Indomethacin effect on BMMC migration: Prostaglandin synthesis inhibition or PPAR activation?

CASALI CI; VANINA USACH,; GONZALO PIÑERO; WEBER K; PARRA LEANDRO; CLARA P. SETTON; FERNÁNDEZ TOMÉ MC

Rosario, Santa Fe, Argentina

Congreso; Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2014

Sociedad Argentina de Investigación en Bioquímica y Biología Molecular

Indomethacin effect on BMMC migration: Prostaglandin synthesis inhibition or PPAR activation? Casali, C*, Usach, V*, Piñero, G, Weber, K, Parra, L, Setton-Avruj, P**, Fernández Tome, MC** *Ambas deben ser considerados primeros autores **Ambas deben ser considerados últimos autores Química Biológica Patológica y Biología Celular y Molecular. FFyB-UBA. IQUIFIB-CONICET. We have previously described the reorganization of major myelin and axonal proteins during sciatic nerve demyelination, as well as the migration of bone marrow mononuclear cells (BMMC) exclusively to the injured nerve. Once in the ipsilateral nerve, some BMMC colocalize with Schwann cell and nerve fiber markers. In this context, BMMC accelerate the degeneration process and, as a consequence, promote the onset of regeneration. The aim of the present work was to determine whether lesion-associated inflammation is involved in cell recruitment. To that end, animals subjected to sciatic nerve crush and transplanted or not with BMMC, were treated with indomethacin or vehicle and sacrificed at different survival times. Then BMMC migration, COX expression and prostaglandin (PGs) biosynthesis were evaluated. Results showed an injury-mediated induction of COX-2 expression. Treatment with indomethacin blocked BMMC migration but did not inhibit PG synthesis as evidenced by an increase in PGJ2. In the light of these results we can suggest that indomethacin action on BMMC migration occurs through an independent PG-mediated mechanism such as the PPAR pathway. Further experiments are necessary to elucidate indomethacin effect on BMMC migration.