• Title/Summary/Keyword: Rat cortical cells

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Increased α2,3-Sialylation and Hyperglycosylation of N-Glycans in Embryonic Rat Cortical Neurons During Camptothecin-induced Apoptosis

  • Kim, Sung-Min;Lee, Jung-Sun;Lee, Yoon-Hee;Kim, Woo-Jung;Do, Su-Il;Choo, Young-Kug;Park, Yong-Il
    • Molecules and Cells
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    • 제24권3호
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    • pp.416-423
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    • 2007
  • Alterations in the glycan chains of cell surface glycoconjugates are frequently involved biological processes such as cell-cell interaction, cell migration, differentiation and development. Cultured embryonic (E18) rat cortical neurons underwent apoptosis in response to camptothecin, and lectin histochemistry showed that binding to apoptotic neurons of FITC-conjugated Maackia amurensis agglutinin (MAA), which is specific for terminal ${\alpha}2,3$-sialic acid residues, increased progressively with increasing concentrations of camptothecin. Analysis of the total proteins of apoptotic neurons by SDS-PAGE, and lectin blotting using HRP-labeled MAA, revealed that the expression of terminal ${\alpha}2,3$-sialic acid residues on an unknown protein with an apparent molecular mass of 25.6 kDa also increased in apoptotic neurons. NP-HPLC analysis of the total cellular N-glycans of normal and apoptotic neurons demonstrated that the expression of structurally simpler biantennary types of N-glycans fell by 49% during apoptosis whereas the more branched triantennary types of N-glycans with terminal sialic acid residues increased by up to 59%. These results suggest that increased surface expression of ${\alpha}2,3$-sialic acid residues and hyperglycosylation of N-glycans is a common feature of cellular responses to changes in cell physiology such as tumorigenesis and apoptosis.

Essential Role for c-jun N-terminal Kinase on tPA-induced Matrix Metalloproteinase-9 Regulation in Rat Astrocytes

  • Lee, Sun-Ryung
    • Animal cells and systems
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    • 제10권2호
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    • pp.79-83
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    • 2006
  • Tissue plasminogen activator (tPA) is used to lyse clots and reperfuse brain in ischemic stroke. However, sideeffects of intracerebral hemorrhage (ICH) and edema limit their clinical application. In part, these phenomena has been linked with elevations in matrix metalloproteinase-9 (MMP-9) in neurovascular unit. However little is known about their regulatory signaling pathways in brain cells. Here, I examine the role of MAP kinase pathways in tPA-induced MMP-9 regulation in rat cortical astrocytes. tPA $(1-10\;{\mu}g/ml)$ induced dose-dependent elevations in MMP-9 and MMP-2 in conditioned media. Although tPA increased phosphorylation in two MAP kinases (ERK, JNK), only inhibition of the JNK pathway by the JNK inhibitor SP600126 significantly reduced MMP-9 upregulation. Neither ERK inhibition with U0126 nor p38 inhibition with SB203580 had any significant effects. Taken together, these results suggest that c-jun N-terminal kinase (JNK) plays an essential role for tPA-induced MMP-9 upregulation.

Effects of Triclosan on Neural Stem Cell Viability and Survival

  • Park, Bo Kyung;Gonzales, Edson Luck T.;Yang, Sung Min;Bang, Minji;Choi, Chang Soon;Shin, Chan Young
    • Biomolecules & Therapeutics
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    • 제24권1호
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    • pp.99-107
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    • 2016
  • Triclosan is an antimicrobial or sanitizing agent used in personal care and household products such as toothpaste, soaps, mouthwashes and kitchen utensils. There are increasing evidence of the potentially harmful effects of triclosan in many systemic and cellular processes of the body. In this study, we investigated the effects of triclosan in the survivability of cultured rat neural stem cells (NSCs). Cortical cells from embryonic day 14 rat embryos were isolated and cultured in vitro. After stabilizing the culture, triclosan was introduced to the cells with concentrations ranging from $1{\mu}M$ to $50{\mu}M$ and in varied time periods. Thereafter, cell viability parameters were measured using MTT assay and PI staining. TCS decreased the cell viability of treated NSC in a concentration-dependent manner along with increased expressions of apoptotic markers, cleaved caspase-3 and Bax, while reduced expression of Bcl2. To explore the mechanisms underlying the effects of TCS in NSC, we measured the activation of MAPKs and intracellular ROS. TCS at $50{\mu}M$ induced the activations of both p38 and JNK, which may adversely affect cell survival. In contrast, the activities of ERK, Akt and PI3K, which are positively correlated with cell survival, were inhibited. Moreover, TCS at this concentration augmented the ROS generation in treated NSC and depleted the glutathione activity. Taken together, these results suggest that TCS can induce neurodegenerative effects in developing rat brains through mechanisms involving ROS activation and apoptosis initiation.

Neuroprotective effect of woganin in a rodent model of permanent focal cerebral ischemia

  • Cho , Jung-Sook;Lee, Hyung-Kyu
    • 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.303.2-304
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    • 2002
  • Wogonin. a flavonoid originated from the root of Scutellaria baicalensis Georgi. is known to exhibit potent anti-inflammatory effects and variable degrees of antioxidant and free radical scavenging effects depending on the experimental systems. In addition. wogonin has been reported to protect neurons from excitotoxic and oxidative injuries in primary cultured rat cortical cells. (omitted)

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Neuroprotective effects of gossypin on beta-amyloid- and oxidative stress-induced toxicity in primary cultured rat cortical cells

  • Yoon, In-Jae;Lee, Kwang-Heun;Cho, Jung-Sook
    • 대한약학회:학술대회논문집
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    • 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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    • pp.142.1-142.1
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    • 2003
  • Excessive accumulation of beta-amyloid (A$\beta$) peptides is one of the leading hypotheses to explain neurodegenerative processes in Alzheimer's disease (AD). It has been suggested that $A\beta$ toxicity is associated with increases in reactive oxygen species. whose overproduction may in turn initiate neurotoxic events. (omitted)

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발육 중의 백서 태아 대뇌 피질에서 방사선에 의한 아포토시스 (Radiation-induced Apoptosis in Developing Fetal Rat Cerebral Cortex)

  • 정웅기;남택근;이민철;안성자;송주영;박승진;나병식
    • Radiation Oncology Journal
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    • 제21권4호
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    • pp.315-321
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    • 2003
  • 목적: 발육 중인 백서 태아 대뇌 피질에서 방사선조사에 의한 아포토시스 반응에 대하여 알아보고자 하였다 대상 및 방법: 임신 백서의 태령 17 내지 19일(E17$\~$E19)에 선형가속기의 X-ray를 이용하여 어미 쥐의 복부에 방사선을 조사하였다. 방사선량에 따른 아포토시스를 보기 위하여 1, 2, 3, 4 Gy를 전후 조사면으로 방사선조사를 시행하고 5시간 후 백서 태아의 뇌를 획득하였다. 시간 경과에 따른 아포토시스를 보기 위하여 E7$\~$E19에 2 Gy의 방사선을 조사한 후 1, 3, 6, 12, 24시간에 각각 백서 태아의 뇌를 획득하였다. 대조군은 방사선을 조사하지 않은 임신 쥐를 같은 조건하에서 사육하여 각 군당 3마리씩 할당하였다. 아포토시스 세포는 면역조직화학적 방법(TUNEL, In situ 707-mediated dUTP nick end labeling)으로 염색하여 관찰하였다 결과: 백서 태아 대뇌 피질에서 TUNEL 양성인 세포는 광학현미경하에서 전형적인 아포토시스의 형태학적 특징을 나타내었다 대조군에서는 대뇌 피질의 전 층에서 TUNEL 양성세포를 거의 발견할 수 없었다. 1 Gy의 방사선 조사 후 5시간에 대뇌피질 전 층에서 미약하게 관찰되었으나 2 Gy에는 전 층에서 1 Gy 경우보다 더 증가하였고 그중 뇌실대와 중간대에서 피질대보다 더 많이 나타났다. 조사된 1$\~$4 Gy 범위에서 방사선량이 증가할수록 TUNEL양성세포가 더욱 증가하는 것을 볼 수 있었다. 2 Gy의 방사선 조사 후 3시간부터 TUNEL양성세포가 관찰 되기 시작하여 방사선 조사 후 6시간에 최고점을 이루었으며 이는 24시간까지 지속되었다. 결론: 발육 중인 백서 태아 대뇌피질에서 방사선에 의한 아포토시스의 전형적인 형태학적 특징을 관찰할 수 있었다. 아포토시스는 뇌실대와 중간대에서 피질대보다 더 많이 나타났으며 이는 줄기세포와 초기의 분화세포에서 방사선조사에 대한 감수성이 더욱 민감함을 시사하였다.

목향(木香) 및 사향(麝香)이 저산소증 유발 배양 대뇌신경세포에 미치는 영향 (The Effect of Aucklandiae Radix.Moschus(木香.麝香)'s for Delayed Neuronal Death in Hypoxia)

  • 정승현;신길조;이원철;문일수;류도균
    • 대한한방내과학회지
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    • 제24권2호
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    • pp.348-357
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    • 2003
  • Objectives : The purpose of this investigation is to evaluate the effects of Aucklandiae Radix Moschus(木香 麝香)and to study the mechanism for neuronal death protection in hypoxia with Embryonic day 20 (E20) cortical cells of a rat (Sprague Dawley). Methods : E20 cortical cells used in this investigation were dissociated in Neurobasal media and grown for 14 days in vitro (DIV). On 14 DIV, Aucklandiae Radix Moschus(木香 麝香) was added to the culture media for 72 hrs. On 17 DIV, cells were given a hypoxic shock and further incubated in normoxia for another three days. On 20 DIV, Moschus(麝香)'s effects for neuronal death protection were evaluated by LDH assay and the mechanisms were studied by Bcl-2, Bak, Bax, caspase family. Results : This study indicate that Aucklandiae Radix(木香)'s effects for neuronal death protection in normoxia and Scutellariae Radix(麝香)'s effects for neuronal death protection in hypoxia were confirmed by LDH assay in culture method of Embryonic day 20(E20) cortical neuroblast. Moschus(麝香)'s mechanism for neuronal death protection in hypoxia is to increase the anti-apoptosis protein Bcl-2. Conclusions : It may be reasonable to propose that Moschus(麝香) protects delayed neuronal death in hypoxia by increasing Bcl-2, thereby reducing mitochondrial permeability transition(PT) pores, the cytochrome c channels.

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Nephron Heterogeneity of Renin Release in Rat Kidney Slices: Effects of L-Isoproterenol, Angiotensin II and TMB-8

  • Seul, Kyung-Hwan;Kim, Suhn-Hee;Koh, Gou-Young;Cho, Kyung-Woo
    • The Korean Journal of Physiology
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    • 제25권1호
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    • pp.61-67
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    • 1991
  • In order to determine possible relationships between the renin-angiotensin system and nephron heterogeneity, we compared the response of renin release and the angiotensin-converting enzyme (ACE) activity from different areas of the rat kidney. We used the renal cortical slices from the capsular surface to the juxtamedullary junction. Slices from outer one-third of the cortex were designated as outer cortical slices (OC), middle one-third as midcortical slices (MC), and inner one-third as inner cortical slices (IC). The renal renin content markedly decreased from OC and MC to IC. The basal lenin release was higher in OC than in MC or IC. On the contrary the percent change of renin release in response to L-isoproterenol was significantly higher in MC than in OC or IC. By TMB-8, the renin release in MC by $231{\pm}21%$ was higher than OC by $171{\pm}19%$ or IC by $$162{\pm}19. Angiotensin II suppressed renin release in OC and MC by $68{\pm}2,\;71{\pm}4%$ respectively, but only $40{\pm}7%$ in IC. The ACE activity was higher in IC than in OC, MC, medulla and papilla. The present data indicate that renin content and basal lenin release gradulally decreased from outer (OC) to inner (IC) cortex. The renin release in response to beta-adrenergic agonist, L-isoproterenol and intracellular calcium antagonist, TMB-8 were higher in MC than in OC and IC, but angiotensin II suppressed renin release less in IC than in OC and MC. It is suggested that juxtaglomerular cells of outer, mid-and inner cortices show a difference in renin release response to the stimuli.

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