Molecular biology reports · 2026
Phenotype-specific differences in bone morphogenetic protein ligand expression and intracellular signaling pathway activation in chronic rhinosinusitis.
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Eyibilen Ahmet, Hira Serdar
Аннотация
PURPOSE: Chronic rhinosinusitis (CRS) comprises distinct phenotypes with divergent inflammatory and tissue remodeling patterns. Bone morphogenetic proteins (BMPs) are key regulators of airway repair; however, it remains unclear whether phenotypic differences between CRS with nasal polyps (CRSwNP) and without nasal polyps (CRSsNP) are associated with BMP ligand abundance or downstream pathway activity. We investigated phenotype-specific BMP/Smad pathway patterns and their potential relevance to airway remodeling.
METHODS: Sinonasal tissue samples were obtained from patients with CRSwNP (n = 20), CRSsNP (n = 16), and control subjects (n = 10). Expression and localization of BMP-2, BMP-4, TGF-β1, Smad1, Smad5, Smad8, and phospho-Smad1/5/8 were evaluated by immunohistochemistry using semi-quantitative H-SCORE analysis. Tissue protein levels of BMP-2, BMP-4, and TGF-β1 were quantified by enzyme-linked immunosorbent assay (ELISA).
RESULTS: CRSsNP tissues demonstrated increased expression of BMP-2, BMP-4, and TGF-β1 compared with controls, consistent with a fibrotic remodeling profile, whereas CRSwNP tissues exhibited reduced ligand expression. In contrast, phospho-Smad1/5/8 expression was significantly increased in both CRS phenotypes relative to controls. These findings suggest that downstream Smad activation may not directly parallel BMP ligand abundance across CRS phenotypes. BMP-4 expression showed a positive association with phospho-Smad1/5/8 levels in both CRS subgroups, whereas BMP-2 did not. ELISA analyses were largely concordant with immunohistochemical findings.
CONCLUSION: The observed patterns suggest that BMP/Smad pathway activity in CRS may vary according to disease phenotype and tissue context. These findings highlight the importance of interpreting signaling activity alongside ligand expression in tissue-based studies and provide descriptive insight into remodeling-related pathway behavior in CRS.
METHODS: Sinonasal tissue samples were obtained from patients with CRSwNP (n = 20), CRSsNP (n = 16), and control subjects (n = 10). Expression and localization of BMP-2, BMP-4, TGF-β1, Smad1, Smad5, Smad8, and phospho-Smad1/5/8 were evaluated by immunohistochemistry using semi-quantitative H-SCORE analysis. Tissue protein levels of BMP-2, BMP-4, and TGF-β1 were quantified by enzyme-linked immunosorbent assay (ELISA).
RESULTS: CRSsNP tissues demonstrated increased expression of BMP-2, BMP-4, and TGF-β1 compared with controls, consistent with a fibrotic remodeling profile, whereas CRSwNP tissues exhibited reduced ligand expression. In contrast, phospho-Smad1/5/8 expression was significantly increased in both CRS phenotypes relative to controls. These findings suggest that downstream Smad activation may not directly parallel BMP ligand abundance across CRS phenotypes. BMP-4 expression showed a positive association with phospho-Smad1/5/8 levels in both CRS subgroups, whereas BMP-2 did not. ELISA analyses were largely concordant with immunohistochemical findings.
CONCLUSION: The observed patterns suggest that BMP/Smad pathway activity in CRS may vary according to disease phenotype and tissue context. These findings highlight the importance of interpreting signaling activity alongside ligand expression in tissue-based studies and provide descriptive insight into remodeling-related pathway behavior in CRS.