Interleukin-1α (IL-1α), IL-1β, IL-1 receptor type I, IL-1 receptor antagonist, and TGF-β1 mRNAs in pediatric astrocytomas, ependymomas, and primitive neuroectodermal tumors

被引:21
作者
Ilyin, SE
Gonzalez-Gomez, I
Gilles, FH
Plata-Salaman, CR [1 ]
机构
[1] Univ Delaware, Sch Life & Hlth Sci, Div Mol Biol, Newark, DE 19716 USA
[2] Childrens Hosp, Dept Pathol, Los Angeles, CA 90027 USA
关键词
astrocyte; astrocytomas; brain tumor; cytokine; ependymomas; glia; growth factor; interleukins; nervous system; neuron; posterior fossa; RNase protection; TGF;
D O I
10.1007/BF02870186
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Interleukin-1 alpha (IL-1 alpha), IL-1 beta, interleukin-l receptor type I(IL-1RI, signaling receptor), and IL-1 receptor antagonist (IL-1Ra, endogenous inhibitor) are pivotal components of the IL-1 system. IL-1 and other cytokines induced by IL-1, such as TGF-beta 1, may participate in the growth of various tumor cells. In children, primary nervous system tumors represent the most common solid malignancy. We investigated the levels of IL-1 alpha, IL-1 beta, IL-1RI, IL-1Ra, and TGF-beta 1 mRNAs in pediatric astrocytomas (n = 19), ependymomas (n = 13), and primitive neuroectodermal tumors (n = 22) using sensitive and specific RNase protection assays. The data show a significant distinct cytokine mRNA profile among brain tumor types. Pilocytic, nonpilocytic, and anaplastic astrocytomas have significant increased levels of IL-1 beta, IL-1RI, and TGF-beta 1 mRNAs, but low levels of IL-1Ra mRNA; this may have implications for an IL-1 beta feedback system and IL-1 beta <-> TGF-beta 1 interactions in astrocytomas. Ependymomas show increased levels of IL-1 alpha and IL-1 beta mRNAs associated with low levels of IL-1Ra mRNA; primitive neuroectodermal tumors do not exhibit increased levels of any cytokine component examined. The data also suggest that a dysregulation of the balance between stimulatory and inhibitory cytokines may be involved in the growth and development of brain tumors via autocrine/paracrine mechanisms.
引用
收藏
页码:125 / 137
页数:13
相关论文
共 34 条
  • [1] DIFFERENTIAL REGULATION OF C3 GENE-EXPRESSION IN HUMAN ASTROGLIOMA CELLS BY INTERFERON-GAMMA AND INTERLEUKIN-1-BETA
    BARNUM, SR
    JONES, JL
    [J]. NEUROSCIENCE LETTERS, 1995, 197 (02) : 121 - 124
  • [2] CHOMCZYNSKI P, 1993, BIOTECHNIQUES, V15, P532
  • [3] Differential effects of transforming growth factor-beta 1 on interleukin-1-induced cellular inflammation and vascular permeability in the rabbit retina
    Cuff, CA
    Martiney, JA
    Berman, JW
    Brosnan, CF
    [J]. JOURNAL OF NEUROIMMUNOLOGY, 1996, 70 (01) : 21 - 28
  • [4] GLIAL CELL-SPECIFIC MECHANISMS OF TGF-BETA-1 INDUCTION BY IL-1 IN CEREBRAL-CORTEX
    DACUNHA, A
    JEFFERSON, JA
    JACKSON, RW
    VITKOVIC, L
    [J]. JOURNAL OF NEUROIMMUNOLOGY, 1993, 42 (01) : 71 - 86
  • [5] Biologic basis for interleukin-1 in disease
    Dinarello, CA
    [J]. BLOOD, 1996, 87 (06) : 2095 - 2147
  • [6] INTERLEUKIN-1
    DOWER, SK
    BIRD, TA
    SIMS, JE
    [J]. ADVANCES IN NEUROIMMUNOLOGY, 1992, 2 (01): : 1 - 16
  • [7] Effects of NSAIDs on IL-1 beta-induced IL-6 mRNA and protein synthesis in human astrocytoma cells
    Fiebich, BL
    Lieb, K
    Hull, M
    Berger, M
    Bauer, J
    [J]. NEUROREPORT, 1996, 7 (06) : 1209 - 1213
  • [8] GAUTAM SC, 1993, ONCOL RES, V5, P423
  • [9] Classification and grading of low-grade astrocytic tumors in children
    Giannini, C
    Scheithauer, BW
    [J]. BRAIN PATHOLOGY, 1997, 7 (02) : 785 - 798
  • [10] GILLESPIE GY, 1996, CYTOKINES CNS, P269