• Applied Microscopy
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• 제18권2호
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• pp.34-46
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• 1988

췌장비 acinar cell에서 자극-분비 반응 과정을 알아보기 위하여 전자현미경을 이용하였다. 분비 촉진 물질인 아세틸콜린이나 MNNG의 투여에 따른 세포내 반응이 세포의 형태적 변화로서 잘 나타났으며 특히 guanylate cyclase를 활성화시키는 것으로 알려진 MNNG는 투여 후 일정시간 뒤 세포내에 많은 분비물 과립의 형성을 유발하였다. 이러한 결과에서 볼때 췌장의 acinar cell을 아세틸콜린으로 자극할 경우 guanylate cyclase는 지속적 반응 단계의 초기에 분비에 가세하는 것으로 생각되었고 cycloheximide나 dibucaine은 지속적 반응을 억제하는 것으로 나타났다. 또 췌장의 acinar cell에서는 분비물 과립의 형성이 소포체에서 직접 이루어지는 것으로 생각되었다.

• International Journal of Oral Biology
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• 제37권1호
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• pp.37-41
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• 2012

Pancreatic acinar cells exhibit a polarity that is characterized by the localization of secretory granules at the apical membrane. However, the factors that regulate cellular polarity in these cells are not well understood. In this study, we investigated the effect of Mist1, a basic helix-loop-helix transcription factor, on the cellular architecture of pancreatic acinar cells. Mist1-null mice displayed secretory granules that were diffuse throughout the pancreatic acinar cells, from the apical to basolateral membranes, whereas Mist1 heterozygote mice showed apical localization of secretory granules. Deletion of the Mist1 gene decreased the expression of type 3 inositol 1,4,5-triphosphate receptors ($IP_3R$) but did not affect apical localization and expression of $IP_3R2$. Mist1-null mice also displayed an increase in luminal areas and an increase in the expression of zymogen granules in pancreatic acinar cells. These results suggest that Mist1 plays a critical role in polar localization of cellular organelles and in maintaining cellular architecture in mouse pancreatic acinar cells.

• Journal of Yeungnam Medical Science
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• 제25권2호
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• pp.128-133
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• 2008

Acinar cell carcinoma is a rare tumor that represents 1~2% of all pancreatic cancers. Clinical and radiologic findings are inconclusive in this disease. Acinar cell carcinoma is characterized by rapid progression and early metastasis, which lead to its poor prognosis. A 41-year-old man was admitted to our hospital for abdominal pain. Abdominal computed tomography (CT) and positron emission tomography-computed tomography (PET-CT) showed a splenic mass, which was being invaded by a pancreatic tail mass and which had increased $^{18}F$-fluorodeoxyglucose (FDG) uptake. Primary radical distal pancreatectomy and splenectomy were performed. Pathologic findings revealed an acinar cell carcinoma of the pancreas. The patient underwent a total gastrectomy three months later because of gastric recurrence. Four months later, multiple hepatic metastases were discovered, and the patient underwent a left hepatectomy. During treatment with capecitabine, there was no evidence of tumor progression for 14 months. We report a case of metastatic pancreatic acinar cell carcinoma, which did not progress for an extended period while the patient was being treated with capecitabine.

• The Korean Journal of Physiology and Pharmacology
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• 제14권2호
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• pp.105-111
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• 2010

Inositol 1,4,5-trisphosphate receptors ($InsP_3Rs$) modulate $Ca^{2+}$ release from intracellular $Ca^{2+}$ store and are extensively expressed in the membrane of endoplasmic/sarcoplasmic reticulum and Golgi. Although caffeine and 2-aminoethoxydiphenyl borate (2-APB) have been widely used to block $InsP_3Rs$, the use of these is limited due to their multiple actions. In the present study, we examined and compared the ability of caffeine and 2-APB as a blocker of $Ca^{2+}$ release from intracellular $Ca^{2+}$ stores and $Ca^{2+}$ entry through store-operated $Ca^{2+}$ (SOC) channel in the mouse pancreatic acinar cell. Caffeine did not block the $Ca^{2+}$ entry, but significantly inhibited carbamylcholine (CCh)-induced $Ca^{2+}$ release. In contrast, 2-APB did not block CCh-induced $Ca^{2+}$ release, but remarkably blocked SOC-mediated $Ca^{2+}$ entry at lower concentrations. In permeabilized acinar cell, caffeine had an inhibitory effect on InsP3-induced $Ca^{2+}$ release, but 2-APB at lower concentration, which effectively blocked $Ca^{2+}$ entry, had no inhibitory action. At higher concentrations, 2-APB has multiple paradoxical effects including inhibition of Ins$P_3$-induced $Ca^{2+}$ release and direct stimulation of $Ca^{2+}$ release. Based on the results, we concluded that caffeine is useful as an inhibitor of $InsP_3R$, and 2-APB at lower concentration is considered a blocker of $Ca^{2+}$ entry through SOC channels in the pancreatic acinar cell.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2003년도 정기총회 및 학술발표회
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• pp.56-56
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• 2003

Isolated single pancreatic acinar cells have long been used as a good model for studying many kinds of signaling processes due to their good structural and functional polarities without a significant validation. In this study, we have examined morphological and functional changes of the dissociated single pancreatic acinar cells by imaging cytosolic Ca$\^$2+/ concentration, exocytosis of granules, and by observing their shapes with confocal microscopy.

• 생명과학회지
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• 제23권11호
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• pp.1404-1408
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• 2013

본 연구에서는 마우스 췌장의 선포세포(primary acinar cell)에서 에탄올에 의해 유도된 염증성 손상에 미치는 녹차의 생리활성 물질인 EGCG의 효과를 췌장분비 효소의 활성과 선포세포에서의 기능 회복 관련 마크로 알려진 유전자들(AMPK, RKIP 및 Reg1)의 발현 조절 측면에서 조사하였다. 대조군에 비해 에탄올이 처리된 세포에서는 ${\alpha}$-amylase와 chymotrypsin의 활성이 증가되었지만, EGCG 처리에 의하여 그들 활성이 유의적으로 감소하였다. 세포 생존 및 보호와 관련 있는 AMPK 인산화 수준은 에탄올 단독 처리시 그 발현이 감소하였지만, EGCG 처리에 의하여 유의적으로 회복되었다. 세포 사멸과 세포독성 조절과 연관이 있는 RKIP 또한 그 발현 경향이 AMPK인산화 변화의 정도와 유사하였다. 또한 베타세포 재생에 관여하는 Reg1 발현은 에탄올이 처리된 선포세포에 EGCG를 처리하였을 경우 그 발현량이 유의적으로 증가하였다. 이상의 결과들을 종합하여, 항산화성 폴리페놀인 EGCG는 알코올성 췌장염으로 인한 세포의 손상이나 당뇨병 예방과 회복에 치료적 효과를 가질 수 있다고 제안한다.

• Molecules and Cells
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• 제19권2호
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• pp.268-278
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• 2005

We investigated the effect of cytosolic and extracellular $Ca^{2+}$ on $Ca^{2+}$ signals in pancreatic acinar cells by measuring $Ca^{2+}$ concentration in the cytosol($[Ca^{2+}]_c$) and in the lumen of the ER($[Ca^{2+}]_{Lu}$). To control buffers and dye in the cytosol, a patch-clamp microelectrode was employed. Acetylcholine released $Ca^{2+}$ mainly from the basolateral ER-rich part of the cell. The rate of $Ca^{2+}$ release from the ER was highly sensitive to the buffering of $[Ca^{2+}]_c$ whereas ER $Ca^{2+}$ refilling was enhanced by supplying free $Ca^{2+}$ to the cytosol with $[Ca^{2+}]_c$ clamped at resting levels with a patch pipette containing 10 mM BAPTA and 2 mM $Ca^{2+}$. Elevation of extracellular $Ca^{2+}$ to 10 mM from 1 mM raised resting $[Ca^{2+}]_c$ slightly and often generated $[Ca^{2+}]_c$ oscillations in single or clustered cells. Although pancreatic acinar cells are reported to have extracellular $Ca^{2+}$-sensing receptors linked to phospholipase C that mobilize $Ca^{2+}$ from the ER, exposure of cells to 10 mM $Ca^{2+}$ did not decrease $[Ca^{2+}]_{Lu}$ but rather raised it. From these findings we conclude that 1) ER $Ca^{2+}$ release is strictly regulated by feedback inhibition of $[Ca^{2+}]_c$, 2) ER $Ca^{2+}$ refilling is determined by the rate of $Ca^{2+}$ influx and occurs mainly in the tiny subplasmalemmal spaces, 3) extracellular $Ca^{2+}$-induced $[Ca^{2+}]_c$ oscillations appear to be triggered not by activation of extracellular $Ca^{2+}$-sensing receptors but by the ER sensitised by elevated $[Ca^{2+}]_c$ and $[Ca^{2+}]_{Lu}$.

• Asian Pacific Journal of Cancer Prevention
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• 제16권1호
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• pp.373-376
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• 2015

Background: EVA1A (eva-1 homolog A) is a novel gene that regulates programmed cell death through autophagy and apoptosis. Our objective was to investigate the expression profiles and potential role of EVA1A in normal and neoplastic human pancreatic tissues. Materials and Methods: The expression pattern of EVA1A in normal pancreatic tissue was examined by indirect immunofluorescence and confocal microscopy. Protein levels in paraffin-embedded specimens from normal and diseased pancreatic and matched non-tumor tissues were evaluated by immunohistochemistry. Results: EVA1A colocalized with glucagon but not with insulin, demonstrating production in islet alpha cells. Itwas strongly expressed in chronic pancreatitis, moderately or weakly expressed in the plasma membrane and cytoplasm in pancreatic acinar cell carcinoma, and absent in normal pancreatic acinar cells. Although the tissue architecture was deformed, EVA1A was absent in the alpha cells of pancreatic ductal adenocarcinomas, intraductal papillary mucinous neoplasms, mucinous cystadenomas, solid papillary tumors and pancreatic neuroendocrine tumors. Conclusions: EVA1A protein is specifically expressed in islet alpha cells, suggesting it may play an important role in regulating alpha-cell function. The ectopic expression of EVA1A in pancreatic neoplasms may contribute to their pathogenesis and warrants further investigation.

• The Korean Journal of Physiology and Pharmacology
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• 제3권5호
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• pp.521-528
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• 1999

Reactive oxygen species (ROS), generated by infiltrating neutrophils, are considered as an important regulator in the pathogenesis and deveolpment of pancreatitis. The present study aims to investigate whether neutrophils primed by $4{\beta}-phorbol\;12{\beta}-myristate\;13{\alpha}-acetate$ (PMA) affect the productions $H_2O_2$ and lipid peroxide (LPO), $NF-_{\kappa}B$ activation and cytokine production in pancreatic acinar cells, and whether these alterations were inhibited by an antioxidant, N-acetylcysteine (NAC) and superoxide dismutase (SOD). $H_2O_2$ (ferrithiocyanate method), LPO (as thiobarbiturate reactive substances), and cytokines $(IL-l{\bata},\; IL-6,\;TNF-{\alpha};\;enzyme-linked\;immunosorbent\;assay)$ and $NF-_{\kappa}B$ activation (electrophoretic mobility shift assay) were analyzed in acinar cells treated with or without PMA-primed neutrophils in the absence or presence of NAC (10 mM) or SOD (300 U/ml). As a result, the productions of H2O2, LPO and $TNF-{\alpha}$ were increased with the ratio of PMA-primed neutrophils to acinar cells while the productions of LPO, $IL-l{\beta},\;IL-6\;and\;TNF-{\alpha}$ were increased with time. PMA-primed neutrophils resulted in the activation of $NF-_{\kappa}B.$ Both NAC and SOD inhibited neutrophil-induced alterations in acinar cells. In conclusion, ROS, generated by neutrophils, activates $NF-_{\kappa}B,$ resulting in upregulation of inflammatary cytokines in acinar cells. Antioxidants might be clinically useful antiinflammatory agents by inhibiting oxidant-mediated activation of $NF-_{\kappa}B$ and decreasing cytokine production.

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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• pp.27-27
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• 2001

In exocrine acinar cells, $Ca^{2＋}$ -activated Cl$^{[-10]}$ channels in the apical membrane are essential for fluid secretion, but it is unclear whether such channels are important for Cl$^{[-10]}$ uptake at the base. Whole cell current recording, combined with local uncaging of caged $Ca^{2＋}$, was used to reveal the Cl$^{[-10]}$ channel distribution in mouse pancreatic acinar cells, where ~90％ of the current activated by $Ca^{2＋}$ in response toacetylcholine was carried by Cl$^{[-10]}$ .(omitted)