• Journal of Plant Biology
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• 제36권3호
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• pp.285-292
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• 1993

Cellular compatibility in the self-parasitism of Cuscuta australis R. Brown was studied at the ultrastructural level. The front cells of the haustorium penetrated the host stems independently grew within the host tissues and transformed into elongate, filamentous hyphae. Each hyphal cells contained a large nucleus and dense cytoplasm with abundant cell organelles. Multilamellar structures were contained in the cytoplasm and cell walls of the penetrating hyphal cells. When the hyphal cells did not yet invade the host cells, the middle lamella and the fused cellulosic cell walls of the two partners at the host-parasite interface were preserved well. As the invasion of the parasitic hyphal cells progressed, however, the middle lamella was not found at the interface and the host cell walls and plasma membranes were partially broken down. A hyphal cell penetrated deeply into the host cell had a more darkly stained cytoplasm with numerous of cell organelles. In the host cells attacked by the hyphal cells the limiting membranes of plastids were broken down and several vesicles were arrayed near the cell walls. No plasmodesmatal connections between the host and parasite cell walls were found; however, half-plasmodesmata were observed frequently on the side of the hyphal cell walls. These results suggested that the compatibility response in the self-parasitism of Cuscuta was expressed by cell walls, not by plasmodesmata, between the host and the parasite cells.

• Molecules and Cells
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• 제46권12호
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• pp.727-735
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• 2023

Stem cells require high amounts of energy to replicate their genome and organelles and differentiate into numerous cell types. Therefore, metabolic stress has a major impact on stem cell fate determination, including self-renewal, quiescence, and differentiation. Lysosomes are catabolic organelles that influence stem cell function and fate by regulating the degradation of intracellular components and maintaining cellular homeostasis in response to metabolic stress. Lysosomal functions altered by metabolic stress are tightly regulated by the transcription factor EB (TFEB) and TFE3, critical regulators of lysosomal gene expression. Therefore, understanding the regulatory mechanism of TFEB-mediated lysosomal function may provide some insight into stem cell fate determination under metabolic stress. In this review, we summarize the molecular mechanism of TFEB/TFE3 in modulating stem cell lysosomal function and then elucidate the role of TFEB/TFE3-mediated transcriptional activity in the determination of stem cell fate under metabolic stress.

• Molecules and Cells
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• 제40권9호
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• pp.607-612
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• 2017

When mammalian cells and animals face a variety of internal or external stresses, they need to make homeostatic changes so as to cope with various stresses. To this end, mammalian cells are equipped with two critical stress responses, autophagy and cellular senescence. Autophagy and cellular senescence share a number of stimuli including telomere shortening, DNA damage, oncogenic stress and oxidative stress, suggesting their intimate relationship. Autophagy is originally thought to suppress cellular senescence by removing damaged macromolecules or organelles, yet recent studies also indicated that autophagy promotes cellular senescence by facilitating the synthesis of senescence-associated secretory proteins. These seemingly opposite roles of autophagy may reflect a complex picture of autophagic regulation on cellular senescence, including different types of autophagy or a unique spatiotemporal activation of autophagy. Thus, a better understanding of autophagy process will lead us to not only elucidate the conundrum how autophagy plays dual roles in the regulation of cellular senescence but also helps the development of new therapeutic strategies for many human diseases associated with cellular senescence. We address the pro-senescence and anti-senescence roles of autophagy while focusing on the potential mechanistic aspects of this complex relationship between autophagy and cellular senescence.

• Mass Spectrometry Letters
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• 제14권4호
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• pp.121-140
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• 2023

It is becoming more and more clear that each cell, even those of the same type, has a unique identity. This sophistication and the diversity of cell types in tissue are what are pushing the necessity for spatially distributed omics at the single-cell (SC) level. Single-cell chemical assessment, which also provides considerable insight into biological, clinical, pharmacodynamic, pathological, and toxicity studies, is crucial to the investigation of cellular omics (genomics, metabolomics, etc.). Mass spectrometry (MS) as a tool to image and profile single cells and subcellular organelles facilitates novel technical expertise for biochemical and biomedical research, such as assessing the intracellular distribution of drugs and the biochemical diversity of cellular populations. It has been illustrated that ambient mass spectrometry (AMS) is a valuable tool for the rapid, straightforward, and simple analysis of cellular and sub-cellular constituents and metabolites in their native state. This short review examines the advances in ambient mass spectrometry (AMS) and ambient mass spectrometry imaging (AMSI) on single-cell analysis that have been authored in recent years. The discussion also touches on typical single-cell AMS assessments and implementations.

• Reproductive and Developmental Biology
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• 제39권2호
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• pp.37-41
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• 2015

The oocyte undergoes various events during maturation and requires many substances for the maturation process. Various intracellular organelles are also involved in maturation of the oocyte. During the process glucose is essential for nuclear and cytoplasmic maturation, and adenosine triphosphate is needed for reorganization of the organelles and cytoskeleton. If mitochondrial function is lost, several developmental defects in meiotic chromosome segregation and maturation cause fertilization failure. The endoplasmic reticulum, a store for $Ca^{2+}$, releases $Ca^{2+}$ into the cytoplasm in response to various cellular signaling molecules. This event stimulates secretion of hormones, growth factors and antioxidants in oocyte during maturation. Also, oocyte nuclear maturation is stimulated by growth factors such as epidermal growth factor. This review summarizes roles of organelles with focus on the Golgi apparatus during maturation in oocyte.

• Applied Microscopy
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• 제26권4호
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• pp.401-410
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• 1996

The microwave fixator has recently been introduced in morphological research. The present study was carried out to investigate the ultrastructural effects of microwave fixation of rat brain. kidney, liver and skeletal muscle tissues. The results are as follows: In the case of microwave fixed cerebrum. the cytoplasmic processes of neurons and the various membranous organelles such as nuclear envelope, mitochondria, rough endoplasmic reticulum and Golgi apparatus were well preserved, The myelin sheath wrapping neuronal axon was prominent. Microwave fixed hepatocytes showed the microvilli on the free surface of bile canaliculus, the evident nucleolar components, and typical organelles. In nephron, ultrastructures of glomerulus and Bowman's capsule were preserved, and also tubular wall were structurally observed. Among the skeletal muscle cells, plentiful collagen fibers were appeared, myofibrils and mitochondria were typically observed. In conclusion, the microwave fixation procedures result in an good preservation of the tissues and would be time- and reagent-saving.

• The Korean Journal of Physiology and Pharmacology
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• 제21권6호
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• pp.567-577
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• 2017

Obesity is known to induce inhibition of glucose uptake, reduction of lipid metabolism, and progressive loss of skeletal muscle function, which are all associated with mitochondrial dysfunction in skeletal muscle. Mitochondria are dynamic organelles that regulate cellular metabolism and bioenergetics, including ATP production via oxidative phosphorylation. Due to these critical roles of mitochondria, mitochondrial dysfunction results in various diseases such as obesity and type 2 diabetes. Obesity is associated with impairment of mitochondrial function (e.g., decrease in $O_2$ respiration and increase in oxidative stress) in skeletal muscle. The balance between mitochondrial fusion and fission is critical to maintain mitochondrial homeostasis in skeletal muscle. Obesity impairs mitochondrial dynamics, leading to an unbalance between fusion and fission by favorably shifting fission or reducing fusion proteins. Mitophagy is the catabolic process of damaged or unnecessary mitochondria. Obesity reduces mitochondrial biogenesis in skeletal muscle and increases accumulation of dysfunctional cellular organelles, suggesting that mitophagy does not work properly in obesity. Mitochondrial dysfunction and oxidative stress are reported to trigger apoptosis, and mitochondrial apoptosis is induced by obesity in skeletal muscle. It is well known that exercise is the most effective intervention to protect against obesity. Although the cellular and molecular mechanisms by which exercise protects against obesity-induced mitochondrial dysfunction in skeletal muscle are not clearly elucidated, exercise training attenuates mitochondrial dysfunction, allows mitochondria to maintain the balance between mitochondrial dynamics and mitophagy, and reduces apoptotic signaling in obese skeletal muscle.

• 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.

• 한국미생물생명공학회:학술대회논문집
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• 한국미생물생명공학회 1979년도 춘계학술대회
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• pp.115.4-116
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• 1979

Acetone-dried cells of Arthrobacter simplex were entrapped in several preparations of hydrophilic urethane prepolymers and their steroid converting ability was examined. SeVeral solvents, such as methanol and propylone glycol, wereeffective for the conversion of hydrocortisone to prednisolone. The stability of the immobilized cells during storage and on repeated reactions was also examined. Thisconvenient entrapping method was also applicable for the immobilization of cellular organelles. yeast peroxisomes. The entrapped peroxi-somessh owed the activities of alcohol oxidase and catalase.

• 치위생과학회지
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• 제22권3호
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• pp.164-170
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• 2022

Background: When cells are damaged by nicotine, cellular senescence due to oxidative stress accelerates. In addition, stress-induced inflammatory response and cellular senescence cause the accumulation of damaged organelles in cells, and autophagy appears to remove them. Conversely, when autophagy is reduced, harmful cell components accumulate, and aging is accelerated. This study aimed to determine the association between nicotine-induced cellular senescence and autophagy expression patterns in human gingival fibroblasts. Methods: Cells were treated with various concentrations of nicotine (0, 0.1, 0.5, 1, 2, and 5 mM) and 10 nM rapamycin was added to 1 mM nicotine to investigate the relationship between autophagy and cellular senescence. Cell viability was confirmed using WST-8 and the degree of cellular senescence was measured by SA-β-gal staining. The expression of the inflammatory proteins (COX-2 and iNOS) and autophagy markers (LC3-II, p62, and Beclin-1) was analyzed by western blotting. Results: The cell viability tended to decrease in a concentration-dependent manner. COX-2 showed no concentration-dependent expression and iNOS increased in the 0.5 mM nicotine treated group. The degree of cellular senescence was the highest in the 1 mM nicotine treatment group. In the group treated with rapamycin and nicotine, the conversion ratio of LC3-II to LC3-I was the highest, that of p62 was the lowest, and the level of Beclin-1 proteins was significantly increased. Furthermore, the degree of cellular senescence was reduced in the group in which rapamycin was added to nicotine compared to that in the group treated with nicotine alone. Conclusion: This study provides evidence that autophagy activated in an aging environment reduces cellular senescence to a certain some extent.