Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3065814 | Journal of Neuroimmunology | 2007 | 13 Pages |
Abstract
Proopiomelanocortin (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 12Â h of inflammation, END increased in popliteal lymph nodes and at 96Â 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.
Keywords
CFAlymph node(s)RPL19i.pl.IntraplantarRIACRFPOMCqRT-PCRribosomal protein L19PPTcomplete Freund's adjuvantquantitative RT-PCRpaw pressure thresholdimmunoreactiveBeta-endorphinReverse transcriptaseNeuro-immune interactionSIGPainImmune systemSignal sequenceradioimmunoassaycorticotropin releasing factorPituitarycrossing pointWild type.endproopiomelanocortinOpioid peptidesnegative control
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Authors
Nicolle Sitte, Melanie Busch, Shaaban A. Mousa, Dominika Labuz, Heike Rittner, Carmen Gore, Hans Krause, Christoph Stein, Michael Schäfer,