Glucocorticoid-induced DNA fragmentation: role of protein-kinase-C activity

G Migliorati; M C Pagliacci; F D'Adamio; F Crocicchio; I Nicoletti; C Riccardi

doi:10.1016/1043-6618(92)90574-u

Glucocorticoid-induced DNA fragmentation: role of protein-kinase-C activity

Pharmacol Res. 1992 Sep:26 Suppl 2:5-9. doi: 10.1016/1043-6618(92)90574-u.

Authors

G Migliorati¹, M C Pagliacci, F D'Adamio, F Crocicchio, I Nicoletti, C Riccardi

Affiliation

¹ Istituto di Farmacologia Medica, Perugia University Medical School, Italy.

PMID: 1409324
DOI: 10.1016/1043-6618(92)90574-u

Abstract

Glucocorticoid hormones (GCH) and IL-2 induce apoptotic cell death by a PKC-dependent mechanism. IL-4 counteracts apoptosis by inhibiting PKC activity. GCH and IL-2 show antagonistic effects on apoptosis when administered together. These data indicate that PKC activation in response to different stimuli can both enhance or reduce thymocyte survival.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Animals
Apoptosis / drug effects
Cell Death / drug effects
DNA / metabolism*
Dexamethasone / pharmacology
Flow Cytometry
Glucocorticoids / pharmacology*
In Vitro Techniques
Mice
Mice, Inbred C3H
Protein Kinase C / metabolism*
T-Lymphocytes / drug effects
Tetradecanoylphorbol Acetate / pharmacology

Substances

Glucocorticoids
Dexamethasone
DNA
Protein Kinase C
Tetradecanoylphorbol Acetate