Peripheral endothelin A receptor antagonism attenuates carcinoma-induced pain - 22/08/11
, Victoria Pickering a, Stanley Liu a, Phuong Quang a, John Dolan a, S. Thaddeus Connelly a, Richard C.K. Jordan b, c
Corresponding author. Tel.: +1 415 502 3297; fax: +1 415 476 6305.Abstract |
In this study we investigated the role of endothelin-1 (ET-1) and its peripheral receptor (ET-A) in carcinoma-induced pain in a mouse cancer pain model. Tumors were induced in the hind paw of female mice by local injection of cells derived from a human oral squamous cell carcinoma (SCC). Significant pain, as indicated by reduction in withdrawal thresholds in response to mechanical stimulation, began at four days after SCC inoculation and lasted to 28 days, the last day of measurement. Intra-tumor expression of both ET-1 mRNA and ET-1 protein were significantly upregulated compared to normal tissue, and local administration of the ET-A receptor selective antagonist, BQ-123 (100μM) significantly elevated withdrawal thresholds, indicating the induction of an antinociceptive effect. These findings support the suggestion that ET-1 and ET-A receptors contribute to the severity of carcinoma-induced soft tissue cancer pain.
Le texte complet de cet article est disponible en PDF.Keywords : Oral cancer, Cancer pain, Mouse model, Endothelin, Endothelin A receptor
Plan
Vol 11 - N° 4
P. 406-414 - mai 2007 Retour au numéro
Article précédent
- Hypertonic saline-induced muscle nociception and c-fos activation are partially mediated by peripheral NMDA receptors
- Jin Y. Ro, Norman F. Capra, Jong-seok Lee, Radi Masri, Yang-Hyun Chun
- Generalized deep-tissue hyperalgesia in patients with chronic low-back pain
- Søren O’Neill, Claus Manniche, Thomas Graven-Nielsen, Lars Arendt-Nielsen
Bienvenue sur EM-consulte, la référence des professionnels de santé.
L’accès au texte intégral de cet article nécessite un abonnement.
Déjà abonné à cette revue ?