Abstract:
BACKGROUND:One of the earliest prerequisites for the development of inflammation after ischemia-reperfusion (I/R) is local chemokine expression. We recently demonstrated that apoptosis, characterized by intracellular caspase-activation, contributes to the development of inflammation after I/R. METHODS:The contribution of apoptosis was investigated using the pan-caspase inhibitor Z-Val-Ala-Asp(OMe)-CH2F in a murine model of renal I/R. Renal expression of the chemokines macrophage inflammatory protein-2 (MIP-2) and KC was studied using RT-PCR and immunohistology. Measuring myeloperoxidase activity and serum ureum and creatinine levels assessed neutrophil influx and kidney dysfunction. RESULTS:We demonstrate renal up-regulation of KC and MIP-2 after 1 to 16 hr of reperfusion. Treatment with the caspase inhibitor Z-Val-Ala-Asp(OMe)-CH2F effectively prevented I/R-induced renal apoptosis, KC, and MIP-2 up-regulation after 2 hr of reperfusion as well as neutrophil influx and functional impairment after 24 hr of reperfusion. CONCLUSIONS:These data for the first time show that chemokine induction following I/R is dependent on caspase activation.
journal_name
Transplantationjournal_title
Transplantationauthors
Daemen MA,de Vries B,van't Veer C,Wolfs TG,Buurman WAdoi
10.1097/00007890-200104150-00032subject
Has Abstractpub_date
2001-04-15 00:00:00pages
1007-11issue
7eissn
0041-1337issn
1534-6080journal_volume
71pub_type
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