• Korean Journal of Veterinary Research
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• v.39 no.5
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• pp.930-937
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• 1999

Atrial natriuretic peptide(ANP) is a hormone with potent natriuretic, diuretic and relaxing properties on vascular smooth muscle. Specific chemical modulator in response for the ANP secretion has not been found yet. Therefore, we have investigated the role of $Ca^{2+}$ responsible for the regulation of ANP induced by protein kinase C(PKC) on mechanically stretch-induced ANP secretion in the rat atria. The results obtained were as follows ; 1. ANP secretion and ANP concentration were increased to more in $Ca^{2+}$-free buffer than in the Kreb-Henseleit buffer on mechanically stretch-induced ANP secretion(p < 0.05), but extracellular fluid translocation(ECF) was not significant. Phorbol 12-myristate 13-acetate(PMA, $10^{-7}M$) induced ANP secretion and ANP concentration in $Ca^{2+}$-free buffer shown to more accentuate on mechanically stretch-induced ANP secretion than in the $Ca^{2+}$-free buffer(p < 0.05), but ECF translocation was not significant. 2. In the presence of ryanodine($3{\times}10^{-6}M$), PMA($10^{-7}M$) induced ANP secretion and ANP concentration in the Kreb-Henseleit buffer were shown to more increase on mechanically stretch-induced ANP secretion than in the ryanodine($3{\times}10^{-6}M$) with the Kreb-Henseleit buffer(p < 0.05), but ECF translocation was not significant. 3. In the presence of ryanodine($3{\times}10^{-6}M$), PMA($10^{-7}M$) induced ANP secretion and ANP concentration in the $Ca^{2+}$-free buffer was shown to more increase on mechanically stretch-induced ANP secretion than in the ryanodine($3{\times}10^{-6}M$) with the $Ca^{2+}$-free buffer on mechanically induced ANP secretion(p < 0.05), but ECF translocation was not significant. The results suggest that PKC-induced ANP secretion may not be related to the change of $Ca^{2+}$ on mechanically induced ANP secretion in the rat atria.

• Korean Journal of Microbiology
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• v.36 no.4
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• pp.254-258
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• 2000

Invasion process of bacterial cell into intestinal epithelium is important in Salmonella infection. The invasion is induced by the proteins secreted by type III secretion appratus of Salmonella. It has been known that the proteins do not have N-terminal signal peptide existing in general secreted proteins. Recent studies on Yersinia reported that secretion signal of type III appratus may lie on 5'end secondary structure of mRNA of secreted protein. In this study, we constructed translational fusion of ompR and sopE, encoding type III secretion protein of Salmonella, and observed secretion of the fusion protein for investigating the secretion signal of Salmonella type III appratus. The sopE DNA fragments of the translational fusion contain the region of promoter and from start code to tenth or to fifth code. These translational fusions indicate that type III secretion signal of Salmonella is located on 5'end of mRNA encoding secreted protein. We constructed prototype of secretion vector using this signal to produce useful foreign protein.

• The Korean Journal of Zoology
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• v.3 no.1
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• pp.19-23
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• 1960

A method for determination of thyroid secretion rate in rabbit by means of radioactive iodine presented. After injection of radioactive iodine, in vivo determination so f radioactivity in thyroid gland were made during a 19 day-experimental period. In the same period blood samples were drawn and analyzed for protein-bound iodine (PBI) and for protein-bound radioactive iodine(PBI181). A rate constant for secretion of thyroid hormone was calculated from the disappearance rate of radioactive iodine in thyroid gland. The secretion rate of radioactive hormone iodine was calculated by multiplying this rate constant by the amount of radioactive iodine present in thyroid gland. Assuming that the specific radioactiveness of the circulating thyroid hormone and of the hormone just secreted were identical , thyroid secretion rate was calculated by the equation. {{{{ { Secreted hormone-iodine , gamma /hr} over { Secreted hormone-I^131, % dose/hr }= { PBI, ${\gamma}$/ml.Serum} over { PBI^131 , % dose/ml . Serum } }} The method presented consisted of measurements for series of independent criteria on thyroid function, and the resulting thyroid secretion rate was calculated by combination of those.

• Korean Journal of Microbiology
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• v.30 no.1
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• pp.60-64
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• 1992

The secretion vector with promoter and signal sequence region of neutral protease gene (npr) from Bacillus amyloliquefaciens was constructed by the technique of polymerase chain reaction (PCR). A unique restriction iste was introduced into the 3' of the signal coding region by the synthesis of PCR primer. To demonstrate the function of cloned promoter and signal sequence, we used the E. coli .betha.-lactamase structural gene as a foreign gene. The signal sequence of .betha.-lactamase gene was deleted by Bal31 exonuclease and only mature region was introduced into the secretion vector. Bacillus subtilis cells transformed by the recombinant vector synthesized the fusion protein and were also capable of removing the signal peptide from the original fusion protein, as judged by the assay of .betha.-lactamase activity and secretion into the growth medium by western blotting.

• YAKHAK HOEJI
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• v.46 no.3
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• pp.192-196
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• 2002

To investigate the effect of intravenous ethanol administration on pancreatic exocrine secretion, we measured volume and protein amount in pancreatic juice and assayed amylase activity and phospholipase $A_2$ activity in pancreatic fragments and serum. Acute pancreatitis induced by obstruction of common bile-pancreatic duct (CBPD) and caerulein infusion (5 $\mu\textrm{g}$/kg/hr) showed typical characteristics, such as hyperamylasemia and pancreatic edema and increase of phospholipase $A_2$ activity in pancreatic fragments and serum. Intravenous ethanol infusion (50 mg/kg/hr) significantly stimulated pancreatic exocrine secretion, but such a stimulatory effect of ethanol disappeared at dose of 100 mg/kg/hr without typical symptoms of acute pancreatitis. In microscopic examination, there were no typical changes of edematous pancreatitis in ethanol administrated rats. These results suggest that acute ethanol administration has dual effect on exocrine pancreatic secretion: low dose of ethanol (50 mg/kg/hr) stimulates pancreatic exocrine secretion, whereas high dose of ethanol (100 mg/kg/hr) does not without typical changes of edematous pancreatitis.

• Tuberculosis and Respiratory Diseases
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• v.43 no.2
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• pp.123-127
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• 1996

Secretion of surfactant phospholipid can be stimulated by a variety of agonists acting via at least three different signal transduction mechanisms. These include the adenylate cyclase system with activation of cAMP-dependent protein kinase; activation of protein kinase C either directly or subsequent to activation of phosphoinositide-specific phospholipase C and generation of diacylglycerols and inositol trisphosphate; and a third mechanism that involves incresed $Ca^{2+}$ levels and a calmodulin-dependent step. ATP stimulates secretion via all three mechanisms. The protein kinase C pathway is also coupled to phopholipase D which, acting on relatively abundant cellular phospholipids, generates diacylglycerols that further activate protein kinase C. Sustained protein kinase C activation can maintain phosphatidylcholine secretion for a prolonged period of time. It is likely that interactions between the different signaling pathways have an important role in the overall physiological regulation of surfactant secretion.

• Molecules and Cells
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• v.28 no.3
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• pp.167-174
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• 2009

Genistein has been reported to potentiate glucose-stimulated insulin secretion (GSIS). Inhibitory activity on tyrosine kinase or activation of protein kinase A (PKA) was shown to play a role in the genistein-induced potentiation effect on GSIS. The aim of the present study was to elucidate the mechanism of genistein-induced potentiation of insulin secretion. Genistein augmented insulin secretion in INS-1 cells stimulated by various energygenerating nutrients such as glucose, pyruvate, or leucine/glutamine (Leu/Gln), but not the secretion stimulated by depolarizing agents such as KCl and tolbutamide, or $Ca^{2+}$ channel opener Bay K8644. Genistein at a concentration of $50{\mu}M$ showed a maximum potentiation effect on Leu/Gln-stimulated insulin secretion, but this was not sufficient to inhibit the activity of tyrosine kinase. Inhibitor studies as well as immunoblotting analysis demonstrated that activation of PKA was little involved in genistein-induced potentiation of Leu/Gln-stimulated insulin secretion. On the other hand, all the inhibitors of $Ca^{2+}$/calmodulin kinase II tested, significantly diminished genistein-induced potentiation. Genistein also elevated the levels of $[Ca^{2+}]_i$ and phospho-CaMK II. Furthermore, genistein augmented Leu/Gln-stimulated insulin secretion in CaMK II-overexpressing INS-1 cells. These data suggest that the activation of CaMK II played a role in genistein-induced potentiation of insulin secretion.

• The Korean Journal of Pharmacology
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• v.31 no.1 s.57
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• pp.75-84
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• 1995

Acid secretion and NO synthase activity were determined in isolated gastric glands following hypoxia/reoxygenation and acidosis to investigate the involvement of NO in acid secretion. Isolated gastric glands were exposed to hypoxia (30 min)/reoxygenation (1 h) and/or to acidosis (pH 6.0 and 4.0). Acid secretion was measured by the ratio of $[^{14}C]-aminopyrine$ accumulation between intra- and extraglands. NO synthase activity was determined by percent conversion to $[^{14}C]-citrulline\;from\;[^{14}C]L-arginine$, a precursor of NO. The results indicate that dibutyryl cAMP stimulated acid secretion dose-dependently but had no effect on NO synthase activity in basal gastric glands. Hypoxia/reoxygenation significantly suppressed acid secretion both in unstimulated and stimulated gastric glands, which was exaggerated by acidosis. Constitutive NO synthase, activity, not responded to dibutyryl cAMP, was also inhibited by hypoxia/reoxygenation and acidosis. In conclusion, pathologic state of gastric mucosa such as hypoxia/reoxygenation and acidosis suppresses both acid secretion and NO release but the role of NO in acid secretion stimulated by dibutyryl cAMP in basal gastric glands is not significant.

• IMMUNE NETWORK
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• v.13 no.5
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• pp.213-217
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• 2013

Enterotoxigenic Bacteroides fragilis (ETBF) is a human gut commensal bacteria that causes inflammatory diarrhea and colitis. ETBF also promotes colorectal tumorigenesis in the Min mouse model. The key virulence factor is a secreted metalloprotease called B. fragilis toxin (BFT). BFT induces E-cadherin cleavage, cell rounding, activation of the ${\beta}$-catenin pathway and secretion of IL-8 in colonic epithelial cells. However, the precise mechanism by which these processes occur and how these processes are interrelated is still unclear. E-cadherin form homophilic interactions which tethers adjacent cells. Loss of E-cadherin results in detachment of adjacent cells. Prior studies have suggested that BFT induces IL-8 expression by inducing E-cadherin cleavage; cells that do not express E-cadherin do not secrete IL-8 in response to BFT. In the current study, we found that HT29/C1cells treated with dilute trypsin solution induced E-cadherin degradation and IL-8 secretion, consistent with the hypothesis that E-cadherin cleavage causes IL-8 secretion. However, physical damage to the cell monolayer did not induce IL-8 secretion. We also show that EDTA-mediated disruption of E-cadherin interactions without E-cadherin degradation was sufficient to induce IL-8 secretion. Finally, we determined that HT29/C1 cells treated with LiCl (${\beta}$-catenin activator) induced IL-8 secretion in a dose-dependent and time-dependent manner. Taken together, our results suggest that BFT induced IL-8 secretion may occur by the following process: E-cadherin cleavage, disruption of cellular interactions, activation of the ${\beta}$-catenin pathway and IL-8 expression. However, we further propose that E-cadherin cleavage per se may not be required for BFT induced IL-8 secretion.

• Journal of Oriental Neuropsychiatry
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• v.12 no.2
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• pp.173-183
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• 2001

Substance P can stimulate secretion of tumor necrosis $factor-\;{\alpha}\;(TNF-\;{\alpha}\;)$ from astrocytes stimulated with lipopolysaccharide (LPS). Here I report that Chilbogeum can modulate cytokines secretion from primary cultures of rat astrocytes. Chilbogeum $(10\;{\mu}g/ml)$ significantly inhibited the $TNF-\;{\alpha}$ secretion by astrocytes stimulated with LPS and Substance P. Interleukin-1 (IL-1) has been shown to elevate $TNF-\;{\alpha}$ secretion from LPS-stimulated astrocytes while having no effect on astrocytes in the absence of LPS. Treatment of Chilbogeum $(10,\;100\;{\mu}g/ml)$ to astrocytes stimulated with both LPS and Substance P decreased IL-1 secretion significantly. The secretion of $TNF-\;{\alpha}$ by LPS and Substance P in astrocytes was progressively inhibited with increasing amount of IL-1 neutralizing antibody. Upon stimulation from various agents, these cells adopt a reactive phenotype, a morphological hallmark in Alzheimer's disease (AD) pathology, during which they themselves may produce still more inflammatory cytokines. Chilbogeum $(10,\;100\;{\mu}g/ml)$ significantly inhibited the $TNF-\;{\alpha}$ secretion by CCF-STTG1 astrocytoma cells stimulated with $A\;{\beta}$ and IL-1. These results suggest that Chilbogeum may inhibit $TNF-\;{\alpha}$ secretion by inhibiting IL-1 secretion and that Chilbogeum has an antiinflammatory activity in AD brain.