title: Putative innate immunity of antiatherogenic paraoxanase-2 via STAT5 signal transduction in HIV-1 infection of hematopoietic TF-1 cells and in SCID-hu mice.
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.
authors.affiliation: Laboratory of Stem Cell Biology, Torrey Pines Institute for Molecular Studies, 3550 General Atomics Court, San Diego, California 92121, USA.
authors.forename: Jinyun
authors.initials: J
authors.lastname: Yuan
authors.forename: Asokan
authors.initials: A
authors.lastname: Devarajan
authors.forename: Rosita
authors.initials: R
authors.lastname: Moya-Castro
authors.forename: Menghua
authors.initials: M
authors.lastname: Zhang
authors.forename: Stella
authors.initials: S
authors.lastname: Evans
authors.forename: Noam
authors.initials: N
authors.lastname: Bourquard
authors.forename: Peter
authors.initials: P
authors.lastname: Dias
authors.forename: Catherine
authors.initials: C
authors.lastname: Lacout
authors.forename: William
authors.initials: W
authors.lastname: Vainchenker
authors.forename: Srinivasa T
authors.initials: ST
authors.lastname: Reddy
authors.forename: Prasad S
authors.initials: PS
authors.lastname: Koka
mesh_terms: D000818:Animals; D018952:Antigens, CD34 / Q000378:metabolism; D043303:Aryldialkylphosphatase / Q000235:genetics / Q000378:metabolism*; D050197:Atherosclerosis / Q000517:prevention & control; D015153:Blotting, Western; D002316:Cardiotonic Agents / Q000378:metabolism; D002478:Cells, Cultured; D005333:Fetus / Q000166:cytology; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000494:pharmacology; D015658:HIV Infections / Q000276:immunology* / Q000378:metabolism / Q000821:virology; D015497:HIV-1 / Q000502:physiology*; D006412:Hematopoietic Stem Cells / Q000502:physiology*; D006801:Humans; D007113:Immunity, Innate; D008099:Liver / Q000276:immunology / Q000821:virology; D051379:Mice; D016513:Mice, SCID; D010766:Phosphorylation; D012333:RNA, Messenger / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050799:STAT5 Transcription Factor / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015398:Signal Transduction; D013950:Thymus Gland / Q000276:immunology / Q000821:virology
chemical_list: D018952:Antigens, CD34; D002316:Cardiotonic Agents; D012333:RNA, Messenger; D050799:STAT5 Transcription Factor; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D043303:Aryldialkylphosphatase