalamic regulatory proteins, FOS and FTO. Expression of these proteins was very sensitive to hypoglycemia. We demonstrated that hypoglycemia modulates the expression of hypothalamic miRNAs that are related to FOS and FTO.

Sign in / Sign up

Export Citation Format

Share Document