Background: Allergic rhinitis is characterized by a remodeling of nasal epithelium. Since the Notch and TGF-β signaling pathways are known to be involved in cell differentiation and remodeling processes and leptin adipokine has already been identified as a marker for homeostasis in human bronchial and nasal epithelial cells of asthmatics, roles played by these pathways have been investigated for chronic allergic rhinitis. Methods: The leptin/leptin receptor expression has been investigated in a study with 40 biopsies from allergic (AR, n = 18) and non-allergic (C, n = 22) inferior turbinates, using immunohistochemistry, immunofluorescence staining and RT-PCR. In addition, extracts from in vitro samples prepared from primary cells of inferior turbinates as well as in vitro cultured human nasal epithelial RPMI 2650 cells (ATCC-CCL-30) were also tested for leptin expression and activation of the Notch-1 pathway. Results: With regards to AR, in vivo expression levels of both leptin and its receptor significantly decreased in comparison to C. Furthermore, leptin receptor mRNA was significantly reduced in AR as compared to C. Immunofluorescence showed an apparent co-expression of leptin receptor with Notch-1, which was not seen with TGF-β. In vitro, in primary turbinate epithelial cells, the expression of leptin receptor and Notch-1 significantly decreased in AR as compared to C. Moreover, in RPMI 2650 cells, leptin receptor expression was shown to be induced by Notch-1 ligand signaling. Conclusion: Thus, both the leptin and Notch-1 pathways appear to represent markers for epithelial homeostasis in allergic rhinitis.

Bruno, A., Di Sano, C., Lorusso, F., Dino, P., Russo, D., Ballacchino, A., et al. (2019). Notch-1 decreased expression contributes to leptin receptor downregulation in nasal epithelium from allergic turbinates. BIOCHIMICA ET BIOPHYSICA ACTA. MOLECULAR BASIS OF DISEASE, 1865(6), 1642-1650 [10.1016/j.bbadis.2019.03.016].

Notch-1 decreased expression contributes to leptin receptor downregulation in nasal epithelium from allergic turbinates

Bruno, A;Di Sano, C;Lorusso, F;Dino, P;Ballacchino, A;Gallina, S;
2019-01-01

Abstract

Background: Allergic rhinitis is characterized by a remodeling of nasal epithelium. Since the Notch and TGF-β signaling pathways are known to be involved in cell differentiation and remodeling processes and leptin adipokine has already been identified as a marker for homeostasis in human bronchial and nasal epithelial cells of asthmatics, roles played by these pathways have been investigated for chronic allergic rhinitis. Methods: The leptin/leptin receptor expression has been investigated in a study with 40 biopsies from allergic (AR, n = 18) and non-allergic (C, n = 22) inferior turbinates, using immunohistochemistry, immunofluorescence staining and RT-PCR. In addition, extracts from in vitro samples prepared from primary cells of inferior turbinates as well as in vitro cultured human nasal epithelial RPMI 2650 cells (ATCC-CCL-30) were also tested for leptin expression and activation of the Notch-1 pathway. Results: With regards to AR, in vivo expression levels of both leptin and its receptor significantly decreased in comparison to C. Furthermore, leptin receptor mRNA was significantly reduced in AR as compared to C. Immunofluorescence showed an apparent co-expression of leptin receptor with Notch-1, which was not seen with TGF-β. In vitro, in primary turbinate epithelial cells, the expression of leptin receptor and Notch-1 significantly decreased in AR as compared to C. Moreover, in RPMI 2650 cells, leptin receptor expression was shown to be induced by Notch-1 ligand signaling. Conclusion: Thus, both the leptin and Notch-1 pathways appear to represent markers for epithelial homeostasis in allergic rhinitis.
Bruno, A., Di Sano, C., Lorusso, F., Dino, P., Russo, D., Ballacchino, A., et al. (2019). Notch-1 decreased expression contributes to leptin receptor downregulation in nasal epithelium from allergic turbinates. BIOCHIMICA ET BIOPHYSICA ACTA. MOLECULAR BASIS OF DISEASE, 1865(6), 1642-1650 [10.1016/j.bbadis.2019.03.016].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10447/398129
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