• 한국미생물·생명공학회지
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• 제19권4호
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• pp.413-418
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• 1991

L.bulgaricus KFCC 35462와 S.uvarum KFCC 32021을 두유에 혼합하였을 때 L.bulgaricus의 생육은 크게 촉진되었으나 젖산발효는 거의 촉진되지 않았고, S.uvarum의 생육과 알코올 발효는 억제되지 않았다. 젖산균과 효모의 혼합배양에 의한 두유음료의 산도증가 등의 발효적성의 향상에는 젖산균에 의한 효모의 억제작용 등의 배합균주 상호간의 특이적 작용이 중요하였다.

• BMB Reports
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• 제52권4호
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• pp.239-249
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• 2019

Membrane-anchored full-length MET stimulated by its ligand HGF/SF induces various biological responses, including survival, growth, and invasion. This panel of responses, referred to invasive growth, is required for embryogenesis and tissue regeneration in adults. On the contrary, MET deregulation is associated with tumorigenesis in many kinds of cancer. In addition to its well-documented ligand-stimulated downstream signaling, the receptor can be cleaved by proteases such as secretases, caspases, and calpains. These cleavages are involved either in MET receptor inactivation or, more interestingly, in generating active fragments that can modify cell fate. For instance, MET fragments can promote cell death or invasion. Given a large number of proteases capable of cleaving MET, this receptor appears as a prototype of proteolytic-cleavage-regulated receptor tyrosine kinase. In this review, we describe and discuss the mechanisms and consequences, both physiological and pathological, of MET proteolytic cleavages.

• 한국미생물·생명공학회지
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• 제8권4호
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• pp.221-227
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• 1980

포도당을 포함한 생장 배지속에 L-사과산을 첨가하면 Leuconostoc oenos균들의 생장률을 크게 촉진 시켰다. L-사과산은 동시에 C-젖산탈수소 효소(D-LDH)의 합성과 활성도를 촉진시켜 포도당에서 D-젖산의 생산을 빠르게 하였다. L-사과산 존재 하에서 이렇게 빨라진 포도당의 이용이 leuconostoc 균들의 생장률을 촉진시키는 것 같다.

• The Korean Journal of Physiology and Pharmacology
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• 제17권4호
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• pp.307-314
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• 2013

Connective tissue growth factor (CTGF) is a potent pro-fibrotic factor, which is implicated in fibrosis through extracellular matrix (ECM) induction in diabetic cardiovascular complications. It is an important downstream mediator in the fibrotic action of transforming growth factor ${\beta}$ ($TGF{\beta}$) and is potentially induced by hyperglycemia in human vascular smooth muscle cells (VSMCs). Therefore, the goal of this study is to identify the signaling pathways of CTGF effects on ECM accumulation and cell proliferation in VSMCs under hyperglycemia. We found that high glucose stimulated the levels of CTGF mRNA and protein and followed by VSMC proliferation and ECM components accumulation such as collagen type 1, collagen type 3 and fibronectin. By depleting endogenous CTGF we showed that CTGF is indispensable for the cell proliferation and ECM components accumulation in high glucose-stimulated VSMCs. In addition, pretreatment with the MEK1/2 specific inhibitors, PD98059 or U0126 potently inhibited the CTGF production and ECM components accumulation in high glucose-stimulated VSMCs. Furthermore, knockdown with ERK1/2 MAPK siRNA resulted in significantly down regulated of CTGF production, ECM components accumulation and cell proliferation in high glucose-stimulated VSMCs. Finally, ERK1/2 signaling regulated Egr-1 protein expression and treatment with recombinant CTGF reversed the Egr-1 expression in high glucose-induced VSMCs. It is conceivable that ERK1/2 MAPK signaling pathway plays an important role in regulating CTGF expression and suggests that blockade of CTGF through ERK1/2 MAPK signaling may be beneficial for therapeutic target of diabetic cardiovascular complication such as atherosclerosis.

• Archives of Pharmacal Research
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• 제20권6호
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• pp.572-578
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• 1997

To gain further insight into how antiestrogens modulate cell function, the effects of antiestrogen on cell proliferation were studied in human breast cancer cells. We examined the effects of trans-tamoxifen on the proliferation of three human breast cancer cell lines that differed in their estrogen receptor contents. Trans-tamoxifen $(1{\mu}M)$ markedly inhibited the estrogen stimulated proliferation of MCF-7 human breast cancer cells that contained high levels of estrogen receptor $(1.15{\pm}0.03 pmole/mg protein)$ over that of control. In T47D cells that contained low levels of estrogen receptor $(0.23{\pm}0.05 pmole/mg protein)$, trans-tamoxifen $(1{\mu}M)$ showed minimal inhibition of estrogen stimulated cell proliferation over that of control. MDA-MB-231 cells, that contained no detectable levels of estrogen receptors, had their growth unaffected by trans-tamoxifen treatment. These results showed their sensitivity to growth inhibition by antiestrogen conrrelated well with their estrogen receptor content. Also we examined the effect of antiestrogen on cellular progestrone receptor level as well as plasminogen activator activity in MCF-7 cells. Trans-tamoxifen $(1{\mu}M)$ showed maximal inhibition of estrogen stimulated progestrone receptor level as well as plasminogen activator activity in MCF-7 cells that were stimulated by estrogen. It is not clear whether these inhibitions of progestrone receptor and plasminogen activator activity by estrogen are related to the antiestrogen inhibition of cell proliferation of MCF-7 cells. From the results of this study, it is clearly demonstrated that trans-tamoxifen is an antiestrogen in MCF-7 human breast cancer cells. Our data suggest that the biological effectiveness of trans-tamoxifen appear to result from its affinity of interaction with the estrogen receptor.

• 한국어병학회지
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• 제31권2호
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• pp.109-113
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• 2018

The purpose of the present study was to determine whether the scuticocidal activity of olive flounder (Paralichthys olivaceus) head-kidney leucocytes can be enhanced by stimulation with polyinosine-polycytosine [poly (I:C)]. The growth of Miamiensis avidus was not affected by exposure to unstimulated or poly (I:C)-stimulated leucocytes alone, heat-inactivated immune serum alone, or unstimulated leucocytes plus heat-inactivated immune serum. However, leucocytes stimulated with poly (I:C) showed clearly high scuticocidal activity against M. avidus in the presence of heat-inactivated immune serum. Furthermore, numerous poly (I:C)-stimulated leucocytes occupied the surface of scuticociliates in the presence of the heat-inactivated immune serum, which led to lysis of scuticociliates. These results suggest that both of the stimulation of leukocytes and the immobilization of scuticociliates are necessary to kill scuticociliates by leukocytes.

• 해양환경안전학회지
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• 제12권2호
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• pp.81-87
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• 2006

본 연구는 남해안 북만 해역을 대상으로 조류성장잠재력(AGP) 시험을 통하여 H. akashiwo의 성장제한요인을 평가하였다. 영양물질의 첨가 및 미생물과의 동시배양에 의하면 적조발생 단계별 H. akashiwo의 성장은 서로 다른 제한요인에 의하여 영향을 받는 것으로 나타났다. 적조발생 전의 H. akashiwo 성장은 질산질소 $50{\mu}M$과 연산인 $5{\mu}M$을 복합첨가하면 크게 증가하였지만 인산인을 단독 첨가하거나 미생물과 동시 배양하여도 전혀 영향이 없었다. 적조발생 전의 H. akashiwo 성장제한요인은 질산질소로 나타났다. 적조발생시기의 H. akashiwo 성장은 질산질소 $50{\mu}M$ 또는 인산인 $5{\mu}M$을 단독첨가하면 증가하였지만 미량영양물질이나 $vitamin\;B_{12}$을 첨가해도 전혀 영향이 없었다. 적조발생 시기의 H. akashiwo 성장제한요인은 질산질소와 인산인이 동시에 작용하는 것으로 나타났다. 반면에 적조소멸시기의 H. akashiwo 성장은 질산질소와 인산인을 첨가하면 약간 증가하였지만 미생물과 동시 배양하면 현저히 감소하였다. 그러므로 적조 소멸시기의 H. akashiwo 성장제한은 미생물요인에 의한 것으로 평가되었다.

• Preventive Nutrition and Food Science
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• 제11권1호
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• pp.1-5
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• 2006

Conjugated linoleic acid (CLA) is a group of positional and geometric isomers of linoleic acid that have been used to reduce the incidence, growth and metastasis of breast, colon, prostate and gastric cancer in animals. CLA could reduce tumor growth by altering angiogenesis; a process requiring associated angiogenic factors such as vascular endothelial growth factor (VEGF). In this study, we determined whether CLA could modulate the expression of VEGF in murine mammary tumor cells and adipocytes. The c9, t11-CLA isomer reduced VEGF transcripts and protein when mammary tumor cells were stimulated with PMA. That isomer also reduced VEGF expression in un stimulated mouse 3T3-L1 adipocytes. Since VEGF can be regulated by cyclooxygenase-2 (COX-2), we determined whether CLA could alter COX-2 enzyme expression and $PGE_2$ production. The c9, t11-CLA isomer reduced not only COX-2 enzyme expression but also $PGE_2$ production. Thus, c9, t11-CLA could modulate neovascularization by alteration of VEGF expression from mammary tumor cells and adipocytes by reducing COX-2 metabolites.

• BMB Reports
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• 제56권9호
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• pp.496-501
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• 2023

Elongation of most bones occur at the growth plate through endochondral ossification in postnatal mammals. The maturation of chondrocyte is a crucial factor in longitudinal bone growth, which is regulated by a complex network of paracrine and endocrine signaling pathways. Here, we show that a phytochemical sulfuretin can stimulate hypertrophic chondrocyte differentiation in vitro and in vivo. We found that sulfuretin stabilized nuclear factor (erythroid-derived 2)-like 2 (Nrf2), stimulated its transcriptional activity, and induced expression of its target genes. Sulfuretin treatment resulted in an increase in body length of zebrafish larvae and induced the expression of chondrocyte markers. Consistently, a clinically available Nrf2 activator, dimethyl fumarate (DMF), induced the expression of hypertrophic chondrocyte markers and increased the body length of zebrafish. Importantly, we found that chondrocyte gene expression in cell culture and skeletal growth in zebrafish stimulated by sulfuretin were significantly abrogated by Nrf2 depletion, suggesting that such stimulatory effects of sulfuretin were dependent on Nrf2, at least in part. Taken together, these data show that sulfuretin has a potential use as supporting ingredients for enhancing bone growth.

• 생명과학회지
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• 제5권3호
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• pp.117-120
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• 1995

Human milk was examined for antiangiogenic activities by using the chick embryo chorioallantoic membrane (CAM) assay and endothelial cell growth. The low molecular weight (20 KD>$\sim$ ) fraction of human milk stimulated the angiogenesis and increased the endothelial cell growth. These results suggest that the increase of angiogenesis and endothelial cell growth might be attributed to several growth factors and/or angiogenic factors in low molecular fraction (20 KD>$\sim$) of human milk.