Objective: To investigate the histogenesis of pulmonary sclerosing hemangioma (PSH).
Methods: Tissue microarray and immunohistochemical technique were used to detect the expression of pan-cytokeratin, epithelial membrane antigen(EMA), vimentin, thyroid transcription factor (TTF)-1, napsin A, synaptophysin, chromogranin A, CD56, E-cadherin, β-catenin, CD117, CD68 and transforming growth factor(TGF)-β1 in 49 cases of PSH.
Results: Immunohistochemistry revealed that all cuboidal surface cells expressed pan-cytokeratin, EMA, TTF-1 and napsin A. The polygonal cells expressed EMA, TTF-1, napsin A (positive rate 16.3%, 8/49), but not pan-cytokeratin. Both types of cells were negative for synaptophysin, chromogranin A and CD56. Strong positive staining for E-cadherin and β-catenin appeared on the membrane of cuboidal cells in all PSH, with cytoplasm staining for β-catenin as well. The expression levels of these adhesion molecules decreased in the polygonal cells, with the staining localized to the cytoplasm. E-cadherin staining was not detected or was weak. β-catenin staining was not detected on the cell membrane but partially in the cytoplasm. The polygonal cells stained strongly for vimentin, while only a few cuboidal cells were positive. CD117 and CD68 positive inflammatory cells were scattered between the polygonal cells, which was consistent with the distribution of TGF-β1 positive cells.
Conclusions: PSH originates from the primitive respiratory epithelium, and polygonal stromal cells may be derived from epithelial-mesenchymal transformation of the cuboidal cells. TGF-β1 may play an important role in the formation of sclerosing hemangioma.