Abstract:
:The activation of c-jun N-terminal kinase (JNK) in pancreatic islets is associated with impaired function and viability, and JNK inhibitory peptides (JNKIs) are cytoprotective. In particular, l-isoforms of JNKIs were shown to improve islets viability, while the d-retroinverso isoform of JNKI (RI-JNKI), with a higher therapeutic potential due to longer half-life, has not been studied. We compared the cytoprotective properties of L-JNKI and RI-JNKI. Treatment of murine islets with L-JNKI resulted in preservation of islet equivalents and greater percentage of viable beta-cells in culture. In contrast, RI-JNKI was not protective. We found that L-JNKI but not RI-JNKI prevents endogenous c-jun phosphorylation in insulinoma cells. Moreover, RI-JNKI induced islet cells necrosis and activates the p-38 kinase. In conclusion, L-JNKI directly affects beta-cells and ameliorates islet viability and function, while RI-JNKI has toxic effects, limiting its biological application to islet cell biology.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Fornoni A,Cobianchi L,Sanabria NY,Pileggi A,Molano RD,Ichii H,Rosero S,Inverardi L,Ricordi C,Pastori RLdoi
10.1016/j.bbrc.2006.12.186subject
Has Abstractpub_date
2007-03-02 00:00:00pages
227-33issue
1eissn
0006-291Xissn
1090-2104pii
S0006-291X(06)02865-8journal_volume
354pub_type
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journal_title:Biochemical and biophysical research communications
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