• Title/Summary/Keyword: cell organelle

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Protective Effects of Dohongsamul-tang on 2-deoxy-D-glucose Induced Autophagic Cell Death in C6 Glial Cells (도홍사물탕(挑紅四物湯)이 C6 신경교세포의 2-DG에 의한 오토파지성 세포사멸에 미치는 영향)

  • Shin, Hak-Soo;Lee, Seung-Geun;Moon, Byung-Soon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.23 no.3
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    • pp.581-589
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    • 2009
  • The water extract of Dohongsamul-tang(DHSMT) has been traditionally used in treatment of ischemic heart and brain diseases in Oriental Medicine. However, little is known about the mechanism by which DHSMT protects C6 glial cells from glucose deprevation induced damages. Therefore, this study was designed to evaluate the protective effects of DHSMT on 2-deoxy-D-glucose induced autophagy of C6 glial cells. Autophagic phenotype is evaluated by fluorescence microscopy and flow cytometry with specific biological staining dyes, including monodansylcadaverine and acridine orange, as well as Western blot analysis with microtubule-associated protein 1 light chain 3(LC3) and Beclin-1. Treatment with 2-deoxy-D-glucose significantly resulted in a decrease of the viability of C6 glial cells and increase of the extracellular LDH release in a dose and time-dependent manner. However, pretreatment with DHSMT protected C6 glial cells from glucose deprivation with 2-deoxy-D-glucose. The author also observed the fact that autophagy phenotype occurred by 2-deoxy-D-glucose in C6 glial cells. Pretreatment with 3-MA, a pharmacological inhibitior of autophagy, abolished the formation of acidic vesicle organelle in C6 glial cells treated with 2-deoxy-D-glucose. However, pretreatment with DHSMT inhibited the formation of autophagic phenotypes, including formation of acidic vesicle organelle, and increase of the expression of LC-3 II Beclin-1 proteins in C6 glial cells treated with 2-deoxy-D-glucose. Taken together, these data suggest that DHSMT is able to protect C6 glial cells from glucose deprivation with marked inhibition of autophagy formation.

The role of cell type-specific mitochondrial dysfunction in the pathogenesis of Alzheimer's disease

  • Kim, Dong Kyu;MookJung, Inhee
    • BMB Reports
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    • v.52 no.12
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    • pp.679-688
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    • 2019
  • The decrease of metabolism in the brain has been observed as the important lesions of Alzheimer's disease (AD) from the early stages of diagnosis. The cumulative evidence has reported that the failure of mitochondria, an organelle involved in diverse biological processes as well as energy production, maybe the cause or effect of the pathogenesis of AD. Both amyloid and tau pathologies have an impact upon mitochondria through physical interaction or indirect signaling pathways, resulting in the disruption of mitochondrial function and dynamics which can trigger AD. In addition, mitochondria are involved in different biological processes depending on the specific functions of each cell type in the brain. Thus, it is necessary to understand mitochondrial dysfunction as part of the pathological phenotypes of AD according to each cell type. In this review, we summarize that 1) the effects of AD pathology inducing mitochondrial dysfunction and 2) the contribution of mitochondrial dysfunction in each cell type to AD pathogenesis.

Ab ovo or de novo? Mechanisms of Centriole Duplication

  • Loncarek, Jadranka;Khodjakov, Alexey
    • Molecules and Cells
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    • v.27 no.2
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    • pp.135-142
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    • 2009
  • The centrosome, an organelle comprising centrioles and associated pericentriolar material, is the major microtubule organizing center in animal cells. For the cell to form a bipolar mitotic spindle and ensure proper chromosome segregation at the end of each cell cycle, it is paramount that the cell contains two and only two centrosomes. Because the number of centrosomes in the cell is determined by the number of centrioles, cells have evolved elaborate mechanisms to control centriole biogenesis and to tightly coordinate this process with DNA replication. Here we review key proteins involved in centriole assembly, compare two major modes of centriole biogenesis, and discuss the mechanisms that ensure stringency of centriole number.

Repeated restraint stress promotes hippocampal neuronal cell ciliogenesis and proliferation in mice

  • Lee, Kyounghye;Ko, Hyuk Wan
    • Laboraroty Animal Research
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    • v.34 no.4
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    • pp.203-210
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    • 2018
  • Stress severely disturbs physiological and mental homeostasis which includes adult neurogenesis in hippocampus. Neurogenesis in hippocampus is a key feature to adapt to environmental changes and highly regulated by multiple cellular signaling pathways. The primary cilium is a cellular organelle, which acts as a signaling center during development and neurogenesis in adult mice. However, it is not clear how the primary cilia are involved in the process of restraint (RST) stress response. Using a mouse model, we examined the role of primary cilia in repeated and acute RST stress response. Interestingly, RST stress increased the number of ciliated cells in the adult hippocampal dentate gyrus (DG). In our RST model, cell proliferation in the DG also increased in a time-dependent manner. Moreover, the analysis of ciliated cells in the hippocampal DG with cell type markers indicated that cells that were ciliated in response to acute RST stress are neurons. Taken together, these findings suggest that RST stress response is closely associated with an increase in the number of ciliated neurons and leads to an increase in cell proliferation.

Mitochondria: The Secret Chamber of Therapeutic Targets for Age-Associated Degenerative Diseases

  • KimPak, Young-Mi;Jeong, Jae-Hoon
    • Biomolecules & Therapeutics
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    • v.18 no.3
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    • pp.235-245
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    • 2010
  • Mitochondria have long been recognized as ATP engines for the cell and recently as a dynamic and mobile organelles that control cell death and life. This exquisite organelle is the site of reactive oxygen species production and is highly vulnerable to exogenous stresses, resulting in catastrophic damage to the cell. Mitochondrial dysfunction is linked to a wide range of age-associated degenerative diseases, such as metabolic syndrome, cardiovascular disease, and neurodegenerative diseases. Understanding the molecular mechanisms of mitochondria-dependent pathogenesis may provide important strategies to treat these diseases. Indeed, mitochondria are emerging therapeutic targets for the mitochondria-related diseases. In this paper, we review the recent concepts of mitochondrial biology and how mitochondria are involved in age-associated degenerative diseases. Furthermore, we summarize the therapeutics which target to improve mitochondrial functions.

Role of Sphingolipids and Metabolizing Enzymes in Hematological Malignancies

  • Kitatani, Kazuyuki;Taniguchi, Makoto;Okazaki, Toshiro
    • Molecules and Cells
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    • v.38 no.6
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    • pp.482-495
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    • 2015
  • Sphingolipids such as ceramide, sphingosine-1-phosphate and sphingomyelin have been emerging as bioactive lipids since ceramide was reported to play a role in human leukemia HL-60 cell differentiation and death. Recently, it is well-known that ceramide acts as an inducer of cell death, that sphingomyelin works as a regulator for microdomain function of the cell membrane, and that sphingosine-1-phosphate plays a role in cell survival/proliferation. The lipids are metabolized by the specific enzymes, and each metabolite could be again returned to the original form by the reverse action of the different enzyme or after a long journey of many metabolizing/synthesizing pathways. In addition, the metabolites may serve as reciprocal biomodulators like the rheostat between ceramide and sphingosine-1-phosphate. Therefore, the change of lipid amount in the cells, the subcellular localization and the downstream signal in a specific subcellular organelle should be clarified to understand the pathobiological significance of sphingolipids when extracellular stimulation induces a diverse of cell functions such as cell death, proliferation and migration. In this review, we focus on how sphingolipids and their metabolizing enzymes cooperatively exert their function in proliferation, migration, autophagy and death of hematopoetic cells, and discuss the way developing a novel therapeutic device through the regulation of sphingolipids for effectively inhibiting cell proliferation and inducing cell death in hematological malignancies such as leukemia, malignant lymphoma and multiple myeloma.

Characterizing Organelles in Live Stem Cells Using Label-Free Optical Diffraction Tomography

  • Kim, Youngkyu;Kim, Tae-Keun;Shin, Yeonhee;Tak, Eunyoung;Song, Gi-Won;Oh, Yeon-Mok;Kim, Jun Ki;Pack, Chan-Gi
    • Molecules and Cells
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    • v.44 no.11
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    • pp.851-860
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    • 2021
  • Label-free optical diffraction tomography (ODT), an imaging technology that does not require fluorescent labeling or other pre-processing, can overcome the limitations of conventional cell imaging technologies, such as fluorescence and electron microscopy. In this study, we used ODT to characterize the cellular organelles of three different stem cells-namely, human liver derived stem cell, human umbilical cord matrix derived mesenchymal stem cell, and human induced pluripotent stem cell-based on their refractive index and volume of organelles. The physical property of each stem cell was compared with that of fibroblast. Based on our findings, the characteristic physical properties of specific stem cells can be quantitatively distinguished based on their refractive index and volume of cellular organelles. Altogether, the method employed herein could aid in the distinction of living stem cells from normal cells without the use of fluorescence or specific biomarkers.

Studies on the Toxicity of $\delta$-endotoxin of Bacillus thuringiensis to the Several Tissues of Hyphantria cunea Drury (미국흰불나방(Hyphantria cunea Drury)에 대한 Bacillus thuringiensis 내독소단백질의 독성효과에 관한 연구)

  • 전향미;조자향;강석권;서숙재
    • Journal of Sericultural and Entomological Science
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    • v.37 no.1
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    • pp.62-67
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    • 1995
  • Ultrastructural changes of tissues caused by Bacillus thuringiensis var. kurstaki $\delta$-endotoxin intoxication of Hyphantria cunea were observed by transmission electron microscopy. Bt $\delta$-endotoxin crystals induced the disruption of microvilli, vacuolation of cytoplasm, changes in the cisternae of the endoplasmic reticulum, disappearance of basal striations, loss of ribosomes, and changes in the configurations of mitochondria in the columnar cell of midgut. The fat body cells also showed spherical endoplasmic reticulum and distorted mitochondria, and then the cells were destroyed.

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Roles of Endoplasmic Reticulum Stress in Immune Responses

  • So, Jae-Seon
    • Molecules and Cells
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    • v.41 no.8
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    • pp.705-716
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    • 2018
  • The endoplasmic reticulum (ER) is a critical organelle for protein synthesis, folding and modification, and lipid synthesis and calcium storage. Dysregulation of ER functions leads to the accumulation of misfolded- or unfolded-protein in the ER lumen, and this triggers the unfolded protein response (UPR), which restores ER homeostasis. The UPR is characterized by three distinct downstream signaling pathways that promote cell survival or apoptosis depending on the stressor, the intensity and duration of ER stress, and the cell type. Mammalian cells express the UPR transducers IRE1, PERK, and ATF6, which control transcriptional and translational responses to ER stress. Direct links between ER stress and immune responses are also evident, but the mechanisms by which UPR signaling cascades are coordinated with immunity remain unclear. This review discusses recent investigations of the roles of ER stress in immune responses that lead to differentiation, maturation, and cytokine expression in immune cells. Further understanding of how ER stress contributes to the pathogenesis of immune disorders will facilitate the development of novel therapies that target UPR pathways.

Morphological Diversity of Mitochondria in Cultured Astrocyte, HeLa, COS7 Cells under High Voltage Electron Microscopy

  • Kim, Hyun-Wook;Park, Seung Nam;Moon, Younghye;Oh, Seung Hak;Rhyu, Im Joo
    • Applied Microscopy
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    • v.43 no.3
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    • pp.117-121
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    • 2013
  • Mitochondrion is an important intracellular organelle controlling energy production essential for cell survival. In addition, it is closely related to cellular apoptosis and necrosis. Linear, branched, circular, and ball-shaped mitochondria have been reported. Recent research suggests that mitochondrial morphology may reflect functional status of the cell. In this study, we investigated the density and ratio of the each morphological categories of mitochondria in a few normal cultured cells; astrocyte, HeLa and COS7 cells, of which metabolic activities are different, with high voltage electron microscopy. The absolute number and relative number per unit area of mitochondria was largest in astrocyte. But, the proportion of different mitochondrial shape was similar among cells. These results shows the numerical profiles but not morphological profiles of mitochondria are related to the metabolic activity of each cell line.