Preferencje help
Polish version English version Język
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 9

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  pancreatic acinar cell
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
1
Content available remote

The effect of concomitant stimulation with cholecystokinin and epidermal growth factor on extracellular signal-regulated kinase (ERK) activity in pancreatic acinar cells

100%
Daniluk J., Dabrowski A.
Journal of Physiology and Pharmacology
|
2007
|
tom 58
|
nr 3
The transmission of extracellular proliferation and differentiation signals into their intracellular targets is mediated by a signaling cascade culminating in mitogen-activated protein kinase (MAPK) also known as ERK. In pancreatic acinar cells both cholecystokinin (CCK) and epidermal growth factor (EGF) are known to stimulate ERK. Regulatory interactions among individual receptor-coupled signaling cascades are critically important for establishing cellular responses in the face of multiple stimuli. The aim of our study was to evaluate the effect of concomitant stimulation of G protein-coupled receptors (GPCR) and EGF receptors on ERK activity in isolated pancreatic acinar cells. ERK activity was determined by means of Western-blotting, with the use of the antibody which recognizes active, tyrosine-phosphorylated kinase (pY-ERK). pY-ERK level was strongly elevated by 10 nM CCK-8, 100 µM carbachol (CAR), or 100 nM EGF. The addition of EGF to 60 min-lasting incubations of acini with CCK-8 or CAR caused abrupt decrease of pY-ERK level to 56 and 59% of control, respectively. Similar phenomenon was observed when short stimulation with CCK-8 or CAR was superimposed on the effect of EGF. After the addition of EGF to acini incubated previously with phorbol ester TPA, strong decrease in pY-ERK level was also observed. In conclusion, in pancreatic acinar cells, concomitant stimulation with CCK or CAR and EGF has strong inhibitory effect on ERK cascade. This inhibitory cross-talk may be mediated, at least partially, by protein kinase C (PKC). These mutual inhibitory interactions demonstrate novel mechanism for integration of multiple signals generated by activation of G-protein-coupled and growth factor receptors in pancreatic acinar cells.
2
Content available remote

Pancreatitis-associated protein-1 suppresses apoptosis in cerulein-stimulated pancreatic acinar cells in response to nuclear factor-kappaB activation

84%
Yu J. H., Lim J. W., Kim H.
Journal of Physiology and Pharmacology
|
2019
|
tom 70
|
nr 6
3
Content available remote

Exocrine pancreas; molecular basis for intracellular signaling, damage and protection - Polish experience

84%
Dabrowski A.
Journal of Physiology and Pharmacology. Supplement
|
2003
|
tom 54
|
nr 3
167-181
Polish experience in molecular pancreatology mostly involves experimental work on intracellular signal transduction mechanisms in pancreatic acinar cells. It was found that stimulation with cholecystokinin (CCK) or exposure of pancreatic acini to reactive oxygen species induces three separate signaling cascades leading to activation of ERKs, JNK/SAPKs and p38 MAPK. In pancreatic acini, ERK cascade is also activated by epidermal growth factor (EGF). However, CCK and EGF activate this cascade by different mechanisms. EGF activates the cascade in a classical Ras-dependent manner, while CCK-induced activation of the ERK cascade is Ras-independent. Furthermore, stimulation with CCK leads to a rapid activation of PKC, which in turn may directly activate Raf family of kinases. Freshly isolated pancreatic acini contain pancreatic stellate cells which respond to EGF by activation of ERK cascade. It is possible that stimulation with CCK and EGF induces a cross-talk between acinar and stellate cells. Isolated pancreatic acinar cells irradiated with UV-B die predominantly by apoptosis while necrosis predominates among the cells subjected to supraphysiological concentrations of CCK. In pancreatic acini subjected to stressful stimuli the regulation of apoptosis may involve interaction between ERK and p38 MAPK signaling pathways. Acute pancreatitis in rats and in humans is associated with a marked increase in the plasma level of leptin which is caused by increased production of this peptide in the inflamed pancreas. It is possible that exogenous leptin protects the pancreas against development of acute pancreatitis by the activation of nitric oxide pathway.
4
Content available remote

Missorting of cathepsin B into the secretory compartment of CI-MPR/IGFII-deficient mice does not induce spontaneous trypsinogen activation but leads to enhanced trypsin activity during experimental pancreatitis - without affecting disease severity

84%
Meister T., Niehues R., Hahn D., Domschke W., Sendler M., Lerch M. M., Schnekenburger J.
Journal of Physiology and Pharmacology
|
2010
|
tom 61
|
nr 5
5
Content available remote

Increase of heat shock protein gene expression by melatonin in AR42J cells

84%
Bonior J., Jaworek J., Konturek S. J., Pawlik W. W.
Journal of Physiology and Pharmacology
|
2005
|
tom 56
|
nr 3
Heat shock proteins (HSPs) have been reported to protect the pancreatic cells from the acute damage produced by caerulein overstimulation. However the effects of caerulein, melatonin or hyperthermia preconditioning on mRNA signal for HSP60 in the pancreatic acinar cells has not been examined yet. The aims of this study were: 1. To investigate the gene expression for HSP60 in the pancreatic AR42J cells stimulated by melatonin, caerulein or combination of both these substances. 2. To compare above changes with mRNA signal for HSP60 in pancreatic AR42J cells subjected to hyperthermia preconditioning. AR42J cells were incubated in standard medium at 37°C for: 0, 1, 3, 5, 12 or 24 h, under basal conditions. Above cells were then subjected to heat shock (42°C) for 0, 1 or 3 h. In the next part of the study AR42J cells were incubated in presence of caerulein (10-11, 10-9 or 10-7M), melatonin (10-8 or 10-6M), or combination of above under basal conditions or following heat shock pretreatment. Gene expression for HSP60 was determined by RT-PCR. The mRNA signal for HSP60 has been observed in AR42J cells under basal conditions, and this signal was markedly and time-dependently increased in these cells subjected to hyperthermia preconditioning. Incubation of AR42J cells in presence of melatonin (10-8 or 10-6M) resulted in the significant and dose-dependent increase of gene expression for HSP60 in both groups of AR42J cells: preconditioned and in those, which were not subjected to hyperthermia. Caerulein stimulation reduced mRNA signal for HSP60. The strongest signal has been observed after the exposition of AR42J cells to hyperthermia preconditioning, combined with melatonin and caerulein. We conclude that: 1. Gene expression for HSP60 has been detected in pancreatic AR42J cells under basal conditions. 2. Hyperthermia preconditioning resulted in a significant and time-dependent increase of HSP60 signal in pancreatic AR42J cells. 3. HSP60 gene expression was significantly increased in pancreatic AR42J cells stimulated by melatonin whereas caerulein reduced this signal. 4. The strongest gene expression for HSP60 has been found in the cells subjected to the combination of hyperthermia preconditioning, caerulein and melatonin.
6

Intracellular signalling in pancreatic acinar cells

84%
Dabrowski A.
Journal of Physiology and Pharmacology. Supplement
|
1998
|
tom 49
|
nr 2
7
Content available remote

Modulation of CCK-8-evoked intracellular Ca2+ waves by hydrogen peroxide in mouse pancreatic acinar cells

84%
Granados M. P., Salido G. M., Pariente J. A., Gonzalez A.
Journal of Physiology and Pharmacology
|
2007
|
tom 58
|
nr 3
In the present study we have employed single cell imaging analysis to monitor the propagation of cholecystokinin-evoked Ca2+ waves in mouse pancreatic acinar cells. Stimulation of cells with 1 nM CCK-8 led to an initial Ca2+ release at the luminal cell pole and subsequent spreading of the Ca2+ signal towards the basolateral membrane in the form of a Ca2+ wave. Inhibition of sarcoendoplasmic reticulum Ca2+-ATPase (SERCA) activity by 1 µM thapsigargin, preincubation in the presence of 100 µM H2O2 or inhibition of PKC with either 5 µM Ro31-8220 or 3 µM GF-109203-X all led to a faster propagation of CCK-8-induced Ca2+ signals. The propagation of CCK-8-evoked Ca2+ signals was slowed down by activation of PKC with 1 µM PMA, and preincubation of cells in the presence of H2O2 counteracted the effect of PKC inhibition. The protonophore FCCP (100 nM) and the inhibitor of the mitochondrial Ca2+-uniporter Ru360 (10 µM) led to an increase in the propagation rate of CCK-8-evoked Ca2+ waves. Finally, depolymerisation of actin cytoskeleton with cytochalasin D (10 µM) led to a faster propagation of CCK-8-evoked Ca2+ signals. Stabilization of actin cytoskeleton with jasplakinolide (10 µM) did not induce significant changes on CCK-8-evoked Ca2+ waves. Preincubation of cells in the presence of H2O2 counteracted the effect of cytochalasin D on CCK-8-evoked Ca2+ wave propagation. Our results suggest that spreading of cytosolic Ca2+ waves evoked by CCK-8 can be modulated by low levels of oxidants acting on multiple Ca2+-handling mechanisms.
8
Content available remote

Endotoxemia in the infant rats modulates HSP60 protein level in the pancreatic acinar cells

67%
Bonior J., Jaworek J., Kot M., Konturek S. J., Pawlik W. W.
Journal of Physiology and Pharmacology. Supplement
|
2007
|
tom 58
|
nr 3
189-198
9
Content available remote

Brain-gut axis in the modulation of pancreatic enzyme secretion

67%
Jaworek J., Nawrot-Porabka K., Leja-Szpak A., Konturek S. J.
Journal of Physiology and Pharmacology
|
2010
|
tom 61
|
nr 5
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.