Histamine methyltransferase in dispersed cells from rabbit fundic mucosa

1989 ◽  
Vol 28 (1-2) ◽  
pp. 39-44 ◽  
Author(s):  
J. Loiselle ◽  
A. Wollin
Keyword(s):  
Fundic Mucosa ◽  
Histamine Methyltransferase ◽  
Dispersed Cells

STIMULATION BY HUMAN CHORIONIC GONADOTROPHIN OF OESTRADIOL PRODUCTION BY DISPERSED CELLS FROM HUMAN CORPUS LUTEUM: COMPARISON WITH PROGESTERONE PRODUCTION; UTILIZATION OF EXOGENOUS TESTOSTERONE

1981 ◽  
Vol 91 (2) ◽  
pp. 197-203 ◽  
Author(s):  
M. C. RICHARDSON ◽  
G. M. MASSON
Keyword(s):  
Luteal Phase ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Cell Suspensions ◽  
Corpora Lutea ◽  
Progesterone Production ◽  
Late Luteal Phase ◽  
Oestradiol Production ◽  
Dispersed Cells

Cell suspensions were prepared from tissue samples of human corpora lutea obtained during the mid- and late-luteal phase of the menstrual cycle. Both oestradiol and progesterone production by dispersed cells were stimulated by similar concentrations of human chorionic gonadotrophin (hCG). As the degree of stimulation of production by hCG was greater for progesterone than for oestradiol (five- to tenfold compared with two- to threefold higher than basal production), the ratio of progesterone to oestradiol produced varied according to the level of trophic stimulation. A comparison of cell suspensions prepared from mid- and late-luteal phase corpora lutea, exposed to the same concentration of hCG (10 i.u./ml) in vitro, did not reveal a shift to oestradiol production in the late-luteal phase. Provision of additional testosterone during incubation raised the level of oestradiol production by dispersed luteal cells. At an optimum concentration of testosterone (1 μmol/l), oestradiol synthesis was not raised further in the presence of hCG or N6, O2-dibutyryl cyclic AMP, suggesting a lack of induction or activation of the aromatase system by gonadotrophin in short-term cultures. Basal and stimulated levels of progesterone production were not significantly impaired in the presence of testosterone.

Histamine H3 and H4 receptors are expressed on distinct endocrine cell types in the rat fundic mucosa

2008 ◽  
Vol 57 (S1) ◽  
pp. 57-58 ◽  
Author(s):  
G. Morini ◽  
G. Becchi ◽  
F. C. Shenton ◽  
P. L. Chazot ◽  
D. Grandi
Keyword(s):  
Endocrine Cell ◽  
Cell Types ◽  
Fundic Mucosa ◽  
Histamine H3

Prostaglandin E2-histamine in interactions on cAMP, cGMP, and acid production in isolated fundic glands

1982 ◽  
Vol 242 (1) ◽  
pp. G21-G26 ◽  
Author(s):  
R. A. Levine ◽  
K. R. Kohen ◽  
E. H. Schwartzel ◽  
C. E. Ramsay
Keyword(s):  
Prostaglandin E2 ◽  
Acid Secretion ◽  
Acid Production ◽  
Camp Production ◽  
Histamine Stimulation ◽  
Fundic Mucosa ◽  
Biochemical Responses ◽  
Camp Levels ◽  
Camp And Cgmp ◽  
Stimulation Of

Relations among cAMP, cGMP, acid production [measured by the intraglandular accumulation of [14C]aminopyrine (AP)], and prostaglandin E2 (PGE2) activity were studied in isolated glands from rabbit fundic mucosa. AP, cAMP, and cGMP responses to histamine, PGE2, and 3-isobutyl-1-methylxanthine (IMX) were compared with controls. Histamine and PGE2 significantly increased glandular cAMP levels twofold, and histamine and IMX stimulated AP uptake two- to fourfold. PGE2 significantly inhibited both histamine- and IMX-stimulated AP accumulation, but it did not alter basal AP uptake. PGE2 also decreased histamine-stimulated cAMP production but only at a low concentration (10(-7) M). This dose of PGE2 was near to the endogenous PGE2 content found in unstimulated glands (10(-8) M). Intraglandular cGMP levels in unstimulated glands (10(-8) M). Intraglandular cGMP levels were increased by IMX but not by PGE2 or histamine. It is concluded that histamine stimulation of acid secretion is mediated by cAMP, that secretory and biochemical responses to histamine are modulated by PGE2 because PGE2 antagonized histamine-stimulated cAMP and AP uptake, and that the rise in cAMP induced solely by PGE2 appears to be localized within nonparietal cells because PGE2 alone did not stimulate AP accumulation.

scholarly journals Susceptibility of Pseudomonas aeruginosa Dispersed Cells to Antimicrobial Agents Is Dependent on the Dispersion Cue and Class of the Antimicrobial Agent Used

2017 ◽  
Vol 61 (12) ◽  
Author(s):  
Jacob R. Chambers ◽  
Kathryn E. Cherny ◽  
Karin Sauer
Keyword(s):  
Antimicrobial Agents ◽  
Expression Patterns ◽  
Drug Susceptibility ◽  
Exponential Phase ◽  
Planktonic Cells ◽  
Additional Time ◽  
Modification System ◽  
Expression Of Genes ◽  
The Difference ◽  
Dispersed Cells

ABSTRACT The biofilm life cycle is characterized by the transition of planktonic cells exhibiting high susceptibly to antimicrobial agents to a biofilm mode of growth characterized by high tolerance to antimicrobials, followed by dispersion of cells from the biofilm back into the environment. Dispersed cells, however, are not identical to planktonic cells but have been characterized as having a unique transitionary phenotype relative to biofilm and planktonic cells, with dispersed cells attaching in a manner similar to exponential-phase cells, but demonstrating gene expression patterns that are distinct from both exponential and stationary-phase planktonic cells. This raised the question whether dispersed cells are as susceptible as planktonic cells and whether the dispersion inducer or the antibiotic class affects the drug susceptibility of dispersed cells. Dispersed cells obtained in response to dispersion cues glutamate and nitric oxide (NO) were thus exposed to tobramycin and colistin. Although NO-induced dispersed cells were as susceptible to colistin and tobramycin as exponential-phase planktonic cells, glutamate-induced dispersed cells were susceptible to tobramycin but resistant to colistin. The difference in colistin susceptibility was independent of cellular c-di-GMP levels, with modulation of c-di-GMP failing to induce dispersion. Instead, drug susceptibility was inversely correlated with LPS modification system and the biofilm-specific transcriptional regulator BrlR. The susceptibility phenotype of glutamate-induced dispersed cells to colistin was found to be reversible, with dispersed cells being rendered as susceptible to colistin within 2 h postdispersion, though additional time was required for dispersed cells to display expression of genes indicative of exponential growth.

Relationship between interleukin-1β mRNA level in gastric fundic mucosa and gastric juice pH in patients infected with Helicobacter pylori

1998 ◽  
Vol 114 ◽  
pp. A225
Author(s):  
Wang Mengchun ◽  
Takahisa Furuta ◽  
Misako Takashima ◽  
Hajime Futami ◽  
Hiroyuki Hanai ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Juice ◽  
Mrna Level ◽  
Interleukin 1Β ◽  
Fundic Mucosa

scholarly journals Chlorotetracycline as a fluorescent Ca2+ probe in pancreatic islet cells.

1978 ◽  
Vol 76 (3) ◽  
pp. 652-674 ◽  
Author(s):  
I B Täljedal
Keyword(s):  
Plasma Membranes ◽  
Islet Cells ◽  
Dependent Manner ◽  
Cell Surfaces ◽  
Noticeable Effect ◽  
Cell Plasma ◽  
Glass Capillaries ◽  
Asymmetrically Distributed ◽  
Dose Dependent ◽  
Dispersed Cells

Pancreatic islets, or suspensions of islet cells, from noninbred ob/ob-mice were incubated with chlorotetracycline and analyzed for Ca2+-dependent fluorescence in a microscope. Unless logarithmically transformed, signals from islets were asymmetrically distributed with unstable variance. Signals from cells pelleted in glass capillaries were more homogeneous and depended linearly on the thickness of the sample. The effect of sample thickness and a significant enhancement of fluorescence by alloxan suggest that beta-cells were involved in producing the signal from whole islets. The signal from dispersed cells was probably diagnostic of Ca2+ in beta-cell plasma membranes because it was suppressed by La3+ and had a spectrum indicative of an apolar micromilieu; fluorescent staining of cell surfaces was directly seen at high magnification. Fluorescence from cells was enhanced by 0.5-10 mM Ca2+ in a dose-dependent manner, whereas less than 0.5 mM Ca2+ saturated the probe alone in methanol. The signal from islets or dispersed cells was suppressed by 5 mM theophylline; that from cells was also suppressed by 0.5 mM 3-isobutyl-1-methylxanthine, 1.2 or 15 mM Mg2+, 3-20 mM D-glucose, and, to a lesser extent, 20 mM 3-O-methyl-D-glucose. D-glucose was more inhibitory in the absence than in the presence of Mg2+, as if Mg2+ and D-glucose influenced the same Ca2+ pool. L-glucose, D-mannopheptulose, or diazoxide had no noticeable effect and 20 mM bicarbonate was stimulatory. The results suggest that microscopy of chlorotetracycline-stained cells can aid in characterizing calcium pools of importance for secretion. Initiation of insulin release may be associated with an increas

scholarly journals Pseudomonas aeruginosa Requires the DNA-Specific Endonuclease EndA To Degrade Extracellular Genomic DNA To Disperse from the Biofilm

2019 ◽  
Vol 201 (18) ◽  
Author(s):  
Kathryn E. Cherny ◽  
Karin Sauer
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Biofilm Formation ◽  
Genomic Dna ◽  
Early Stage ◽  
Content Type ◽  
Biofilm Dispersion ◽  
Biofilm Structure ◽  
First Time ◽  
Biofilm Matrix ◽  
Dispersed Cells

ABSTRACT The dispersion of biofilms is an active process resulting in the release of planktonic cells from the biofilm structure. While much is known about the process of dispersion cue perception and the subsequent modulation of the c-di-GMP pool, little is known about subsequent events resulting in the release of cells from the biofilm. Given that dispersion coincides with void formation and an overall erosion of the biofilm structure, we asked whether dispersion involves degradation of the biofilm matrix. Here, we focused on extracellular genomic DNA (eDNA) due to its almost universal presence in the matrix of biofilm-forming species. We identified two probable nucleases, endA and eddB, and eddA encoding a phosphatase that were significantly increased in transcript abundance in dispersed cells. However, only inactivation of endA but not eddA or eddB impaired dispersion by Pseudomonas aeruginosa biofilms in response to glutamate and nitric oxide (NO). Heterologously produced EndA was found to be secreted and active in degrading genomic DNA. While endA inactivation had little effect on biofilm formation and the presence of eDNA in biofilms, eDNA degradation upon induction of dispersion was impaired. In contrast, induction of endA expression coincided with eDNA degradation and resulted in biofilm dispersion. Thus, released cells demonstrated a hyperattaching phenotype but remained as resistant to tobramycin as biofilm cells from which they egress, indicating EndA-dispersed cells adopted some but not all of the phenotypes associated with dispersed cells. Our findings indicate for the first time a role of DNase EndA in dispersion and suggest weakening of the biofilm matrix is a requisite for biofilm dispersion. IMPORTANCE The finding that exposure to DNase I impairs biofilm formation or leads to the dispersal of early stage biofilms has led to the realization of extracellular genomic DNA (eDNA) as a structural component of the biofilm matrix. However, little is known about the contribution of intrinsic DNases to the weakening of the biofilm matrix and dispersion of established biofilms. Here, we demonstrate for the first time that nucleases are induced in dispersed Pseudomonas aeruginosa cells and are essential to the dispersion response and that degradation of matrix eDNA by endogenously produced/secreted EndA is required for P. aeruginosa biofilm dispersion. Our findings suggest that dispersing cells mediate their active release from the biofilm matrix via the induction of nucleases.

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