Document 0576
 DOCN  M9490576
 TI    CD4 engagement by HIV-1 in TF-1 hematopoietic progenitor cells increases
       protein kinase C activity and reduces intracellular Ca2+ levels.
 DT    9411
 AU    Gibellini D; Zauli G; Re MC; Furlini G; Lolli S; Borgatti P; Capitani S;
       La Placa M; Institute of Microbiology, University of Bologna, Italy.
 SO    Microbiologica. 1994 Apr;17(2):85-92. Unique Identifier : AIDSLINE
       MED/94344050
 AB    Starting from our previous observations that the HIV-1-mediated
       engagement of CD4 induced apoptotic death of TF-1 hematopoietic
       progenitor cells, in this study we evaluated PKC activity and
       intracellular Ca2+ levels in TF-1 cells treated with viable and
       heat-inactivated HIV-1 (strain IIIB) or anti-CD4 Leu3a monoclonal
       antibody (mAb). Both viable and heat-inactivated HIV-1 or anti-CD4 mAb,
       but not anti-human cytomegalovirus (HCMV) 66kD protein or anti-CD8 mAb
       induced a rapid (5-10 min) increase in PKC activity under both
       serum-containing and serum-free conditions. The same treatment also
       induced both a transient and a long-lasting (48 hours) decrease (p <
       0.05) in intracellular Ca2+ levels in serum-containing cultures. We
       propose that the observed changes in PKC activity and intracellular Ca2+
       levels might be involved in the HIV-1 mediated apoptosis of
       hematopoietic progenitor cells.
 DE    Antibodies, Monoclonal/IMMUNOLOGY  Antigens, CD4/IMMUNOLOGY/*METABOLISM
       Apoptosis  Calcium/*METABOLISM  Cell Line  Enzyme Activation
       Hematopoietic Stem Cells/METABOLISM/*MICROBIOLOGY  Human
       HIV-1/*METABOLISM  Protein Kinase C/*METABOLISM  Support, Non-U.S. Gov't
       JOURNAL ARTICLE

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