       Document 0869
 DOCN  M95A0869
 TI    Induction of MMP9 (92 kDa gelatinase) activity and expression of tissue
       inhibitor of metalloproteinase-2 mRNA (TIMP-2) in primitive
       neuroectodermal cells infected with retrovirus HTLV-I.
 DT    9510
 AU    Giraudon P; Thomasset N; Bernard A; Verrier B; Belin MF; INSERM, Faculte
       de Medecine A, Lyon, France.
 SO    Eur J Neurosci. 1995 May 1;7(5):841-8. Unique Identifier : AIDSLINE
       MED/95338326
 AB    Matrix-degrading proteases, including metalloproteinases (MMPs) and
       tissue inhibitors of metalloproteinases (TIMPs), are involved in
       modulation of the extracellular matrix, which participates in neural
       cell differentiation, brain morphogenesis and tissue integrity.
       Metalloproteinases and TIMPs are associated with inflammatory and
       degenerative processes in the central nervous system and are regulated
       by cytokines. Human retroviral infections are frequently associated with
       neurological disturbances. In the present paper, we have studied the
       changes occurring in human primitive neuroectodermal cells following
       infection with human T cell lymphotropic virus type 1 (HTLV-I), a
       retrovirus responsible for HTLV-I-associated myelopathy. Infected neural
       cells were found to have high metalloproteinase 9 (MMP9-92 kDa
       gelatinase) activity. MMP9 induction is dependent on HTLV-I infection of
       neural cells. In addition, soluble factors, especially tumour necrosis
       factor alpha, secreted by infected cells, act as mediators of induction.
       HTLV-I infection also induces expression of RNA coding for tissue
       inhibitor of metalloproteinase 2. These observations indicate that
       HTLV-I infection selectively modulates the expression of molecules
       involved in the dynamic equilibrium between the synthesis and
       degradation of the neural cell matrix and leads to its remodelling,
       which modifies cell-cell interactions and cellular function.
 DE    Animal  Antineoplastic Agents/*PHARMACOLOGY  Cell Differentiation  Cell
       Line  Enzyme Induction  Extracellular Matrix/*PHYSIOLOGY
       Gelatinases/*GENETICS/METABOLISM  Gene Expression  HTLV-I/GROWTH &
       DEVELOPMENT  Immunohistochemistry  Neuroglia/METABOLISM
       Neurons/VIROLOGY  Proteins/*METABOLISM  Rats  Retroviridae/GENETICS
       RNA, Messenger/METABOLISM  Support, Non-U.S. Gov't
       T-Lymphocytes/*METABOLISM  Virus Replication  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

