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1. Ricci-Vitiani L, Casalbore P, Petrucci G, Lauretti L, Montano N, Larocca LM, Falchetti ML, Lombardi DG, Gerevini VD, Cenciarelli C, D'Alessandris QG, Fernandez E, De Maria R, Maira G, Peschle C, Parati E, Pallini R: Influence of local environment on the differentiation of neural stem cells engrafted onto the injured spinal cord. Neurol Res; 2006 Jul;28(5):488-92
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  • [Title] Influence of local environment on the differentiation of neural stem cells engrafted onto the injured spinal cord.
  • These features make NSCs suitable for spinal cord (SC) reconstruction.
  • However, in vivo experiments have demonstrated that in the injured SC transplanted NSCs either remain undifferentiated or differentiate into the astrocytic phenotype.
  • METHODS: As the first step, we used immunohistochemistry to analyse the expression of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta and interferon (IFN)-gamma in the normal SC of mice and following traumatic injury.
  • In culture, exposure of proliferating NSCs to a combination of TNF-alpha, IL-1beta and IFN-gamma was per se sufficient to induce the astrocytic differentiation of these cells even in the absence of serum.
  • CONCLUSIONS: In the traumatically injured SC, differentiation of engrafted NSCs is restricted towards the astrocytic lineage because of the inflammatory environment.
  • [MeSH-major] Cytokines / metabolism. Neurons / transplantation. Spinal Cord Injuries / therapy. Stem Cell Transplantation
  • [MeSH-minor] Animals. Astrocytes / cytology. Astrocytes / drug effects. Cell Differentiation / drug effects. Cell Differentiation / physiology. Female. Immunohistochemistry. Interferon-gamma / metabolism. Interferon-gamma / pharmacology. Interleukin-1 / metabolism. Interleukin-1 / pharmacology. Mice. Tumor Necrosis Factor-alpha / metabolism. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16808877.001).
  • [ISSN] 0161-6412
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / Interleukin-1; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma
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2. Giraud SN, Caron CM, Pham-Dinh D, Kitabgi P, Nicot AB: Estradiol inhibits ongoing autoimmune neuroinflammation and NFkappaB-dependent CCL2 expression in reactive astrocytes. Proc Natl Acad Sci U S A; 2010 May 4;107(18):8416-21
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  • The use of estrogens as potential anti-inflammatory and neuroprotective drugs is a matter of debate.
  • Using mouse experimental allergic encephalomyelitis (EAE) as a model of chronic neuroinflammation, we report that implants reproducing pregnancy levels of 17beta-estradiol (E2) alleviate ongoing disease and decrease astrocytic production of CCL2, a proinflammatory chemokine that drives the local recruitment of inflammatory myeloid cells.
  • Immunohistochemistry and confocal imaging reveal that, in spinal cord white matter EAE lesions, reactive astrocytes express estrogen receptor (ER)alpha (and to a lesser extent ERbeta) with a preferential nuclear localization, whereas other cells including infiltrated leukocytes express ERs only in their membranes or cytosol.
  • These data uncover reactive astrocytes as an important target for nuclear ERalpha inhibitory action on chemokine expression and suggest that targeting astrocytic nuclear NFkappaB activation with estrogen receptor alpha modulators may improve therapies of chronic neurodegenerative disorders involving astroglial neuroinflammation.
  • [MeSH-minor] Active Transport, Cell Nucleus. Animals. Cells, Cultured. Estrogen Receptor alpha / metabolism. Estrogen Receptor beta / metabolism. Female. Leukocytes / metabolism. Mice. Mice, Inbred C57BL. Rats. Spinal Cord / metabolism. Transcription, Genetic. Tumor Necrosis Factor-alpha / metabolism

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  • [Cites] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9614-9 [12878732.001]
  • [Cites] Exp Gerontol. 2007 Jan-Feb;42(1-2):70-5 [16872778.001]
  • [Cites] J Immunol. 2003 Dec 15;171(12):6936-40 [14662901.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Apr 3;104(14):6013-8 [17389368.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Sep 11;104(37):14813-8 [17785421.001]
  • [Cites] J Cell Physiol. 2008 Feb;214(2):456-64 [17654501.001]
  • [Cites] Mol Endocrinol. 2008 Feb;22(2):263-72 [17932106.001]
  • [Cites] J Neuroinflammation. 2008;5:6 [18237444.001]
  • [Cites] Glia. 2008 Apr 15;56(6):659-74 [18286612.001]
  • [Cites] Nat Chem Biol. 2008 Apr;4(4):241-7 [18344977.001]
  • [Cites] J Endocrinol. 2008 Jul;198(1):219-30 [18460549.001]
  • [Cites] Neuron. 2008 Nov 6;60(3):430-40 [18995817.001]
  • [Cites] J Immunol. 2009 Mar 1;182(5):2628-40 [19234157.001]
  • [Cites] J Immunol. 2009 Mar 1;182(5):3294-303 [19234228.001]
  • [Cites] Cell. 2009 Apr 3;137(1):26-8 [19345183.001]
  • [Cites] Glia. 2009 May;57(7):777-90 [19031437.001]
  • [Cites] Brain. 2009 Sep;132(Pt 9):2487-500 [19531531.001]
  • [Cites] J Neuroimmunol. 2009 Sep 29;214(1-2):67-77 [19664827.001]
  • [Cites] Lab Invest. 2009 Oct;89(10):1076-83 [19668239.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 23;101(12):4130-5 [15024130.001]
  • [Cites] J Immunol. 2004 Aug 15;173(4):2435-42 [15294957.001]
  • [Cites] FASEB J. 1993 Apr 1;7(6):592-600 [8472896.001]
  • [Cites] Blood. 1997 Aug 1;90(3):909-28 [9242519.001]
  • [Cites] Am J Pathol. 1999 Jan;154(1):45-51 [9916917.001]
  • [Cites] Neurology. 1999 Apr 12;52(6):1230-8 [10214749.001]
  • [Cites] Endocr Rev. 1999 Aug;20(4):435-59 [10453354.001]
  • [Cites] J Neurosci Res. 2004 Dec 1;78(5):603-24 [15515048.001]
  • [Cites] Am J Pathol. 2004 Dec;165(6):2069-77 [15579449.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2005 Feb;76(2):272-5 [15654051.001]
  • [Cites] Am J Pathol. 1999 Nov;155(5):1433-8 [10550297.001]
  • [Cites] J Neurosci. 2000 Jan 1;20(1):401-8 [10627616.001]
  • [Cites] J Neuroimmunol. 2000 Aug 1;108(1-2):192-200 [10900353.001]
  • [Cites] J Exp Med. 2000 Sep 18;192(6):899-905 [10993920.001]
  • [Cites] J Immunol. 2001 Feb 1;166(3):2080-9 [11160259.001]
  • [Cites] J Comp Neurol. 2001 Apr 23;433(1):115-23 [11283953.001]
  • [Cites] Cell Tissue Res. 2001 May;304(2):193-214 [11396714.001]
  • [Cites] Science. 2001 Nov 23;294(5547):1731-5 [11721059.001]
  • [Cites] Oncogene. 2002 May 16;21(22):3603-10 [12032862.001]
  • [Cites] J Comp Neurol. 2002 Aug 26;450(3):256-71 [12209854.001]
  • [Cites] Ann Neurol. 2002 Oct;52(4):421-8 [12325070.001]
  • [Cites] J Neurosci. 2002 Dec 15;22(24):10633-42 [12486156.001]
  • [Cites] J Immunol. 2003 Feb 1;170(3):1548-55 [12538720.001]
  • [Cites] Neuron. 2003 Jun 5;38(5):685-8 [12797954.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Feb 15;102(7):2543-8 [15699342.001]
  • [Cites] Mol Cell Biol. 2005 Apr;25(8):2957-68 [15798185.001]
  • [Cites] J Immunol. 2003 Dec 1;171(11):6267-74 [14634144.001]
  • (PMID = 20404154.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ccl2 protein, mouse; 0 / Chemokine CCL2; 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta; 0 / NF-kappa B; 0 / Tumor Necrosis Factor-alpha; 4TI98Z838E / Estradiol
  • [Other-IDs] NLM/ PMC2889572
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3. Maria BL, Gupta N, Gilg AG, Abdel-Wahab M, Leonard AP, Slomiany M, Wheeler WG, Tolliver LB, Babcock MA, Lucas JT Jr, Toole BP: Targeting hyaluronan interactions in spinal cord astrocytomas and diffuse pontine gliomas. J Child Neurol; 2008 Oct;23(10):1214-20
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  • [Title] Targeting hyaluronan interactions in spinal cord astrocytomas and diffuse pontine gliomas.
  • Although significant advances have been made in treating malignant pediatric central nervous system tumors such as medulloblastoma, no effective therapy exists for diffuse pontine glioma or intramedullary spinal astrocytoma.
  • Biology of these 2 tumors is poorly understood, in part because diffuse pontine gliomas are not treated surgically, and tumor specimens from intramedullary spinal astrocytomas are rare and minuscule.
  • We review the clinical course of pediatric intramedullary spinal astrocytoma and diffuse pontine glioma, and show expression of membrane proteins that interact with hyaluronan: CD44, extracellular matrix metalloproteinase inducer, and breast cancer resistance protein (BCRP/ABCG2).
  • [MeSH-major] Astrocytoma / metabolism. Brain Stem Neoplasms / metabolism. Glioma / metabolism. Hyaluronic Acid / metabolism. Spinal Cord Neoplasms / metabolism
  • [MeSH-minor] ATP Binding Cassette Transporter, Sub-Family G, Member 2. ATP-Binding Cassette Transporters / genetics. ATP-Binding Cassette Transporters / metabolism. Animals. Basigin / genetics. Basigin / metabolism. Child. Disease Models, Animal. Drug Resistance, Neoplasm / genetics. Humans. Hyaluronan Receptors / genetics. Hyaluronan Receptors / metabolism. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Rats

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  • [Cites] J Neurosurg. 1998 Feb;88(2):215-20 [9452226.001]
  • [Cites] Clin Cancer Res. 2008 Mar 15;14(6):1804-13 [18347183.001]
  • [Cites] N Engl J Med. 2005 Jul 14;353(2):172-87 [16014887.001]
  • [Cites] Oncogene. 2005 Nov 14;24(50):7482-92 [16288295.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2006 Mar 15;64(4):1060-71 [16373081.001]
  • [Cites] Nature. 2006 Dec 7;444(7120):756-60 [17051156.001]
  • [Cites] Biochem Biophys Res Commun. 2007 Apr 20;355(4):855-9 [17307142.001]
  • [Cites] Br J Cancer. 1999 Nov;81(5):835-40 [10555754.001]
  • [Cites] Int J Cancer. 2000 Oct 1;88(1):21-7 [10962435.001]
  • [Cites] Am J Pathol. 2001 Jun;158(6):1921-8 [11395366.001]
  • [Cites] J Surg Oncol. 2002 Jan;79(1):30-5; discussion 35-6 [11754374.001]
  • [Cites] J Neurooncol. 2002 Nov;60(2):127-34 [12635659.001]
  • [Cites] Am J Pathol. 2003 May;162(5):1403-9 [12707023.001]
  • [Cites] Cancer Res. 2004 Feb 15;64(4):1229-32 [14983875.001]
  • [Cites] Int J Biochem Cell Biol. 2004 Jun;36(6):1046-69 [15094120.001]
  • [Cites] Nat Rev Cancer. 2004 Jul;4(7):528-39 [15229478.001]
  • [Cites] Eur J Cancer. 1993;29A(7):1012-7 [7684596.001]
  • [Cites] Cancer Res. 1995 Jan 15;55(2):434-9 [7812975.001]
  • [Cites] Int J Cancer. 1996 Apr 10;66(2):255-60 [8603821.001]
  • [Cites] J Pathol. 1997 Apr;181(4):434-8 [9196442.001]
  • [Cites] Glia. 1997 Jul;20(3):193-202 [9215728.001]
  • [Cites] Regen Med. 2006 Jul;1(4):437-45 [17465836.001]
  • [Cites] Nat Rev Cancer. 2005 Apr;5(4):275-84 [15803154.001]
  • (PMID = 18952588.001).
  • [ISSN] 1708-8283
  • [Journal-full-title] Journal of child neurology
  • [ISO-abbreviation] J. Child Neurol.
  • [Language] eng
  • [Grant] United States / NINDS NIH HHS / NS / R13 NS040925; United States / NCI NIH HHS / CA / R01 CA073839; United States / NINDS NIH HHS / NS / 5R13NS040925-09; United States / NCRR NIH HHS / RR / C06RR015455; United States / NCI NIH HHS / CA / R01 CA082867; United States / NCI NIH HHS / CA / CA073839; United States / NCRR NIH HHS / RR / C06 RR015455; United States / NCI NIH HHS / CA / CA082867
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / ATP Binding Cassette Transporter, Sub-Family G, Member 2; 0 / ATP-Binding Cassette Transporters; 0 / BSG protein, human; 0 / Hyaluronan Receptors; 0 / Neoplasm Proteins; 136894-56-9 / Basigin; 9004-61-9 / Hyaluronic Acid
  • [Number-of-references] 23
  • [Other-IDs] NLM/ NIHMS463105; NLM/ PMC3641563
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4. Marchan EM, Sekula RF Jr, Jannetta PJ, Quigley MR: Long-term survival enhanced by cordectomy in a patient with a spinal glioblastoma multiforme and paraplegia. Case report. J Neurosurg Spine; 2007 Dec;7(6):656-9
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  • [Title] Long-term survival enhanced by cordectomy in a patient with a spinal glioblastoma multiforme and paraplegia. Case report.
  • Spinal glioblastomas multiforme (GBMs) are rare lesions of the central nervous system with a prognosis as poor as that of their intracranial counterpart.
  • The authors present a case of a 50-year-old man with a GBM of the spinal cord treated with surgical removal of the mass and cordectomy after the onset of paraplegia.
  • Although intracranial dissemination of spinal GBMs has been reported, this case illustrates the longest reported interval between the occurrence of a spinal GBM and its intracranial dissemination.
  • Thus, cordectomy should be considered as a reasonable alternative in patients with complete loss of neurological function at and below the level where they harbor a malignant spinal cord astrocytoma.
  • [MeSH-major] Glioblastoma / complications. Glioblastoma / surgery. Neurosurgical Procedures. Paraplegia / etiology. Spinal Cord Neoplasms / complications. Spinal Cord Neoplasms / surgery
  • [MeSH-minor] Antiviral Agents / therapeutic use. Cerebellar Neoplasms / secondary. Fatal Outcome. Hepatitis C / complications. Hepatitis C / drug therapy. Humans. Interferon-alpha / therapeutic use. Magnetic Resonance Imaging. Male. Middle Aged. Polyethylene Glycols. Recombinant Proteins. Spinal Cord / surgery. Survival Analysis

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  • (PMID = 18074692.001).
  • [ISSN] 1547-5654
  • [Journal-full-title] Journal of neurosurgery. Spine
  • [ISO-abbreviation] J Neurosurg Spine
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Interferon-alpha; 0 / Recombinant Proteins; 0 / peginterferon alfa-2b; 30IQX730WE / Polyethylene Glycols; 99210-65-8 / interferon alfa-2b
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5. Winkelstein BA, Rutkowski MD, Sweitzer SM, Pahl JL, DeLeo JA: Nerve injury proximal or distal to the DRG induces similar spinal glial activation and selective cytokine expression but differential behavioral responses to pharmacologic treatment. J Comp Neurol; 2001 Oct 15;439(2):127-39
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  • [Title] Nerve injury proximal or distal to the DRG induces similar spinal glial activation and selective cytokine expression but differential behavioral responses to pharmacologic treatment.
  • This study investigated the role of injury site relative to the DRG in (1) eliciting behavioral responses, (2) inducing spinal neuroimmune activation, and (3) responding to pharmacologic interventions.
  • Rats received either an L5 spinal nerve transection distal to the DRG or an L5 nerve root injury proximal to the DRG.
  • Comparative studies assessed behavioral nociceptive responses, spinal cytokine mRNA and protein expression, and glial activation after injury.
  • In separate studies, intrathecal pharmacologic interventions by using selective cytokine antagonists (interleukin-1 [IL-1] receptor antagonist and soluble tumor necrosis factor [TNF] receptor) and a global immunosuppressant (leflunomide) were performed to determine their relative effectiveness in these injury paradigms.
  • Spinal IL-1beta, IL-6, IL-10, and TNF mRNA and IL-6 protein were significantly elevated in both injuries.
  • The degree of microglial and astrocytic activation in the L5 spinal cord was also similar for both injuries.
  • In contrast, the pharmacologic treatments were more effective in alleviating mechanical allodynia for peripheral nerve injury than nerve root injury, suggesting that nerve root injury elicits a more robust, centrally mediated response than peripheral nerve injury.
  • [MeSH-major] Antigens, CD. Antigens, Neoplasm. Antigens, Surface. Avian Proteins. Blood Proteins. Cytokines / metabolism. Ganglia, Spinal / injuries. Gliosis / metabolism. Neuroglia / metabolism. Pain / physiopathology. Peripheral Nervous System Diseases / metabolism. Spinal Cord / metabolism
  • [MeSH-minor] Animals. Antigens, CD147. Disease Models, Animal. Dose-Response Relationship, Drug. Glial Fibrillary Acidic Protein / metabolism. Hyperalgesia / etiology. Hyperalgesia / metabolism. Hyperalgesia / physiopathology. Immunohistochemistry. Interleukin 1 Receptor Antagonist Protein. Interleukin-1 / genetics. Interleukin-1 / metabolism. Interleukin-10 / genetics. Interleukin-10 / metabolism. Interleukin-6 / genetics. Interleukin-6 / metabolism. Lumbar Vertebrae. Male. Membrane Glycoproteins / metabolism. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Receptors, Tumor Necrosis Factor / therapeutic use. Sialoglycoproteins / pharmacology. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • [Copyright] Copyright 2001 Wiley-Liss, Inc.
  • (PMID = 11596043.001).
  • [ISSN] 0021-9967
  • [Journal-full-title] The Journal of comparative neurology
  • [ISO-abbreviation] J. Comp. Neurol.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR44757; United States / NIDA NIH HHS / DA / DA05969; United States / NIDA NIH HHS / DA / DA11276
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antigens, Surface; 0 / Avian Proteins; 0 / Blood Proteins; 0 / Bsg protein, Gallus gallus; 0 / Bsg protein, rat; 0 / Cytokines; 0 / Glial Fibrillary Acidic Protein; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Interleukin-1; 0 / Interleukin-6; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / Receptors, Tumor Necrosis Factor; 0 / Sialoglycoproteins; 0 / Tumor Necrosis Factor-alpha; 130068-27-8 / Interleukin-10; 136894-56-9 / Antigens, CD147
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6. Sweitzer S, Martin D, DeLeo JA: Intrathecal interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor exhibits an anti-allodynic action in a rat model of neuropathic pain. Neuroscience; 2001;103(2):529-39
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  • [Title] Intrathecal interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor exhibits an anti-allodynic action in a rat model of neuropathic pain.
  • The expression of interleukin-1beta and tumor necrosis factor has previously been shown to be up-regulated in the spinal cord of several rat mononeuropathy models.
  • This present study was undertaken to determine whether blocking the action of central interleukin-1beta and tumor necrosis factor attenuates mechanical allodynia in a gender-specific manner in a rodent L5 spinal nerve transection model of neuropathic pain, and whether this inhibition occurs via down-regulation of the central cytokine cascade or blockade of glial activation.
  • Interleukin-1 receptor antagonist or soluble tumor necrosis factor receptor was administered intrathecally via lumbar puncture to male Holtzman rats in a preventative pain strategy, in which therapy was initiated 1h prior to surgery.
  • Administration of soluble tumor necrosis factor receptor attenuated mechanical allodynia, while interleukin-1 receptor antagonist alone was unable to decrease allodynia.
  • Interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor, administered to both male and female rats in a preventative pain strategy, significantly reduced mechanical allodynia in a dose-dependent manner (P<0.01).
  • Immunohistochemistry on L5 spinal cord revealed similar astrocytic and microglial activation regardless of treatment.
  • At days 3 and 7 post-transection, animals receiving daily interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor exhibited significantly less interleukin-6, but not interleukin-1beta, in the L5 spinal cord compared to vehicle-treated animals.
  • In an existing pain paradigm, in which treatment was initiated on day 7 post-transection, interleukin-1 receptor antagonist in combination with soluble tumor necrosis factor receptor attenuated mechanical allodynia (P<0.05) in male rats.
  • These findings further support a role for central interleukin-1beta and tumor necrosis factor in the development and maintenance of neuropathic pain through induction of a proinflammatory cytokine cascade.
  • [MeSH-major] Immunoglobulin G / pharmacology. Neuralgia / drug therapy. Neuralgia / metabolism. Sialoglycoproteins / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Drug Therapy, Combination. Etanercept. Female. Injections, Spinal. Interleukin 1 Receptor Antagonist Protein. Interleukin-1 / metabolism. Interleukin-6 / metabolism. Male. Neuroglia / immunology. Neuroglia / metabolism. Neurons / immunology. Neurons / metabolism. Rats. Rats, Sprague-Dawley. Receptors, Tumor Necrosis Factor. Sex Factors. Spinal Cord / cytology. Spinal Cord / metabolism. Spinal Cord / physiology. Spinal Nerves / physiopathology. Spinal Nerves / surgery. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 11246166.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA11276; United States / NIDA NIH HHS / DA / F31 DA05969
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunoglobulin G; 0 / Interleukin 1 Receptor Antagonist Protein; 0 / Interleukin-1; 0 / Interleukin-6; 0 / Receptors, Tumor Necrosis Factor; 0 / Sialoglycoproteins; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
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7. Chio CC, Lin JW, Chang MW, Wang CC, Kuo JR, Yang CZ, Chang CP: Therapeutic evaluation of etanercept in a model of traumatic brain injury. J Neurochem; 2010 Nov;115(4):921-9
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  • Antagonism of tumor necrosis factor-alpha with etanercept has proved to be effective in the treatment of spinal cord injury and centrally endotoxin-induced brain injury.
  • TBI-induced neuronal apoptosis (e.g., increased numbers of terminal deoxynucleotidyl transferase αUTP nick-end labeling and neuronal-specific nuclear protein double-positive cells), glial apoptosis (e.g., increased numbers of terminal deoxynucleotidyl transferase αUTP nick-end labeling and glial fibrillary acidic protein double-positive cells), astrocytic (e.g., increased numbers of glial fibrillary acidic protein positive cells) and microglial (e.g., increased numbers of ionized calcium-binding adapter molecule 1-positive cells) activation and activated inflammation (e.g., increased levels of tumor necrosis factor-alpha, interleukin-1β and interleukin-6) were all significantly reduced by etanercept treatment.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Brain Injuries / drug therapy. Disease Models, Animal. Immunoglobulin G / therapeutic use. Receptors, Tumor Necrosis Factor / therapeutic use
  • [MeSH-minor] Animals. Drug Evaluation, Preclinical / methods. Etanercept. Hippocampus / metabolism. Hippocampus / pathology. Male. Random Allocation. Rats. Rats, Sprague-Dawley. Tumor Necrosis Factor-alpha / antagonists & inhibitors. Tumor Necrosis Factor-alpha / metabolism

  • Hazardous Substances Data Bank. Etanercept .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
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  • [Copyright] © 2010 The Authors. Journal of Neurochemistry © 2010 International Society for Neurochemistry.
  • (PMID = 20796174.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunoglobulin G; 0 / Receptors, Tumor Necrosis Factor; 0 / Tumor Necrosis Factor-alpha; OP401G7OJC / Etanercept
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