Apoptosis is a physiologic mode of cell death that plays critical roles cu- a: development, normal cell turnover, target cell killing by different effectors : me immune response, and pathologic disorders such as Alzheimer’s disease anc - I The process is characterized by several morphologic and biochemical char a* including plasma and nuclear membrane blebbing, cell shrinkage, chromatr . m densation, protease activation, and DNA fragmentation. Tissue-transglutaminase (tTG) meets the criteria of a killer gene in apcc Direct evidences come from sense and antisense transfections in human me. n lastoma SK-N-BE cells. Also in vivo, in SCID mice, tTG-transfected ce: ' a drastic reduction in tumor growth capacity. tTG is regulated by retinoid' iimi receptors, which have been identified. The activity of tTG is also linked activity of ornithine decarboxylase, which promoter is transactivated by the intracellular levels of polyamines. We raise the possibility of an involve'-*: - TGase in the apoptosis of alveolar macrophages. Monocytes are known to : p spontaneous apoptosis upon leaving the circulation unless provided with or mi survival signals, while mature tissue macrophages are normally resistar.: it: event. Indeed, during differentiation monocytes rapidly loose their sens!:: m apoptosis triggered by passive cytokine withdrawal. We now show that _ a macrophages (AM), after activation with specific stimuli (e.g. zymosan), dc ~ LIIIIII their programmed cell death. We also found that AM apoptosis was upreguLat: exposure to some proinflammatory cytokines, such as interferon-)/, since ap:: MI affected only those macrophages IFNy-primed. Consistent with a possible role for TGase in the biochemical pathway le_: mi cell death, the TGase inhibitor cisteamine was protective against zymosar- -: apoptosis in IFNy-primed alveolar macrophages. Our study therefore describe a novel form of activation-induced AM ap•?: II which is regulated by two relevant proteins: tGG and IFNy.

APOPTOSIS OF ALVEOLAR MACROPHAGES: TISSUE TRANSGLUTAMINASE AND -/-INTERFERON INVOLVEMENT

MAZZARELLA, Gennaro;
1996

Abstract

Apoptosis is a physiologic mode of cell death that plays critical roles cu- a: development, normal cell turnover, target cell killing by different effectors : me immune response, and pathologic disorders such as Alzheimer’s disease anc - I The process is characterized by several morphologic and biochemical char a* including plasma and nuclear membrane blebbing, cell shrinkage, chromatr . m densation, protease activation, and DNA fragmentation. Tissue-transglutaminase (tTG) meets the criteria of a killer gene in apcc Direct evidences come from sense and antisense transfections in human me. n lastoma SK-N-BE cells. Also in vivo, in SCID mice, tTG-transfected ce: ' a drastic reduction in tumor growth capacity. tTG is regulated by retinoid' iimi receptors, which have been identified. The activity of tTG is also linked activity of ornithine decarboxylase, which promoter is transactivated by the intracellular levels of polyamines. We raise the possibility of an involve'-*: - TGase in the apoptosis of alveolar macrophages. Monocytes are known to : p spontaneous apoptosis upon leaving the circulation unless provided with or mi survival signals, while mature tissue macrophages are normally resistar.: it: event. Indeed, during differentiation monocytes rapidly loose their sens!:: m apoptosis triggered by passive cytokine withdrawal. We now show that _ a macrophages (AM), after activation with specific stimuli (e.g. zymosan), dc ~ LIIIIII their programmed cell death. We also found that AM apoptosis was upreguLat: exposure to some proinflammatory cytokines, such as interferon-)/, since ap:: MI affected only those macrophages IFNy-primed. Consistent with a possible role for TGase in the biochemical pathway le_: mi cell death, the TGase inhibitor cisteamine was protective against zymosar- -: apoptosis in IFNy-primed alveolar macrophages. Our study therefore describe a novel form of activation-induced AM ap•?: II which is regulated by two relevant proteins: tGG and IFNy.
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11591/217764
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact