Abstract:
:The mechanisms underlying the inhibition of bile acid-induced apoptosis by cyclic AMP (cAMP) were studied in 24-h-cultured rat hepatocytes. Taurolithocholate 3-sulfate (TLCS, 100 micromol/l) led to a sustained activation of mitogen activated protein (MAP) kinases (JNK, p38(MAPK), and ERKs), dephosphorylation of protein kinase B (PKB), activation of caspases 3 and 8, and hepatocyte apoptosis. cAMP prevented TLCS-induced apoptosis, shifted the persistent TLCS-induced MAP kinase response to a transient pattern, and prevented PKB dephosphorylation. TLCS-induced CD95 and TRAIL receptor-2 trafficking to the plasma membrane were significantly inhibited. Blockade of protein kinase A (PKA) abolished the inhibitory effect of cAMP on TLCS-induced CD95 membrane targeting, but not TRAIL receptor-2 membrane targeting, PKB and MAP kinase responses. H89, an inhibitor of PKA, had no effect on cAMP-induced inhibition of TLCS-triggered poly(ADP) ribose polymerase (PARP) cleavage and caspase activation, but abolished the cAMP-induced inhibition of TLCS-triggered TUNEL- and Annexin V staining. It is concluded that cAMP inhibits bile acid-induced apoptosis via PKA-dependent and -independent mechanisms.
journal_name
Arch Biochem Biophysjournal_title
Archives of biochemistry and biophysicsauthors
Graf D,Reinehr R,Kurz AK,Fischer R,Häussinger Ddoi
10.1016/s0003-9861(03)00224-8subject
Has Abstractpub_date
2003-07-01 00:00:00pages
34-42issue
1eissn
0003-9861issn
1096-0384pii
S0003986103002248journal_volume
415pub_type
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journal_title:Archives of biochemistry and biophysics
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journal_title:Archives of biochemistry and biophysics
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journal_title:Archives of biochemistry and biophysics
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