Cellular mechanisms in activation of Na-K-Cl cotransport in nasal gland acinar cells of guinea pigs

1995 ◽  
Vol 146 (3) ◽  
Author(s):  
K. Ikeda ◽  
D. Wu ◽  
T. Takasaka
1953 ◽  
Vol 31 (4) ◽  
pp. 343-357
Author(s):  
Christine E. Rice ◽  
Paul Boulanger ◽  
P. J. G. Plummer ◽  
E. Annau

Fatty livers were produced in guinea pigs by the repeated feeding or injection of ethionine; the acinar cells of the pancreas were also affected in some of the animals. Marked changes in plasma coagulability always occurred as well as a definite reduction in complement titer in which two or more of the major complement components were involved. Methionine displayed some protective effect against the fatty liver induced by the ethionine and was partially effective in controlling the coagulative changes and the decline in complement titer. In some animals, choline likewise ameliorated these conditions, whereas cystine tended to aggravate them. A combination of cystine and choline was more effective than choline alone.


1995 ◽  
Vol 98 (5) ◽  
pp. 761-769,925
Author(s):  
MOTOAKI ISHIGAKI ◽  
KATSUHISA IKEDA ◽  
HIROSHI SUNOSE ◽  
MASAAKI SUZUKI ◽  
TOMONORI TAKASAKA
Keyword(s):  

1994 ◽  
Vol 266 (6) ◽  
pp. G1130-G1138 ◽  
Author(s):  
N. Rivard ◽  
D. Lebel ◽  
J. Laine ◽  
J. Morisset

Phosphorylation and dephosphorylation of proteins on tyrosyl residues are important reactions involved in cellular activities, namely, those associated with growth and differentiation. Although it is accepted that cholecystokinin (CCK) and somatostatin (SS) stimulate and inhibit pancreatic growth and secretion, the cellular mechanisms by which these two hormones trigger their stimulatory and inhibitory effects are not well known. It has recently been suggested that, in acinar cells, one of the early signals of SS would involve activation of a membrane tyrosine phosphatase, whereas the signal associated with CCK may involve stimulation of protein tyrosine phosphorylation. This study examines the effects of caerulein (Cae) and SMS-201-995 (SMS) on pancreatic growth, particulate and crude cytosolic tyrosine kinase (TRK), and phosphotyrosine phosphatase (PTase) activities. Rats infused intravenously with 0.05% bovine serum albumin (control), Cae (0.25 micrograms.kg-1.h-1), or SMS (5 micrograms.kg-1.h-1) were killed after 0.5, 1, 2, 3, 4, 8, 12, 24, and 48 h of infusion. The pancreas was excised, weighed, and evaluated for contents of DNA and protein and for TRK and PTase activities. The effects of subtotal pancreatectomy on TRK and PTase activities were also examined after 1, 2, 3, 4, and 7 days. In response to Cae, pancreatic growth was evident after 48 h and was accompanied by sustained increases in particulate TRK and particulate PTase. Increases in membrane PTase activities were localized on membranes of the zymogen granules. SMS treatment was associated with increases in pancreatic weight and protein as a result of inhibition of secretion.(ABSTRACT TRUNCATED AT 250 WORDS)


2004 ◽  
Vol 72 (1) ◽  
pp. 489-497 ◽  
Author(s):  
Anna I. Bakardjiev ◽  
Brian A. Stacy ◽  
Susan J. Fisher ◽  
Daniel A. Portnoy

ABSTRACT Feto-placental infections represent a major cause of pregnancy complications, and yet the underlying molecular and cellular mechanisms of vertical transmission are poorly understood. Listeria monocytogenes, a facultative intracellular pathogen, is one of a group of pathogens that are known to cause feto-placental infections in humans and other mammals. The purpose of this study was to evaluate possible mechanisms of vertical transmission of L. monocytogenes. Humans and guinea pigs have a hemochorial placenta, where a single layer of fetally derived trophoblasts separates maternal from fetal circulation. We characterized L. monocytogenes infection of the feto-placental unit in a pregnant guinea pig model and in primary human trophoblasts and trophoblast-derived cell lines. The clinical manifestations of listeriosis in the pregnant guinea pigs and the tropism of L. monocytogenes to the guinea pig placenta resembled those in humans. Trophoblast cell culture systems were permissive for listerial growth and cell-to-cell spread and revealed that L. monocytogenes deficient in internalin A, a virulence factor that mediates invasion of nonphagocytic cells, was 100-fold defective in invasion. However, crossing of the feto-placental barrier in the guinea pig model was independent of internalin A, suggesting a negligible role for internalin-mediated direct invasion of trophoblasts in vivo. Further understanding of vertical transmission of L. monocytogenes will help in designing more effective means of treatment and disease prevention.


1995 ◽  
Vol 268 (3) ◽  
pp. L361-L367 ◽  
Author(s):  
K. Ikeda ◽  
M. Ishigaki ◽  
D. Wu ◽  
H. Sunose ◽  
M. Suzuki ◽  
...  

We examined intracellular Ca2+ responses of the nasal gland acinar cells to clarify cellular responses and molecular events with regard to the regulatory mechanism of the nasal secretion. The acinar cells of the serous gland in the nasal septum of guinea pigs were obtained by meticulous and selective dissection with minimal contamination by epithelial lining cells after collagenase treatment. The dispersed acini were incubated in the oxygenated solution supplemented with fura 2 acetoxymethyl ester, and the intracellular Ca2+ concentration ([Ca2+]i) was measured by fluorescence ratio imaging microscopy. The application of acetylcholine (ACh) to the cells induced an initially rapid increased [Ca2+]i followed by a sustained plateau. The increase in [Ca2+]i induced by ACh was concentration dependent, ranging between 10(-8) and 10(-4) M. The [Ca2+]i response was completely inhibited by atropine, further indicating the involvement of muscarinic cholinergic receptors. Removal of external Ca2+ with addition of EGTA resulted in a transient increase without a sustained phase, and the transient increase was abolished by the intracellular Ca2+ antagonist 8-(diethylamino)-octyl-3,4,5-trimethoxybenzoate, indicating that this increase in [Ca2+]i was due to release from internal stores. The initial peak was not altered by changes in external pH, addition of adenosine 3',5'-cyclic monophosphate (cAMP), nor addition of phorbol 12-myristate 13-acetate (PMA) but was augmented by external K(+)-induced depolarization, suggesting that the transient increase was due to a changing in the binding affinity to inositol 1,4,5-trisphosphate. The sustained Ca2+ entry induced by ACh was inhibited by Ni2+, but not by nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)


1996 ◽  
Vol 10 (3) ◽  
pp. 173-179
Author(s):  
Seiichiro Nakabayashi ◽  
Katsuhisa Ikeda ◽  
Akira Shimomura ◽  
DaZheng Wu ◽  
Narihisa Ueda ◽  
...  

Endocrinology ◽  
1984 ◽  
Vol 115 (3) ◽  
pp. 1102-1109 ◽  
Author(s):  
LARS SJÖDIN ◽  
KERSTIN HOLMBERG ◽  
ANNIKA LYDEN

1999 ◽  
Vol 277 (1) ◽  
pp. C74-C82 ◽  
Author(s):  
Bing Han ◽  
Craig D. Logsdon

Inflammatory mediators are involved in the early phase of acute pancreatitis, but the cellular mechanisms responsible for their generation within pancreatic cells are unknown. We examined the role of nuclear factor-κB (NF-κB) in cholecystokinin octapeptide (CCK-8)-induced mob-1 chemokine expression in pancreatic acinar cells in vitro. Supraphysiological, but not physiological, concentrations of CCK-8 increased inhibitory κB (IκB-α) degradation, NF-κB activation, and mob-1 gene expression in isolated pancreatic acinar cells. CCK-8-induced IκB-α degradation was maximal within 1 h. Expression of mob-1 was maximal within 2 h. Neither bombesin nor carbachol significantly increased mob-1 mRNA or induced IκB-α degradation. Thus the concentration, time, and secretagogue dependence of mob-1 gene expression and IκB-α degradation were similar. Inhibition of NF-κB with pharmacological agents or by adenovirus-mediated expression of the inhibitory protein IκB-α also inhibited mob-1 gene expression. These data indicate that the NF-κB signaling pathway is required for CCK-8-mediated induction of mob-1 chemokine expression in pancreatic acinar cells. This supports the hypothesis that NF-κB signaling is of central importance in the initiation of acute pancreatitis.


Author(s):  
I. Bagcivan ◽  
O. Cevit ◽  
M. K. Yildirim ◽  
S. Gursoy ◽  
S. Yildirim ◽  
...  
Keyword(s):  

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