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      KCI등재 SCOPUS SCIE

      Growth Differentiation Factor 15 Expression in Astrocytes After Excitotoxic Lesion in the Mouse Hippocampus

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      https://www.riss.kr/link?id=A104152382

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      다국어 초록 (Multilingual Abstract)

      Growth differentiation factor 15 (GDF15) is, a member of the transforming growth factor β (TGF-β) superfamily of proteins. Although GDF15 is well established as a potent neurotrophic factor for neurons, little is known about its role in glial cells under neuropathological conditions. We monitored GDF15 expression in astrocyte activation after a kainic acid (KA)-induced neurodegeneration in the ICR mice hippocampus. In control, GDF15 immunoreactivity (IR) was evident in the neuronal layer of the hippocampus; however, GDF15 expression had increased in activated astrocytes throughout the hippocampal region at day 3 after the treatment with KA. LPS treatment in astrocytes dramatically increased GDF15 expression in primary astrocytes. In addition, LPS treatment resulted in the decrease of the IκB-α degradation and increase of the phosphorylation level of RelA/p65. These results indicate that GDF15 has a potential link to NF-κB activation, making GDF15 a valuable target for modulating inflammatory conditions.
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      Growth differentiation factor 15 (GDF15) is, a member of the transforming growth factor β (TGF-β) superfamily of proteins. Although GDF15 is well established as a potent neurotrophic factor for neurons, little is known about its role in glial cells ...

      Growth differentiation factor 15 (GDF15) is, a member of the transforming growth factor β (TGF-β) superfamily of proteins. Although GDF15 is well established as a potent neurotrophic factor for neurons, little is known about its role in glial cells under neuropathological conditions. We monitored GDF15 expression in astrocyte activation after a kainic acid (KA)-induced neurodegeneration in the ICR mice hippocampus. In control, GDF15 immunoreactivity (IR) was evident in the neuronal layer of the hippocampus; however, GDF15 expression had increased in activated astrocytes throughout the hippocampal region at day 3 after the treatment with KA. LPS treatment in astrocytes dramatically increased GDF15 expression in primary astrocytes. In addition, LPS treatment resulted in the decrease of the IκB-α degradation and increase of the phosphorylation level of RelA/p65. These results indicate that GDF15 has a potential link to NF-κB activation, making GDF15 a valuable target for modulating inflammatory conditions.

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      참고문헌 (Reference)

      1 Laureys G, "beta(2)-adrenergic agonists modulate TNF-alpha induced astrocytic inflammatory gene expression and brain inflammatory cell populations" 11 : 21-, 2014

      2 Jarrard LE, "Use of excitotoxins to lesion the hippocampus:update" 12 : 405-414, 2002

      3 Unsicker K, "The multiple facets of the TGF-beta family cytokine growth/differentiation factor-15/macrophage inhibitory cytokine-1" 24 : 373-384, 2013

      4 Heiss WD, "The ischemic penumbra: how does tissue injury evolve?" 1268 : 26-34, 2012

      5 Iadecola C, "The immunology of stroke:from mechanisms to translation" 17 : 796-808, 2011

      6 Ransohoff RM, "The anatomical and cellular basis of immune surveillance in the central nervous system" 12 : 623-635, 2012

      7 Doyle KP, "TGFbeta signaling in the brain increases with aging and signals to astrocytes and innate immune cells in the weeks after stroke" 7 : 62-, 2010

      8 Finch CE, "TGF-beta 1 is an organizer of responses to neurodegeneration" 53 : 314-322, 1993

      9 Yi MH, "RhoGDI2 Expression in Astrocytes After an Excitotoxic Lesion in the Mouse Hippocampus" 2014

      10 Schindowski K, "Regulation of GDF-15, a distant TGF-beta superfamily member, in a mouse model of cerebral ischemia" 343 : 399-409, 2011

      1 Laureys G, "beta(2)-adrenergic agonists modulate TNF-alpha induced astrocytic inflammatory gene expression and brain inflammatory cell populations" 11 : 21-, 2014

      2 Jarrard LE, "Use of excitotoxins to lesion the hippocampus:update" 12 : 405-414, 2002

      3 Unsicker K, "The multiple facets of the TGF-beta family cytokine growth/differentiation factor-15/macrophage inhibitory cytokine-1" 24 : 373-384, 2013

      4 Heiss WD, "The ischemic penumbra: how does tissue injury evolve?" 1268 : 26-34, 2012

      5 Iadecola C, "The immunology of stroke:from mechanisms to translation" 17 : 796-808, 2011

      6 Ransohoff RM, "The anatomical and cellular basis of immune surveillance in the central nervous system" 12 : 623-635, 2012

      7 Doyle KP, "TGFbeta signaling in the brain increases with aging and signals to astrocytes and innate immune cells in the weeks after stroke" 7 : 62-, 2010

      8 Finch CE, "TGF-beta 1 is an organizer of responses to neurodegeneration" 53 : 314-322, 1993

      9 Yi MH, "RhoGDI2 Expression in Astrocytes After an Excitotoxic Lesion in the Mouse Hippocampus" 2014

      10 Schindowski K, "Regulation of GDF-15, a distant TGF-beta superfamily member, in a mouse model of cerebral ischemia" 343 : 399-409, 2011

      11 Strelau J, "Progressive postnatal motoneuron loss in mice lacking GDF-15" 29 : 13640-13648, 2009

      12 Yoshioka H, "Nonsteroidal anti-inflammatory drug-activated gene (NAG-1/GDF15) expression is increased by the histone deacetylase inhibitor trichostatin A" 283 : 33129-33137, 2008

      13 Brown GC, "Nitric oxide and neuronal death" 23 : 153-165, 2010

      14 Yi MH, "NFAT5-dependent expression of AQP4in astrocytes" 33 : 223-232, 2013

      15 Bootcov MR, "MIC-1, a novel macrophage inhibitory cytokine, is a divergent member of the TGF-beta superfamily" 94 : 11514-11519, 1997

      16 Brambilla R, "Inhibition of astroglial nuclear factor kappaB reduces inflammation and improves functional recovery after spinal cord injury" 202 : 145-156, 2005

      17 Thompson WL, "Inflammatory cytokines stimulate the chemokines CCL2/MCP-1 and CCL7/MCP-3 through NFkB and MAPK dependent pathways in rat astrocytes" 1287 : 47-57, 2009

      18 Young-Sook Lee, "ID4 mediates proliferation of astrocytes after excitotoxic damage in the mouse hippocampus" 대한해부학회 44 (44): 128-134, 2011

      19 Strelau J, "Growth/differentiation factor-15/macrophage inhibitory cytokine-1 is a novel trophic factor for midbrain dopaminergic neurons in vivo" 20 : 8597-8603, 2000

      20 Subramaniam S, "Growth differentiation factor-15 prevents low potassium-induced cell death of cerebellar granule neurons by differential regulation of Akt and ERK pathways" 278 : 8904-8912, 2003

      21 Meldrum BS, "Glutamate as a neurotransmitter in the brain: review of physiology and pathology" 130 : 1007S-1015S, 2000

      22 Wanner IB, "Glial scar borders are formed by newly proliferated, elongated astrocytes that interact to corral inflammatory and fibrotic cells via STAT3-dependent mechanisms after spinal cord injury" 33 : 12870-12886, 2013

      23 Zamanian JL, "Genomic analysis of reactive astrogliosis" 32 : 6391-6410, 2012

      24 Choi K, "Fas ligation and tumor necrosis factor alpha activation of murine astrocytes promote heat shock factor-1 activation and heat shock protein expression leading to chemokine induction and cell survival" 116 : 438-448, 2011

      25 Schober A, "Expression of growth differentiation factor-15/ macrophage inhibitory cytokine-1 (GDF-15/MIC-1) in the perinatal, adult, and injured rat brain" 439 : 32-45, 2001

      26 Yi MH, "Expression of CD200 in alternative activation of microglia following an excitotoxic lesion in the mouse hippocampus" 1481 : 90-96, 2012

      27 Baek SJ, "Cyclooxygenase inhibitors regulate the expression of a TGF-beta superfamily member that has proapoptotic and antitumorigenic activities" 59 : 901-908, 2001

      28 Babcock AA, "Chemokine expression by glial cells directs leukocytes to sites of axonal injury in the CNS" 23 : 7922-7930, 2003

      29 Faherty CJ, "Caspase-3-dependent neuronal death in the hippocampus following kainic acid treatment" 70 : 159-163, 1999

      30 Cortes-Canteli M, "CCAAT/enhancer binding protein beta deficiency provides cerebral protection following excitotoxic injury" 121 : 1224-1234, 2008

      31 Cekanaviciute E, "Astrocytic transforming growth factorbeta signaling reduces subacute neuroinflammation after stroke in mice" 62 : 1227-1240, 2014

      32 Cekanaviciute E, "Astrocytic TGF-beta signaling limits inflammation and reduces neuronal damage during central nervous system Toxoplasma infection" 193 : 139-149, 2014

      33 Pineau I, "Astrocytes initiate inflammation in the injured mouse spinal cord by promoting the entry of neutrophils and inflammatory monocytes in an IL-1 receptor/MyD88-dependent fashion" 24 : 540-553, 2010

      34 Farina C, "Astrocytes are active players in cerebral innate immunity" 28 : 138-145, 2007

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      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2015-01-01 평가 등재학술지 선정 (계속평가) KCI등재
      2013-01-01 평가 등재후보 1차 FAIL (등재후보1차) KCI등재후보
      2012-01-01 평가 등재후보학술지 유지 (기타) KCI등재후보
      2010-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.25 0.25 0.22
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.2 0.19 0.459 0.05
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