• Applied Microscopy
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• 제35권2호
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• pp.65-72
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• 2005

악하선의 미세구조를 작은땃쥐 Crocidura suaveolens에서 연구하였다. 작은땃쥐의 악하선은 장액선세포와 점액선세포로 구성된 혼합샘이었다. 이 샘포에서 분비된 과립들은 도관을 거쳐 구강으로 분비되었다. 장액선세포와 점액선세포는 잘 발달된 조면소포체와 미토콘드리아 그리고 많은 분비과립을 가지고 있었다. 장액선 분비과립의 경우, 미성숙 분비과립은 무형이면서 전자밀도가 있는 작은 알갱이로만 구성되었고, 성숙 과립은 단일막으로 싸여진 완전한 원형으로 전자밀도가 있는 균질의 중앙부와 전자밀도가 있는 작은 알갱이로 구성된 주변부를 가지고 있었다. 점액선 분비과립의 경우, 미성숙 과립은 원형으로 균질한 기질과 불명확한 경계막을 가지는 반면, 성숙 과립은 균질한 기질 내에 몇 개의 전자밀도가 있는 띠를 가짐으로서 문양의 다양성 가지는 매끈한 원형이었고 명확한 경계막을 가지고 있었다. 즉 작은 땃쥐의 성숙 점액선 분비과립은 문양의 다양성을 가져 다른 포유류와 구분될 뿐만 아니라 매끈한 원형이어서 C. lasiura의 그것과도 구분되었다. 거대한 분비 과립과 미엘린소체가 과립관세포의 세포질과 내강에서 관찰되었다. 3종의 땃쥐류 침샘의 과립관에서 만 보고된 특징적 구조물인 미엘린소체는 분비세포에서 내강으로 분비되었으며 분비과립의 배출방식과 약간의 차이점을 가졌다.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1994년도 춘계학술대회 and 제3회 신약개발 연구발표회
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• pp.88-93
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• 1994

The mechanisms controlling the intensity and duration of synaptic transmission are numerous. Once an action potential reaches a nerve terminal, the stored neurotransmitters are released in a quantum fashion into the synaptic cleft. At that point neurotransmitters can act on post-synaptic receptors to elicit an action on the post-synaptic cell or net at so-called auto-receptors that are located on the presynaptic side and which often regulate the further release of the neutotransmitter. Whereas the action of the neurotransmitter receptors is regulated by desensitization phenomenon, the major mechanism by which the intensity and duration of neurotransmitter action is presumably regulated by either its degradation or its removal from the synaptic cleft. In the central nervous system, specialized proteins located in fe plasma membrane of presynaptic terminals function to rapidly remove neurotransmitters from the synaptic cleft in a sodium chloride-dependent fashion. These proteins have been referred to as uptake sites or neurotransmitter transporters. Once taken up by the plasma membrane transporters, neurotransmitters are repackaged into secretory vesicles by distinct transporters which depend on a proton gradient.

• BMB Reports
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• 제31권1호
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• pp.106-110
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• 1998

We have employed a DNA-native-polyacrylamide gel electrophoresis (DNA-native-PAGE) assay system to characterize the enzyme activity of the endonuclease secreted by human B lymphoblastic IM9 cells. Experimental results clearly demonstrated that the endonuclease activity of IM9 cell culture medium is distinct from that of DNase I in the DNA-native-PAGE assay system. Immunoprecipitation analysis using anti-DNase I antibody showed that the secreted endonuclease is not recognized by the antibody. The secreted endonuclease was estimated using supercoiled plasmid DNA as a substrate. The pH optimum required for the catalytic activity was determined to be in the range of pH 6.6-7.4. No significant difference in the endonuclease secretion was observed by stimulation of the IM9 cells with interferon-${\gamma}$ or interleukin-$1{\beta}$.

• Journal of Microbiology and Biotechnology
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• 제14권1호
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• pp.128-133
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• 2004

The secretion capacity of two E. coli strains (JM109 and AF1000) was evaluated through the expression of two human proinsulin fusion proteins using the translocation signal sequence from Staphylococcal protein A (SpA). Although a 7 to 11-fold difference in the expression levels was attained by the use of different promoters (SpA and malK promoters) and copy-number vectors (700 and 50 copies per cell), the maximum translocation rates for all the systems were around 140,000 amino acids $cell^{-1} min^{-1}$. Moreover, the secretion capacity was found to be independent of the size of the exiting peptide and its translational rate.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.135.1-135.1
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• 2003

The rat mast cell line RBL-2H3 contains both phospholipase D (PLD)1 and PLD2. Previous studies with this cell line indicated that expressed PLD1 and PLD2 are both strongly activated by stimulants of secretion. We now show by use of PLDs tagged with enhanced green fluorescent protein that PLD1, which is largely associated with secretory granules, redistributes to the plasma membrane in stimulated cells by processes reminiscent of exocytosis and fusion of granules with the plasma membrane. (omitted)

• Applied Microscopy
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• 제32권3호
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• pp.265-273
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• 2002

본 연구는 전자현미경을 이용하여 음용 불소가 발생중인 경골의 성장변화와 골모세포의 조직학적 특성에 미치는 영향을 관찰하고 에너지분광분석기를 사용하여 불소의 투여 농도에 따른 골기질 성분변화를 알아보고자 하였다. 전자현미경 관찰 결과, 대조군에서는 입방형의 전형적인 골모세포가 관찰되었다. 100 ppm 불소투여군의 경우, 활성이 강한 골모세포에 의해 생성된 여러층의 반전선과 새로 형성된 골성조직이 관찰되었다. 또한 골모세포의 세포질은 잘 발달된 조면세포체와 미토콘드리아가 관찰되었고 세포막 주위에는 많은 분비소포들이 관찰되었으며, 일부는 세포막과 융합되어 분비물질이 세포 밖으로 방출되었다. 200 ppm 불소투여군에서는 활성이 저하된 골모세포가 관찰되었는데, 세포질내에는 미토콘드리아가 팽창되어 있었고 수조의 형태가 파괴되어 나타났다. 또한, 조면소포체의 표면에는 리보솜이 탈락되어 관찰되었다. 300 ppm의 고농도 불소투여군에서는 골내막과 인접한 골모세포는 불규칙하게 배열되어 있었고, 세포막은 파괴되어 세포성분이 세포 밖으로 용출되어 관찰되었다. 한편, 에너지분산분광분석 결과는 대조군에 비해 100 ppm 불소투여군에서 골기질 성분인 인과 칼슘이 증가하였으나 200 ppm 및 300 ppm 불소투여군에서는 더 이상 증가하지 않았다. 따라서 본 연구결과, 투여된 불소에 의해 골모세포의 활동이 활발해지고 왕성한 골기질 합성이 관찰되었으나, 고농도의 불소 투여는 골모세포를 파괴하고 활동을 억제한다는 것을 확인하였다.

• Nutrition Research and Practice
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• 제8권5호
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• pp.494-500
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• 2014

BACKGROUND/OBJECTIVES: This study investigated whether Padina arborescens extract (PAE) protects INS-1 pancreatic ${\beta}$ cells against glucotoxicity-induced apoptosis. MATERIALS/METHODS: Assays, including cell viability, lipid peroxidation, generation of intracellular ROS, NO production, antioxidant enzyme activity and insulin secretion, were conducted. The expressions of Bax, Bcl-2, and caspase-3 proteins in INS-1 cells were evaluated by western blot analysis, and apoptosis/necrosis induced by high glucose was determined by analysis of FITC-Annexin V/PI staining. RESULTS: Treatment with high concentrations of glucose induced INS-1 cell death, but PAE at concentrations of 25, 50 or $100{\mu}g/ml$ significantly increased cell viability. The treatment with PAE dose dependently reduced the lipid peroxidation and increased the activities of antioxidant enzymes reduced by 30 mM glucose, while intracellular ROS levels increased under conditions of 30 mM glucose. PAE treatment improved the secretory responsiveness following stimulation with glucose. The results also demonstrated that glucotoxicity-induced apoptosis is associated with modulation of the Bax/Bcl-2 ratio. When INS-1 cells were stained with Annexin V/PI, we found that PAE reduced apoptosis by glucotoxicity. CONCLUSIONS: In conclusion, the present study indicates that PAE protects against high glucose-induced apoptosis in pancreatic ${\beta}$ cells by reducing oxidative stress.

• 한국발생생물학회지:발생과생식
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• 제5권2호
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• pp.145-150
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• 2001

인상어 정소는 세관형이며, 각 정소 세관은 여러 개의 정소 소낭으로 구성되어 있는데, 소낭 내의 생식 세포들은 동일한 발달 단계를 보였다. 정자형성과정 동안 소낭 세포에서는 잘 발달된 조면 소포체와 골지체가 관찰되었다. 소낭세포의 분비활성은 후기 정자변태시기에 가장 높은 것으로 나타났다. 정포 내의 정자결합물질은 정소 소낭 세포에서 분비되며, 하나의 정소 소낭에서는 하나의 정포가 만들어진다. 체외로 방출된 정포에서 피막구조는 관찰할 수 없었다. 투과전자현미경 표본에서 횡단된 하나의 정포 내에서는 1,500∼1,700개의 정자 미부가 관찰되었다.

• IMMUNE NETWORK
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• 제10권6호
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• pp.206-211
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• 2010

Background: Dendritic cell (DC)-based tumor vaccine is an attractive modality for the treatment of colon cancer because it has been recurred and produced few side effects in patients. Secretory glycoprotein 90K has been found at elevated level in various cancer tissues and sera. We investigated to establish a more effective DC vaccine for the treatment of colon cancer in which the levels of 90K are elevated. Methods: We obtained the concentrated 90K from 293T cells stably expressing 90K. DCs were cultured from peripheral blood monocytes, and a DC vaccine pulsed with tumor lysate was compared with a DC vaccine pulsed with 90K. We measured the functional activity for CTLs by using IFN-${\gamma}$-enzyme linked immunoabsorbent spot (ELISPOT) assay. Results: DCs pulsed with tumor lysate+90K exhibited the enhanced T cell stimulation, polarization of $\ddot{i}$ T cell toward Th1. The CTLs generated by DCs pulsed with 90K efficiently lysed HCT116 cells. The results indicate that 90K-speicifc-CTLs can recognize 90K proteins naturally presented by colon cancer cells. Conclusion: Our study suggests that 90K-specific CTLs generated by 90K-pulsed DCs could be useful effector cells for immunotherapy in colon cancer.

• BMB Reports
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• 제47권2호
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• pp.51-59
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• 2014

Cellular senescence is a physiological process of irreversible cell-cycle arrest that contributes to various physiological and pathological processes of aging. Whereas replicative senescence is associated with telomere attrition after repeated cell division, stress-induced premature senescence occurs in response to aberrant oncogenic signaling, oxidative stress, and DNA damage which is independent of telomere dysfunction. Recent evidence indicates that cellular senescence provides a barrier to tumorigenesis and is a determinant of the outcome of cancer treatment. However, the senescence-associated secretory phenotype, which contributes to multiple facets of senescent cancer cells, may influence both cancer-inhibitory and cancer-promoting mechanisms of neighboring cells. Conventional treatments, such as chemo- and radiotherapies, preferentially induce premature senescence instead of apoptosis in the appropriate cellular context. In addition, treatment-induced premature senescence could compensate for resistance to apoptosis via alternative signaling pathways. Therefore, we believe that an intensive effort to understand cancer cell senescence could facilitate the development of novel therapeutic strategies for improving the efficacy of anticancer therapies. This review summarizes the current understanding of molecular mechanisms, functions, and clinical applications of cellular senescence for anticancer therapy.