Abstract
Paraoxanase-2 (PON2) activity was increased upon HIV-1 infection of the CD34+CD4+ hematopoietic cell line TF-1. Thymocytes derived from the human fetal conjoint thymus/liver hematopoietic organ of SCID-hu mice also exhibited an increase in PON2 activity. Additionally, a remarkable increase of PON2 mRNA expression was also observed in both TF-1 and thymocytes following HIV-1 infection. The phosphorylation of STAT5 was decreased in TF-1 cells upon HIV-1 infection. Interestingly, phosphorylation of STAT5 does not occur in GM-CSF "starved" TF-1 cells; however, PON2 protein, activity and mRNA expression are increased under these conditions, similar to HIV-1 infection. We conclude that PON2 is induced in HIV-1 infection through a mechanism that may involve STAT5 inactivation.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Antigens, CD34 / metabolism
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Aryldialkylphosphatase / genetics
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Aryldialkylphosphatase / metabolism*
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Atherosclerosis / prevention & control
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Blotting, Western
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Cardiotonic Agents / metabolism
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Cells, Cultured
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Fetus / cytology
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Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology
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HIV Infections / immunology*
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HIV Infections / metabolism
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HIV Infections / virology
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HIV-1 / physiology*
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Hematopoietic Stem Cells / physiology*
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Humans
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Immunity, Innate
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Liver / immunology
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Liver / virology
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Mice
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Mice, SCID
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Phosphorylation
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RNA, Messenger / genetics
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Reverse Transcriptase Polymerase Chain Reaction
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STAT5 Transcription Factor / antagonists & inhibitors
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STAT5 Transcription Factor / metabolism*
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Signal Transduction
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Thymus Gland / immunology
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Thymus Gland / virology
Substances
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Antigens, CD34
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Cardiotonic Agents
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RNA, Messenger
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STAT5 Transcription Factor
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Granulocyte-Macrophage Colony-Stimulating Factor
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Aryldialkylphosphatase