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- Nicolle Sitte, Melanie Busch, Shaaban A Mousa, Dominika Labuz, Heike Rittner, Carmen Gore, Hans Krause, Christoph Stein, and Michael Schäfer.
- Department of Anesthesiology and Critical Care Medicine, Charité University Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany.
- J. Neuroimmunol. 2007 Feb 1;183(1-2):133-45.
AbstractProopiomelanocortin (POMC)-derived beta-endorphin1-31 (END) released from immune cells inhibits inflammatory pain. We examined the expression of END and POMC mRNA encoding the signal sequence required for entry of the nascent polypeptide into the regulated secretory pathway in lymphocytes of rats with inflamed hindpaws. Within 12 h of inflammation, END increased in popliteal lymph nodes and at 96 h the intraplantar neutralization of END exacerbated pain. Lymphocytes expressed POMC, END, and full-length POMC mRNA. Semi-nested PCR revealed 8-fold increased exon 2-3 spanning POMC mRNA. Thus, painful inflammation enhances signal sequence-encoding lymphocytic POMC mRNA needed for regulated secretion of functionally active END.
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