• 한국생물공학회:학술대회논문집
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• 한국생물공학회 2003년도 생물공학의 동향(XII)
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• pp.743-746
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• 2003

The major pathological lesion in Parkinson's disease(PD) is selective degeneration and loss of pigmented dopaminergic neurons in substantia nigra (SN). Although the initial cause and subsequent molecular signaling mechanisms leading to the dopaminergic cell death underlying the PD process is elusive, the potent neurotrophic factors (NTFs), brain derived neurotrophic factor (BDNF) and glial cell line derived neurotrophic factor (GDNF), are known to exert dopaminergic neuroprotection both in vivo and in vitro models of PD employing the neurotoxin, MPTP. BDNF and its receptor, trkB are expressed in SN dopaminergic neurons and their innervation target. Thus, neurotrophins may have autocrine, paracrine and retrograde transport effects on the SN dopaminergic neurons. This study determined the BDNF secretion from SN dopaminergic neurons by ELISA. Regulation of BDNF synthesis/release and changes in signaling pathways are monitored in the presence of free radical donor, NO donor and mitochondrial inhibitors. Also, this study shows that BDNF is able to promote survival and phenotypic differentiation of SN dopaminergic neurons in culture and protect them against MPTP-induced neurotoxicity via MAP kinase pathway.

• BMB Reports
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• 제44권11호
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• pp.699-704
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• 2011

Nitric oxide (NO) is a critical biological mediator involved in numerous diseases. However, the short lifetime of this molecule in biological conditions can make its study in situ complicated. Here, we review some recent results on the role of NO in angiogenesis, obtained using a biocompatible microelectrode array. This simple system allowed for the quick and easy quantification of NO released from cells grown directly on the surface of the sensor. We have used this technology to demonstrate that angiogenin induces NO release, and to partially elucidate its intracellular transduction pathway.

• Biomolecules & Therapeutics
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• 제22권6호
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• pp.503-509
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• 2014

Paraquat has been suggested to induce apoptosis by generation of reactive oxygen species (ROS). However, little is known about the mechanism of paraquat-induced apoptosis. Here, we demonstrate that extracellular signal-regulated protein kinase (ERK) is required for paraquat-induced apoptosis in NIH3T3 cells. Paraquat treatment resulted in activation of ERK, and U0126, inhibitors of the MEK/ERK signaling pathway, prevented apoptosis. Moreover, paraquat-induced apoptosis was associated with cytochrome C release, which could be prevented by treatment with the MEK inhibitors. Taken together, our findings suggest that ERK activation plays an active role in mediating paraquat-induced apoptosis of NIH3T3 cells.

• 환경생물
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• 제21권3호
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• pp.303-307
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• 2003

Tributyltin (TBT) used world-wide in antifouling paints toy ships is a wide-spread environmental pollutant. At low doses, antiproliferative modes of action have been shown to be involved, whereas at higher doses apoptosis seems to be the mechanism of toxicity in reproductive organs by TBT. In this study, we investigated that the mechanisms underlying apoptosis induced by TBT in R2C cell. Effects of TBT on intracellular $Ca^{2+}$ level and reactive oxygen species (ROS) were investigated in R2C cells by fluorescence detector. TBT significantly induced intracellular $Ca^{2+}$ level in a time-dependent manner. The rise in intracellular $Ca^{2+}$ level was followed by a time-dependent generation of reactive oxygen species (ROS) at the cytosol level. Simultaneously, TBT induced the release of cytochrome c from the mitochondrial membrane into the cytosol. Furthermore, ROS production and the release of cytochrome c were reduced by BAPTA, an intracellular $Ca^{2+}$ chelator, indicating the important role of $Ca^{2+}$ in R2C during these early intracellular events. In addition, Z-DEVD FMB, a caspase -3 inhibitor, decreased apoptosis by TBT. Taken together, the present results indicated that the apoptotic pathway by TBT might start with an increase in intracellular $Ca^{2+}$ level, continues with release of ROS and cytochrome c from mitochondria, activation of caspases, and finally results in DNA fragmentation.

• ALGAE
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• 제36권2호
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• pp.147-154
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• 2021

Kelp life history pathways alternate between macroscopic sporophytes that produce spores and microscopic gametophytes that produce gametes. Occasionally, an alternative pathway is seen. This study examined the circumstances by which the high latitude estuarine bull kelp, Nereocystis luetkeana, foregoes the "free-living microscopic stages by releasing embryonic sporophytes directly from sori. Sori were collected from adult N. luetkeana sporophytes from eight locations within Kachemak Bay, Alaska in 2018 and 2020 to examine spatial and temporal development of embryonic sporophytes on sori. Distinctions were made between sori collected from first-generation and overwintered adults to assess the influence of parental age on embryonic sporophyte release. Further distinctions were made between sori collected from attached and drifting individuals to assess the influence of the status of parental attachment to substrate on embryonic sporophyte release. Inspection of propagules released from sori after 48-h incubations indicated that embryonic sporophytes were occasionally released alongside viable spores. Though embryonic sporophytes were released from sori as early as spring, it was not evident that they were bound by seasonal or spatial limits. The percent of propagules that were embryonic sporophytes ranged from 0% to 100% but were not significantly different between first-generation and overwintered adults, nor were they different between attached and drifting individuals. Nevertheless, the characteristic of directly releasing embryonic sporophytes from adult sporophytes might have ecological advantages for N. luetkeana.

• 대한약학회:학술대회논문집
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• 대한약학회 2002년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2
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• pp.268.2-269
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• 2002

The recombinant histamine-releasing factor (rHRF) has been reported to induce a secretion of histamine and cytokines from inflammation-related cell types such as basophils and eosinophils. and to function as a growth factor in immune B cells. Recently. decreased expression level of HRF protein was observed in brain of patients with Alzheimer disease and Downs syndrome. suggesting a possible significant role in neurological systems. (omitted)

• 한국생물물리학회:학술대회논문집
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• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
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• pp.23-23
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• 2001

To evaluate the contribution of cAMP/PKA signal pathway in short-term facilitation, we overexpressed Ap oal receptor in sensory neurons that do not normally express this receptor. We have previously shown that activation of this receptor in sensory cells, by a brief treatment with octopamine (OA), produced short-term facilitation such as membrane depolarization, increase in membrane excitability, spike broadening, and enhanced neurotransmitter release in non-depressed synapse.(omitted)

• 대한의생명과학회지
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• 제12권2호
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• pp.57-63
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• 2006

Deazaadenosine analogs such as 3-deazaadenosine (DZA), 3-deazaaristeromycin (DZAri) and ara-3-deazaadenine (DZAra-A) were developed as inhibitors of S-adenosylhomocysteine (Ado-Hcy) hydrolase (EC 3.3.1.1). These analogs were reported to induce apoptosis in human and murine leukemic cells. But, the mechanism involved in this apoptosis was not clarified yet. In the present study, we analyze the apoptosis induced by deazaadenosine analogs in human cervival cancer cell line, HeLa and the effect of Bcl-2 on this apoptosis. Whereas neither DZAri nor DZAra-A showed inhibitory effect on HeLa cell growth, DZA induced apoptosis in HeLa cells accompanied by cytochrome c release and activation of various caspases such as caspase-2,-8,-9 and -3. In HeLa-bcl-2 cell line, a stable transfectant of HeLa cell to overexpress Bcl-2, cytochrome c release, activation of all these caspases and the resulted apoptosis by DZA were completely prevented. By in vitro assay of cytochrome c release, in addition, DZA induced cytochrome c release from purified mitochondria of HeLa-pcDNA3 cells, but not HeLa-bcl-2 cells, even in the absence of cytosolic fraction. Therefore, it can be suggested that DZA might damage directly mitochondria leading to activate intrinsic pathway of caspase and thus induce apoptosis. DZA-induced apoptosis in HeLa cells may be in a bcl-2-inhibitable manner and irrelative of Ado-Hcy hydrolase.

• Journal of Radiation Protection and Research
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• 제19권3호
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• pp.209-221
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• 1994

원자력발전소의 중대 사고시 대기로 방출된 방사성물질에 의해 피폭자가 사고후 일생동안 받게 될 전신 피폭선량과 핵종의 상대적 중요도를 방출점으로부터 거리에 따라 각 피폭경로에 대해 평가하였다. 방사능운과 지표에 침적된 방사성물질에 의한 외부피폭, 호흡과 오염된 음식물섭취에 의한 내부피폭이 피폭경로로 고려되었다. 오염된 음식물섭취에 의한 영향은 우리나라 환경을 고려하여 개발된 동적 삽식경로모델 KORFOOD을 사용하여 침적시점과 침적후 시간에 따른 음식물내 방사성물질의 농도 변화를 고려하였다. 방출점으로부터 80km까지 피폭선량을 평가한 결과, 오염된 음식물섭취에 의한 영향이 가장 높았다. 핵종별 기여도는 방사능운에 의한 외부피폭과 호흡에 의한 내부피폭의 경우 I, 침적된 방사성물질에 의한 외부피폭의 경우 Cs에 의한 영향이 가장 높았다. 오염된 음식물섭취에 의한 내부피폭의 경우 Cs은 여름철 침적, Sr은 겨울철 침적에 보다 중요한 영향을 미쳤다.

• Journal of Ginseng Research
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• 제43권2호
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• pp.305-311
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• 2019

Background: Gintonin is a ginseng-derived exogenous ligand of the G protein-coupled lysophosphatidic acid (LPA) receptor. We previously reported that gintonin stimulates gliotransmitter release in primary cortical astrocytes. Astrocytes play key roles in the functions of neurovascular systems. Although vascular endothelial growth factor (VEGF) is known to influence the normal growth and maintenance of cranial blood vessels and the nervous system, there is little information about the effect of gintonin on VEGF regulation in primary astrocytes, under normal and hypoxic conditions. Methods: Using primary cortical astrocytes of mice, the effects of gintonin on the release, expression, and distribution of VEGF were examined. We further investigated whether the gintonin-mediated VEGF release protects astrocytes from hypoxia. Results: Gintonin administration stimulated the release and expression of VEGF from astrocytes in a concentration- and time-dependent manner. The gintonin-mediated increase in the release of VEGF was inhibited by the LPA1/3 receptor antagonist, Ki16425; phospholipase C inhibitor, U73122; inositol 1,4,5- triphosphate receptor antagonist, 2-APB; and intracellular $Ca^{2+}$ chelator, BAPTA. Hypoxia further stimulated astrocytic VEGF release. Gintonin treatment stimulated additional VEGF release and restored cell viability that had decreased due to hypoxia, via the VEGF receptor pathway. Altogether, the regulation of VEGF release and expression and astrocytic protection mediated by gintonin under hypoxia are achieved via the LPA receptor-VEGF signaling pathways. Conclusion: The present study shows that the gintonin-mediated regulation of VEGF in cortical astrocytes might be neuroprotective against hypoxic insults and could explain the molecular basis of the beneficial effects of ginseng on the central nervous system.