• Clinical and Experimental Reproductive Medicine
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• v.41 no.3
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• pp.97-107
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• 2014

The placenta is a temporary fetomaternal organ capable of supporting fetal growth and development during pregnancy. In particular, abnormal development and dysfunction of the placenta due to cha nges in the proliferation, differentiation, cell death, and invasion of trophoblasts induce several gynecological diseases as well as abnormal fetal development. Autophagy is a catalytic process that maintains cellular structures by recycling building blocks derived from damaged microorganelles or proteins resulting from digestion in lysosomes. Additionally, autophagy is necessary to maintain homeostasis during cellular growth, development, and differentiation, and to protect cells from nutritional deficiencies or factors related to metabolism inhibition. Induced autophagy by various environmental factors has a dual role: it facilitates cellular survival in normal conditions, but the cascade of cellular death is accelerated by over-activated autophagy. Therefore, cellular death by autophagy has been known as programmed cell death type II. Autophagy causes or inhibits cellular death via the other mechanism, apoptosis, which is programmed cell death type I. Recently, it has been reported that autophagy increases in placenta-related obstetrical diseases such as preeclampsia and intrauterine growth retardation, although the mechanisms are still unclear. In particular, abnormal autophagic mechanisms prevent trophoblast invasion and inhibit trophoblast functions. Therefore, the objectives of this review are to examine the characteristics and functions of autophagy and to investigate the role of autophagy in the placenta and the trophoblast as a regulator of cell death.

• Biomedical Science Letters
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• v.12 no.4
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• pp.385-391
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• 2006

Heterotrimeric GTP binding proteins (G proteins) mediate signals generated by neurotransmitters and hormones Among G proteins, Go is found in a large quantity in brain and growth cone membranes of neurons. In spite of its abundance in neurons, the role of Go is not fully understood. In our previous study, we identified promyelocytic leukemia zinc finger protein (PLZF) as an interacting partner of alpha subunit of Go ($Go{\alpha}$) and confirmed their interaction employing several biochemical assays. To date, it is reported that PLZF functioned as a cell growth suppressor and a transcription repressor. To determine effect of $Go{\alpha}$ and PLZF interaction on the cellular function of PLZF, we performed luciferase reporter gene assay and BrdU incorporation assay. Co-expression of $Go{\alpha}$ and PLZF synergistically increased the effect of PLZF alone. These results suggest that $Go{\alpha}$ may act as cellular activator of PLZF. This novel feature of Go may provide insights into understanding diverse role of Go-coupled receptor as well as its cellular actions.

• Microbiology and Biotechnology Letters
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• v.23 no.5
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• pp.513-518
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• 1995

To evaluate bile salt-tolerance of lactic acid bacteria (LAB, Lactobacillus acidophilus ATCC 4356, Lactobacillus casei IFO 3533, Streptococcus thermnophilus KCTC 2185, Lactobacillus lactis ATCC 4797, and Lactobacillus bulgaricus ATCC 11842), We investigated the survivals, acid production and $\beta $-galactosidase activity of LAB under anaerobic broth system. Cellular permeability of LAB and their cellular retention of $\beta $-galactosidase were also examined in the same system. Although the growth of LAB was slightly suppressed by 0.3% bile salt, they showed normal growth curve. Streptococcus thermophilus KCTC 2185 was significantly more resistant to bile salt than the others. The $\beta $-galactosidase activity from Streptococcus thermophilus KCTC 2185 and Lactobacillus bulgaricus ATCC 11842 and their cellular retention of $\beta $-galactosidase decreased by 0.3% bile salt. The cellular permeability of LAB in the presence of bile salt increased significantly.

• BMB Reports
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• v.50 no.1
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• pp.5-11
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• 2017

One of the characteristics of the neurons that distinguishes them from other cells is their complex and polarized structure consisting of dendrites, cell body, and axon. The complexity and diversity of dendrites are particularly well recognized, and accumulating evidences suggest that the alterations in the dendrite structure are associated with many neurodegenerative diseases. Given the importance of the proper dendritic structures for neuronal functions, the dendrite pathology appears to have crucial contribution to the pathogenesis of neurodegenerative diseases. Nonetheless, the cellular and molecular basis of dendritic changes in the neurodegenerative diseases remains largely elusive. Previous studies in normal condition have revealed that several cellular components, such as local cytoskeletal structures and organelles located locally in dendrites, play crucial roles in dendrite growth. By reviewing what has been unveiled to date regarding dendrite growth in terms of these local cellular components, we aim to provide an insight to categorize the potential cellular basis that can be applied to the dendrite pathology manifested in many neurodegenerative diseases.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.3
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• pp.957-963
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• 2016

Cellular senescence, a barrier to tumorigenesis, controls aberrant proliferation of cells. We here aimed to investigate cellular senescence in immortalized cholangiocyte and cholangiocarcinoma cell lines using five different inducing agents: 5-aza-2'deoxycytidine, bromodeoxyuridine, interferons ($IFN{\beta}$ and $IFN{\gamma}$), and hydrogen peroxide. We analyzed senescence characteristics, colony formation ability, expression of genes involved in cell cycling and interferon signaling pathways, and protein levels. Treatment with all five agents decreased cell proliferation and induced cellular senescence in immortalized cholangiocyte and cholangiocarcinoma cell lines with different degrees of growth-inhibitory effects depending on cell type and origin. Bromodeoxyuridine gave the strongest stimulus to inhibit growth and induce senescence in most cell lines tested. Expression of p21 and interferon related genes was upregulated in most conditions. The fact that bromodeoxyuridine had the strongest effects on growth inhibition and senescence induction implies that senescence in cholangiocarcinoma cells is likely controlled by DNA damage response pathways relating to the p53/p21 signaling. In addition, interferon signaling pathways may partly regulate this mechanism in cholangiocarcinoma cells.

• The Journal of Korean Academy of Prosthodontics
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• v.42 no.2
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• pp.175-191
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• 2004

Statement of problem: Platelet-rich plasma(PRP) is well known to be very effective method to stimulate and accelerate the healing of bone and soft tissue. However, there are few reports which deal with the mechanisms of the PRP on the activation of the osteoblasts. Purpose: This study was aimed to investigate the effect of growth factors in PRP on the activity of osteoblasts. Material and method: To evaluate the effect on human, human osteoblast cell line was cultured. PRP was extracted from the blood of a healthy volunteer. Using the recombinant growth factors of PDGF, $TGFT-\beta$, IGF-1, bFGF which are mainly found at bone matrix and their neutralizing antibody, the effect of PRP on the attachment and proliferation of osteoblasts was evaluated. To evaluate the autocrine and paracrine effects, conditioned media(CM) of PRP was made and compared with PRP. By the western blot analysis, the expression of growth factors in PRP, CM was examined. Cell morphology was compared by the light microscope. Results : 1) The effects of CM on osteoblast were similar to the effects of PRP. 2) PRP, CM, recombinant $TGF-\beta$, bFGF, IGF-1 showed significantly higher cellular attachment than control(p<0.05) in the cell attachment assay. In the cell proliferation assay, PRP, CM, recombinant $TGF-\beta$, IGF-1, bFGF, PDGF increased significantly cell proliferation(p<0.01). Among the recombinant growth factors, IGF-1 showed the highest cellular attachment and proliferation. 3) In the western blot assay, bFGF, IGF-1, PDGF weve equally expressed in PRP and CM. 4) The attachment of osteoblast cell decreased significantly after the addition of neutralizing antibody against $TGF-\beta$, IGF-1(p<0.05). In the cell proliferation assay, the addition of neutralizing antibody against $TGF-\beta$, bFGF, PDGF, IGF-1 decreased significantly the cellular proliferation(p<0.05). The amount of decreasing in the cell attachment and proliferation is the highest in at-lGF-1. 5) The cells in control group were flattened and elongated with a few cellular processes in the a light microscope. But, the cells appeared as spherical, plump cells with well developed cellular processes in experimental groups. The cells in PRP and CM had more prominent developed features than recombinant growth factor groups. Conclusions : These findings imply that PRP maximize the cellular activity in early healing period using the synergistic effect, autocrine, paracrine effects of growth factors and increase the rate and degree of bone formation.

• Korean Journal of Microbiology
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• v.35 no.4
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• pp.283-288
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• 1999

The effect of dissolved oxygen(DO) concentration on the growth of Pseudomonas aeruginosa and it's mutant M-10 was studied the growth kinetics and the possibility of waste treatment for reducing the amount of excess sludge. Different DO concentrations on the growth of wild type Pseudomonas aeruginosa affected to cellular yields, decreasing with increasing DO concentrations. Under these conditions, the maximum 14 folds decrease of cellular yield was achieved at 90 ppm DO levels by screened, being able to reduce their cellular yields under low DO concentration. The optimum mutation conditions were obtained by the treatment of NTG mutagen at 30${\circ}C$ for 1 hr. The growth characteristics of the selected mutant M-10 showed the same as the wild type growth kinetics. However, cellular yields are significantly decreased to 55% compared with those of wild type under DO concentrations increased. We, therefore, expect the application of the mutants to waste treatment for reducing excess sludge.

• Molecules and Cells
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• v.21 no.2
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• pp.224-228
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• 2006

Glypican-3 (GPC3) is a member of the glypican family, which encodes cell-surface heparan-sulfate proteoglycans, and is frequently upregulated in hepatocellular carcinoma (HCC). We have recently reported that blocking endogenous GPC3 expression promotes the growth of HCC cell lines, suggesting that GPC3 plays a negative role in HCC cell proliferation. Here, we report that forced expression of GPC3 reduced the growth of HCC cells. We also found that FGF2-mediated cell proliferation was inhibited by GPC3. In addition, we observed that the adhesion of HCC cells to collagen type I and fibronectin was decreased by GPC3, whereas cellular migration and invasiveness were stimulated. Collectively, these results suggest that progression of hepatocellular carcinoma is associated with upregulation of GPC3.

• Journal of Microbiology and Biotechnology
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• v.15 no.4
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• pp.909-912
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• 2005

In the course of screening for selective growth inhibitors against the mycelial form of Candida albicans, we isolated a Streptomyces sp. A6792 from soils. The inhibitor was isolated from the above bacterium and identified through several spectral analyses with UV and mass spectrophotometries, and various NMR. The compound was determined to be a macrocyclic dilactone antibiotic, IKD-8344 (molecular weight: 844, molecular formula: $C_{48}H_{76}O_{12}$). The compound selectively inhibited the growth of mycelial form of C. albicans with an MIC of 6.25 ${\mu}g/ml$. It also exhibited strong inhibitory effect preferentially on the mycelial form of various Candida spp. including C. krusei, C. tropicalis, and C. lusitaniae, with MICs ranging from 1.56 to 25 ${\mu}g$/ml. Furthermore, the compound showed no significant toxicity against SPF ICR mice up to 60 mg/kg. These results suggest that IKD-8344 is a useful lead compound for the development of novel antifungal agents, based on the preferential growth inhibition against Candida spp.

• Journal of Microbiology and Biotechnology
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• v.25 no.2
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• pp.162-173
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• 2015

The cellular fatty acid composition is important for metabolic plasticity in Rhodobacter sphaeroides. We explored the effects of changing the cellular ratio of unsaturated fatty acids (UFAs) to saturated fatty acids (SFAs) in R. sphaeroides by overexpressing several key fatty acid biosynthetic enzymes through the use of expression plasmid pRK415. Bacteria containing the plasmid pRKfabI₁ with the fabI₁ gene that encodes enoyl-acyl carrier protein (ACP) reductase showed a reduction in the cellular UFA to SFA ratio from 4 (80% UFA) to 2 (65% UFA) and had decreased membrane fluidity and reduced cell growth. Additionally, the ratio of UFA to SFA of the chromatophore vesicles from pRKfabI₁-containing cells was similarly lowered, and the cell had decreased levels of light-harvesting complexes, but no change in intracytoplasmic membrane (ICM) content or photosynthetic (PS) gene expression. Both inhibition of enoyl-ACP reductase with diazaborine and addition of exogenous UFA restored membrane fluidity, cell growth, and the UFA to SFA ratio to wild-type levels in this strain. R. sphaeroides containing the pRKfabB plasmid with the fabB gene that encodes the enzyme β-ketoacyl-ACP synthase I exhibited an increased UFA to SFA ratio from 4 (80% UFA) to 9 (90% UFA), but showed no change in membrane fluidity or growth rate relative to control cells. Thus, membrane fluidity in R. sphaeroides remains fairly unchanged when membrane UFA levels are between 80% and 90%, whereas membrane fluidity, cell growth, and cellular composition are affected when UFA levels are below 80%.