Recently, we investigated the role of substance P (SP) in the lung fibrogenic response to bleomycin (BLM). Since SP exerts its action by activating the NK-1 receptor (NK1-R), we studied the effects of BLM in fibrosis-prone C57 Bl/6J and fibrosis-resistant Balb/C mice treated with L-733,060, a selective NK1-R antagonist. Twenty-one days after BLM challenge, mice treated with L-733,060 did not differ in terms of fibrosis from their respective controls. These data provide evidence that SP does not play a significant role in BLM-induced lung fibrosis. Unexpectedly, we detected areas of bronchiolo-alveolar carcinoma (BAC) in the lungs of L-733,060-treated mice from both strains. The specific role played by NK-1R in the development of BAC was confirmed in NK1-R KO mice generated on C57 Bl/6J and Balb/C background. In these animals, we were able to demonstrate the adenoma-carcinoma sequence (adenomatous hyperplasia → atypical adenomatous hyperplasia →BAC) at various times after BLM. A sequence of alterations in the expression of proliferation markers and cell cycle regulators characterised the adenoma-carcinoma sequence.

Lucattelli, M., Fineschi, S., Geppetti, P., Gerard, N.P., Lungarella, G. (2006). The loss of function of NK1 receptor in mice results in the development of bronchiolo-alveolar carcinoma after bleomycin treatment. FASEB JOURNAL, 20(5), A1328-A1328.

The loss of function of NK1 receptor in mice results in the development of bronchiolo-alveolar carcinoma after bleomycin treatment

Lucattelli, M.;Lungarella, G.
2006-01-01

Abstract

Recently, we investigated the role of substance P (SP) in the lung fibrogenic response to bleomycin (BLM). Since SP exerts its action by activating the NK-1 receptor (NK1-R), we studied the effects of BLM in fibrosis-prone C57 Bl/6J and fibrosis-resistant Balb/C mice treated with L-733,060, a selective NK1-R antagonist. Twenty-one days after BLM challenge, mice treated with L-733,060 did not differ in terms of fibrosis from their respective controls. These data provide evidence that SP does not play a significant role in BLM-induced lung fibrosis. Unexpectedly, we detected areas of bronchiolo-alveolar carcinoma (BAC) in the lungs of L-733,060-treated mice from both strains. The specific role played by NK-1R in the development of BAC was confirmed in NK1-R KO mice generated on C57 Bl/6J and Balb/C background. In these animals, we were able to demonstrate the adenoma-carcinoma sequence (adenomatous hyperplasia → atypical adenomatous hyperplasia →BAC) at various times after BLM. A sequence of alterations in the expression of proliferation markers and cell cycle regulators characterised the adenoma-carcinoma sequence.
2006
Lucattelli, M., Fineschi, S., Geppetti, P., Gerard, N.P., Lungarella, G. (2006). The loss of function of NK1 receptor in mice results in the development of bronchiolo-alveolar carcinoma after bleomycin treatment. FASEB JOURNAL, 20(5), A1328-A1328.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/42497
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