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      KCI등재 SCOPUS SCIE

      Effect of Diesel Exhaust Particles (DEP) on the Activity of Phospholipase D (PLD) in RAW 264.7 Cells

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      https://www.riss.kr/link?id=A75919965

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      다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

      Diesel exhausted particles (DEP), a kind of fine particles with aerodynamic diameters less than 2.5 ㎛ (PM2.5), is of great concern to human health because they remain in atmosphere for long periods, invade an indoor air environment, and can be breathed most deeply into lung and reached the alveoli because of their small size (0.1~0.4 ㎛ in diameter). Epidemiological and experimental studies suggested that DEP may play an active role in the increased respiratory mortality and morbidity. In addition to their physical characteristics, the chemical components including polyaromatic hydrocarbon (PAH) are regarded as a carcinogen causing pulmonary tumors. PLD plays an important role in cell proliferation with various physiological phenomena and affects other enzymes by activating signal transduction pathway. We investigated the cytotoxic mechanism of DEP on RAW 264.7 cells focusing on the role in activation of PLD. Our results suggested DEP induced PLD activity through a specific signaling pathway involving phospholipase A₂, PLC, PKC and Ca<SUP>2+</SUP> mobilization.
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      Diesel exhausted particles (DEP), a kind of fine particles with aerodynamic diameters less than 2.5 ㎛ (PM2.5), is of great concern to human health because they remain in atmosphere for long periods, invade an indoor air environment, and can be breat...

      Diesel exhausted particles (DEP), a kind of fine particles with aerodynamic diameters less than 2.5 ㎛ (PM2.5), is of great concern to human health because they remain in atmosphere for long periods, invade an indoor air environment, and can be breathed most deeply into lung and reached the alveoli because of their small size (0.1~0.4 ㎛ in diameter). Epidemiological and experimental studies suggested that DEP may play an active role in the increased respiratory mortality and morbidity. In addition to their physical characteristics, the chemical components including polyaromatic hydrocarbon (PAH) are regarded as a carcinogen causing pulmonary tumors. PLD plays an important role in cell proliferation with various physiological phenomena and affects other enzymes by activating signal transduction pathway. We investigated the cytotoxic mechanism of DEP on RAW 264.7 cells focusing on the role in activation of PLD. Our results suggested DEP induced PLD activity through a specific signaling pathway involving phospholipase A₂, PLC, PKC and Ca<SUP>2+</SUP> mobilization.

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      목차 (Table of Contents)

      • ABSTRACT
      • INTRODUCTION
      • MATERIALS AND METHODS
      • RESULT
      • DISCUSSION
      • ABSTRACT
      • INTRODUCTION
      • MATERIALS AND METHODS
      • RESULT
      • DISCUSSION
      • ACKNOWLEDGEMENTS
      • REFERENCES
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      참고문헌 (Reference)

      1 "a novel second messenger in cellular signal transduction" i (i): 315-321, 1984

      2 "Vascular smooth-muscle cells contain AT1 angiotensin receptors coupled to phospholipase D activation" 304 : 543-548, 1994

      3 "The relationship of daily mortality to suspended particulates in Santa Clara County" 59-168, 19901980~1986

      4 "The cytotoxic effects of diesel exhaust particles on human pulmonary artery endothelial cells in vitro: role of active oxygen species." 30 : 555-562, 2001

      5 "Role of calcium and protein kinase C in the activation of phospholipase D by angiotensin II in vascular smooth muscle cells" 319 : 84-92, 1995

      6 "Regulation of phospholipase D" 1439 : 121-133, 1999

      7 "Regulation of eukaryotic phosphatynositol-specific phospholipase C and phospholipase D" 66 : 475-509, 1997

      8 "Predictive models for deposition of inhaled diesel exhaust particles in humans and laboratory species" 3-22, 1987

      9 "Phospholipases and phagocytosis: the role of phospholipid-derived second messengers in phagocytosis." 31 : 415-430, 1999

      10 "Peroxynitrite formation by diesel exhaust particles in alveolar cells: Link to pulmonary inflammation." 9 : 1-8, 2000

      1 "a novel second messenger in cellular signal transduction" i (i): 315-321, 1984

      2 "Vascular smooth-muscle cells contain AT1 angiotensin receptors coupled to phospholipase D activation" 304 : 543-548, 1994

      3 "The relationship of daily mortality to suspended particulates in Santa Clara County" 59-168, 19901980~1986

      4 "The cytotoxic effects of diesel exhaust particles on human pulmonary artery endothelial cells in vitro: role of active oxygen species." 30 : 555-562, 2001

      5 "Role of calcium and protein kinase C in the activation of phospholipase D by angiotensin II in vascular smooth muscle cells" 319 : 84-92, 1995

      6 "Regulation of phospholipase D" 1439 : 121-133, 1999

      7 "Regulation of eukaryotic phosphatynositol-specific phospholipase C and phospholipase D" 66 : 475-509, 1997

      8 "Predictive models for deposition of inhaled diesel exhaust particles in humans and laboratory species" 3-22, 1987

      9 "Phospholipases and phagocytosis: the role of phospholipid-derived second messengers in phagocytosis." 31 : 415-430, 1999

      10 "Peroxynitrite formation by diesel exhaust particles in alveolar cells: Link to pulmonary inflammation." 9 : 1-8, 2000

      11 "Peribronchiolar fibrosis in lungs of cats chronically exposed to diesel exhaust" 1985195-206

      12 "Particulate matter in the atmosphere: which particle properties are important for its effects on health" 249 : 85-101, 2000

      13 "PM10 and PM2.5: An international perspective" 2000

      14 "Noninvasive detection of hydroxyl radical generation in lung by diesel exhaust particles" 30 : 516-525, 2001

      15 "Involvement of protein kinase C, phospholipase C, and protein tyrosine kinase pathways in oxygen radical generation by asbestos-stimulated alveolar macrophage" 105 : 1325-1327, 1997

      16 "Inositol phosphates and cell signalling" 341 : 197-205, 1989

      17 "Health effects of exposure to diesel exhaust particles" 279-300, 1987

      18 "Diesel exhaust particles up-regulate expression of intercellular adhension molecule-1 (ICAM-1) in human bronchial epithelial cells" 120 : 356-362, 2000

      19 "Calcium rather than protein kinase C is the major factor to activate phospholipase D in FMLP-stimulated rabbit peritoneal neutrophils" 149 : 622-628, 1992

      20 "Biological effects of diesel exhaust particles (DEP)." 21 : 199-209, 1996

      21 "Biological effects of diesel exhaust particles (DEP)." 99 : 153-167, 1995

      22 "Association of cytoplasmic free Ca2+ gradients with subcellular organelles" 593-609, 1992

      23 "Angiotensin II-induced phosphatidylcholine hydrolysis in cultured vascular smooth-muscle cells" 199119-25

      24 "An association between air pollution and mortality in six US cities New England Journal of Medicine" 1753-1759, 1993

      25 "Acute respiratory effects of particulate air pollution" 15 : 107-132, 1994

      26 "A long-term inhalation study evaluates the pulmonary effect of the diesel emission" 1983

      27 "(1989)Studies and prospectives of the protein kinase c family for cellular regulation" 63 : 1892-1903,

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2010-06-22 학술지명변경 외국어명 : Journal of Toxicology and Public Health -> Toxicological Research KCI등재
      2010-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2008-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2005-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2004-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2002-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.44 0.44 0.36
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.32 0.31 0.707 0.1
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