• 제목/요약/키워드: $C_5-pathway$

검색결과 785건 처리시간 0.029초

신호전달 경로의 저해제를 이용한 혈관 내피세포의 비정상적인 증식 기전에 대한 연구 (A Study for the Mechanism of Abnormal Proliferation in Vascular Endothelial Cells using Inhibitors to the Signal Transduction Pathway)

  • 배용찬;박숙영;남수봉;허재영;강영석
    • Archives of Plastic Surgery
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    • 제33권1호
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    • pp.5-12
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    • 2006
  • Protein tyrosine kinase(PTK), protein kinase C(PKC), oxidase, as a mediator, take a significant role in signal transduction pathway of angiogenesis. The authors utilized the inhibitors, targeting the formation of three co-enzyme in signal transduction pathway in order to quantify the suppression of abnormal vascular endothelial cell proliferation induced by DMH, to compare the level suppression in each up-regulated growth factors, CTGF, CYR61, $ITG{\beta}1$, FHL2, and to identify the relationship between abnormal cell proliferation and signal transduction pathway. Five groups were established; Control group, Group of DMH, Group of DMH-mixed Herbimycin, inhibitor of protein tyrosine kinase, Group of DMH-mixed Calphostin C, inhibitor of protein kinase C, Group Of Dmh-Mixed 10U Catalase, Inhibitor Of oxidase. The rise of vascular endothelial cell was compared by MTT assay, and four growth factors were analysed with RT-PCR method, at pre-administration, 4, 8, 12, and 24 hours after administration. In comparison of abnormal proliferation of vascular endothelial cell induced by DMH, suppression was noticed in Herbimycin and Calphostin C group, and Calphostin C group revealed higher suppression effect. Nevertheless, Catalase group did not have any suppression. In manifestation of four growth factors, Herbimycin and Calphostin C group presented similar manifestation with control group, except in $ITG{\beta}$. Catalse group had similar manifestation with DMH group in all four growth factors. Abnormal proliferation of vascular endothelial cell induced by DMH have a direct relationship with PTK and PKC, more specifically to PKC. Oxidase was confirmed not to have any relevance.

Bacillus cereus 1-1 균주의 5-Aminolevulinic Acid (ALA) 생산 (Production of 5-Aminolevulinic Acid (ALA) by Bacillus cereus 1-1)

  • 안경준
    • 미생물학회지
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    • 제43권4호
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    • pp.304-310
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    • 2007
  • Bacillus cereus 1-1 균주는 광이 없는 호기적 환경에서 levulinic acid와 같은 저해제 처리 없이도 5-aminolevulinic acid (ALA)를2 mM까지 생산하였다. B. cereus 1-1 균주는 TCY 배지에서 전 배양과 본 배양을 18시간 동안 지속하고, 배지의 pH가 6.8에 도달하는 대수기 후기에 acetic acid를 비롯한 유기산들을 16 mM 첨가하였을 때 많은 ALA를 생산하였으며, 본 배양 시작시 0.3% glucose를 첨가하는 것이 효과적이었다. Acetic acid 대신 glutamic acid를 첨가하였을 때 ALA 생산이 8시간 이상 지속되었고, $40\;{\mu}M$의 gabaculine을 첨가하면 생산이 현저히 저해되는 것으로 보아 B. cereus 1-1 균의 ALA 생산은 C-5 경로에 의함을 알 수 있었다.

Glucosylsphingosine Activates Serotonin Receptor 2a and 2b: Implication of a Novel Itch Signaling Pathway

  • Afzal, Ramsha;Shim, Won-Sik
    • Biomolecules & Therapeutics
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    • 제25권5호
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    • pp.497-503
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    • 2017
  • Recent reports claimed that glucosylsphingosine (GS) is highly accumulated and specifically evoking itch-scratch responses in the skins of atopic dermatitis (AD) patients. However, it was unclear how GS can trigger itch-scratch responses, since there were no known molecular singling pathways revealed yet. In the present study, it was verified for the first time that GS can activate mouse serotonin receptor 2a (mHtr2a) and 2b (mHtr2b), but not 2c (mHtr2c) that are expressed in HEK293T cells. Specifically, effects of GS on all mouse serotonin receptor 2 subfamily were evaluated by calcium imaging techniques. The GS-induced intracellular calcium increase was dose-dependent, and antagonists such as ketanserin (Htr2a antagonist) and RS-127445 (Htr2b antagonist) significantly blocked the GS-induced responses. Moreover, the proposed GS-induced responses appear to be mediated by phospholipase C (PLC), since pretreatment of a PLC inhibitor U-73122 abolished the GS-induced responses. Additionally, the GS-induced calcium influx is probably mediated by endogenous TRPC ion channels in HEK293T cells, since pretreatment of SKF-96365, an inhibitor for TRPC, significantly suppressed GS-induced response. In conclusion, the present study revealed for the first time that GS can stimulate mHtr2a and mHtr2b to induce calcium influx, by utilizing PLC-dependent pathway afterwards. Considering that GS is regarded as a pruritogen in AD, the present study implicates a novel GS-induced itch signaling pathway.

5-Aminoisoquinolinone Reduces the Expression of Vascular Endothelial Growth Factor-C via the Nuclear Factor-kappa B Signaling Pathway in CT26 Cells

  • Wu, Wei-Qiang;Fauzee, Nilufer Jasmine Selimah;Wang, Ya-Lan
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권3호
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    • pp.991-994
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    • 2012
  • Objective: VEGF-C has recently been identified as a key molecule which is involved in tumor lymphangiogenesis. The aim of this research was to investigate the role of PARP-1 inhibition in the regulation of VEGF-C expression in CT26 cells. Methods: CT26 cells were treated with or without the PARP-1 inhibitor 5-aminoisoquinolinone (5-AIQ). The expression of PARP-1, NF-kB, and VEGF-C proteins in CT26 cells was measured by Western blot analysis and the VEGF-C mRNA level was determined by reverse transcription polymerase chain reaction (RT-PCR). CT26-secreted VEGF-C was detected by enzyme-linked immunosorbent assay (ELISA). Results: The results of Western blot analysis showed that the expression levels of PARP-1, NF-kB, and VEGF-C were reduced in 5-AIQ treated CT26 cells and the levels of VEGF-C mRNA in 5-AIQ treated CT26 were significantly lower than t in 5-AIQ-untreated cells (P<0.05). The concentrations of CT26-secreted VEGF-C were also dramatically decreased (P<0.05). Conclusion: Here, we provide evidence for the first time that PARP-1 inhibition dramatically reduces VEGF-C expression via the nuclear factor NF-kB signaling pathway. We therefore propose that PARP-1 inhibition has an anti-lymphangiogenic effect and may contribute to the prevention of metastatic dissemination via the lymphatic system.

온열요법이 면역활성의 변화에 미치는 효과 (Effects of the Heat Therapy on Changes of Immune Activities in Human Body)

  • 이상빈
    • 한국콘텐츠학회논문지
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    • 제9권1호
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    • pp.285-292
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    • 2009
  • 본 연구는 온열요법, 그 중 습열(moist heat)과 건열(dry heat)의 적용이 면역 활성의 변동에 미치는 효과를 알아보기 위한 것이다. 건강에 이상이 없는 연령 23${\sim}$32세, 신장 171.0${\pm}$1.2cm, 체중 68.0${\pm}$2.2kg의 남성 15명과 연령 22${\sim}$24세, 신장 159.5${\pm}$1.2cm, 체중 54.6${\pm}$2.4kg의 여성 15명을 대상으로 인체에 온열침수 (핫팩(KRS 12P, Karis Co., Korea))와 적외선 (발광 적외선등(Infrared, Ilshin Co., Korea))을 적용하여 보체와 같은 면역-활성 물질의 추이를 살펴보았다. 연구의 결과로써, 온열침수와 적외선을 적용한 결과 온열침수와 적외선 적용으로 보체 성분의 변동은 온열침수 적용으로 C1q의 유의한 감소와 C3(여성의 경우) 및 C4의 감소가 나타남을 확인할 수 있었다. 그러나 적외선의 경우 C1q와 C3 및 C4의 증감에 별다른 영향을 미치지 못하였다. 이러한 연구의 결과로 미루어 온열침수의 적용으로 보체계의 활성을 확인할 수 있었으며 이러한 면역-활성의 증가는 선택적 경로(alternative pathway)가 아닌 고전적 경로(classical pathway)를 통해 이루어짐을 추정할 수 있었다. 따라서 본 연구의 결과는 극히 부분적 결과를 나타내지만, 온열침수와 적외선 적용으로 면역-증강효과가 다소 존재하는 것으로 사료된다.

문주란의 모발 성장기 유도 기전 (The Mechanism of Crinum asiaticum var. japonicum on the Activation of Anagen)

  • 강정일;최주환;이종건;유은숙;김영호;강희경
    • 생약학회지
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    • 제48권2호
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    • pp.148-154
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    • 2017
  • Crinum asiaticum var. japonicum and its active component, norgalanthamine have been reported to have hair growth-promoting effect via the proliferation of dermal papilla cells. In this study, we investigated the other mechanisms of C. asiaticum extract var. japonicum and norgalanthamine on the hair growth. The C. asiaticum var. japonicum extract inhibited $5{\alpha}$-reductase activity by 16%, which converts testosterone to dihydrotestosterone (DHT), a main cause of androgenetic alopecia, whereas the C. asiaticum var. japonicum extract didn't function as an opener of the $K_{ATP}$ channel. On the other hand, we examined whether norgalanthamine can inhibit transforming growth factor-${\beta}$ (TGF-${\beta}$) signal pathway, which is essential in the regression induction of hair growth. Norgalanthamine inhibited the phosphorylation of Smad2/3 on TGF-${\beta}1$-induced canonical pathway in human keratinocyte HaCaT cells. These results suggested that the C. asiaticum var. japonicum extract and norgalanthamine had the potential to influence hair growth through the inhibition of $5{\alpha}$-reductase activity and TGF-${\beta}1$-induced canonical pathway.

C3 신염의 병리 (Pathology of C3 Glomerulonephritis)

  • 김용진
    • Childhood Kidney Diseases
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    • 제17권1호
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    • pp.1-5
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    • 2013
  • 사구체에 면역글로불린은 음성이면서 C3 만 침착되는 경우, 다른 원인이 없는 경우 C3GN을 의심하여야 한다. 광학현미경으로는 세포의 증식이 있는 경우와 없는 경우가 있지만, 전자현미경으로는 EDD가 내피세포 밑으로 혹은 메산지움 등에 침착함을 확인하여야 한다. 대체보체경로의 조절이상이 원인임으로 혈청 C3 치를 비롯하여 CFH, CFI, CFB 등을 측정하여야 하며, C3 nephritic factor, anti-factor H 자가항체 등을 조사하는 것이 필요하다. 보체 조절이상을 일으키는 유전자 돌연변이를 조사해 보아야 한다. 예후는 안정적이지만, 치료는 대증적이다. 이론적으로 보체의 활성화를 저지하는 약으로 가능할 것으로 생각되며, C5 항체인 eculizumab으로 치유된 보고도 있다.

C형 간염 바이러스 NS5B 단백질과 숙주의 p48 단백질의 상호작용에 의한 인터페론 저항성의 유도 (An Interferon Resistance Induced by the Interaction between HCV NS5B and Host p48)

  • 박소연;이종호;명희준
    • 한국미생물·생명공학회지
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    • 제36권4호
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    • pp.353-359
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    • 2008
  • Hepatitis C virus (HCV) is known as the causative agent of blood transmitted hepatitis. Two viral proteins, E2 and NS5A, are known to exert interferon resistance of HCV via PKR pathway. Here, we report a third protein, the RNA-dependent RNA polymerase (NS5B) of HCV, induced interferon resistance inhibiting p56 pathway. p56 was shown to interact with p48 subunit of eukaryotic initiation factor 3 (eIF3). This interaction inhibited formation of ternary complex in translation initiation. Using dual reporter assay system, we observed that the translation decreased when interferon alpha was added to the culture. But, in the presence of HCV NS5B, the translation partly recovered. NS5B and p48 subunit of eIF3 were shown to interact. This interaction seems to inhibit the interaction between p48 and p56. This is the first report that a virus exerts interferon resistance via p56 pathway.

비만세포에서 Histamine유리에 관여하는 Phospholipase $A_2$의 작용 (Action of Phospholipase $A_2$in Histamine Release from Mast Cells)

  • 이윤혜;이승준;서무현;장용운;윤정이
    • 약학회지
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    • 제45권3호
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    • pp.287-292
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    • 2001
  • To investigate whether phospholipase $A_2$pathway is involved in histamine release of rat peritoneal mast cells, we measured histamine release in the presence of various enzyme inhibitors involved in eicosanoid pathway, such as phospholipase $A_2$, cyclooxygenase and lipoxygenase. Phospholipase $A_2$inhibitors, manoalide and OPC, significantly inhibited histamine release induced by 100 $\mu$M ATP and 1$\mu$g/ml compound 48/80. Cyclooxygenase inhibitors, ibuprofen and indomethacin, significantly inhibited ATP-induced histamine release and lipoxygenase inhibitors, baicalein and caffeic acid, also significantly inhibited. To investigate the involvement of protein kinase in ATP- and compound 48/80-induced histamine release, we observed effects of protein kinase inhibitors on histamine release. Bisindolmaleimide (protein kinase C antagonist) dose-dependently inhibited both ATP and compound 48/80-induced histamine release. Tyrosine kinase inhibitors (methyl 2,5-dihydroxy cinnamate and genistein) dose-dependently inhibited ATP and compound 48/80-induced histamine release. Protein kinase C and tyrosine kinase seem to be involved in histamine release induced by ATP and compound 48/80. These results suggest that phospholipase $A_2$pathway as well as protein kinase C and tyrosine kinase are involved in histamine release of rat peritoneal mast cells by ATP and compound 48/80.

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Role of Nitric Oxide in Pepsinogen Secretion from Rat Gastric Chief Cells

  • Sung, Dae-Suk;Seo, Dong-Wan;Choi, Don-Woong;Ahn, Seong-Hoon;Hong, Sung-Youl;Lee, Hoi-Young;Han, Jeung-Whan;Lee, Hyang-Woo
    • Biomolecules & Therapeutics
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    • 제7권2호
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    • pp.105-111
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    • 1999
  • Nitric oxide (NO), a cellular messenger synthesized from L-arginine by NO synthase (NOS, EC.1.14.13.39), is considered to be a regulator of gastric secretion. In the present study, the role of NO in the regulation of exocrine secretion was investigated in rat gastric chief cells. Treatment of chief cells with carba-chol resulted in an increase in the arginine conversion to citrulline, the amount of $NO_{x}$, the release of pepsine-gen, and the level of cGMP Especially, carbachol-stimulated increase of arginine to citrulline transformation, the amount of $NO_{x}$, cGMP level and the release of pepsinogen were partially reduced by the natural NOS inhibitor, $N^{G}$-monomethyl-L-arginine (MMA) and $N^{G}$, $N^{G}$-dimethyl-L-arginine (DMA). Furthermore, MMA- and DMA-induced decrease of pepsinogen secretion showed dose-dependent patters. Activation of NOS is one of the early events in receptor-mediated cascade of reactions in gastric chief cells and NO, not completely, but partially mediates gastric secretion. Agonist-stimulated pepsinogen secretion in chief cells has been considered to be mediated in adenosine 3',5'-cyclic monophosphate pathway and/or guanosine 3', 5'-cyclic monophosphate (cGMP) pathway. Taken together, the above results suggest that partial decrease of exocrine secretion following treatment of NOS inhibitor may result from the inactivation of NOS and subsequent guano- late cyclase, and NO/cGMP pathway may play a pivotal role in exocrine secretion.

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