Background&Objective: Surfactant protein B (SP-B) is a key component of pulmonary surfactant. SP-B is processed to mature surface-active protein from a pro-peptide by two distinct cleavages at its N-terminal and C-terminal portions. Napsin A is the protease, expressed in type-II pneumocytes, involved in the N-terminal cleavage of this pro-peptide. In this paper, for the first time, we evaluate the immunohistochemical expression of Napsin A in normal human fetal lungs at different gestational ages, and in examples of congenital and acquired pulmonary pathological conditions. Method: Samples of lungs were collected at the Department ofMedicine and Surgery of Parma University, (Italy) from fetal and neonatal autopsies. The immunohistochemical study was performed using primary monoclonal antibody anti-Napsin A (clone MRQ-60). A section of lung adenocarcinoma was used as an external positive control. Results: The results reveal that Napsin A is expressed early in normal fetal lungs and in the entire epitheliumof distal pseudoglandular tracts. At 30 weeks’ gestation and in the newborn at term of pregnancy, immunoreactivity to Napsin A already presents the same distribution as that in adult subjects, affecting isolated cells of the alveolar epithelium. In pathological conditions, such as inflammatory diseases and pulmonary hypoplasia, both in the fetus and in the newborn, this study demonstrates an increase in the expression of Napsin A compared to a control group. Conclusion: In conclusion, this study demonstrates that Napsin A is produced early during fetal life and its production increases in many diseases in the effort to resolve a functional pulmonary deficiency.

Immunohistochemical expression of Napsin A in normal human foetal lungs and congenital and acquired pathologic conditions / Giordano, G; Campanini, Nicoletta; Varotti, Elena. - In: VIRCHOWS ARCHIV. - ISSN 0945-6317. - 473:Suppl1(2018), pp. S309-S309. [10.1007/s00428-018-2422-1]

Immunohistochemical expression of Napsin A in normal human foetal lungs and congenital and acquired pathologic conditions

Giordano G;Nicoletta Campanini;Elena Varotti
2018

Abstract

Background&Objective: Surfactant protein B (SP-B) is a key component of pulmonary surfactant. SP-B is processed to mature surface-active protein from a pro-peptide by two distinct cleavages at its N-terminal and C-terminal portions. Napsin A is the protease, expressed in type-II pneumocytes, involved in the N-terminal cleavage of this pro-peptide. In this paper, for the first time, we evaluate the immunohistochemical expression of Napsin A in normal human fetal lungs at different gestational ages, and in examples of congenital and acquired pulmonary pathological conditions. Method: Samples of lungs were collected at the Department ofMedicine and Surgery of Parma University, (Italy) from fetal and neonatal autopsies. The immunohistochemical study was performed using primary monoclonal antibody anti-Napsin A (clone MRQ-60). A section of lung adenocarcinoma was used as an external positive control. Results: The results reveal that Napsin A is expressed early in normal fetal lungs and in the entire epitheliumof distal pseudoglandular tracts. At 30 weeks’ gestation and in the newborn at term of pregnancy, immunoreactivity to Napsin A already presents the same distribution as that in adult subjects, affecting isolated cells of the alveolar epithelium. In pathological conditions, such as inflammatory diseases and pulmonary hypoplasia, both in the fetus and in the newborn, this study demonstrates an increase in the expression of Napsin A compared to a control group. Conclusion: In conclusion, this study demonstrates that Napsin A is produced early during fetal life and its production increases in many diseases in the effort to resolve a functional pulmonary deficiency.
Immunohistochemical expression of Napsin A in normal human foetal lungs and congenital and acquired pathologic conditions / Giordano, G; Campanini, Nicoletta; Varotti, Elena. - In: VIRCHOWS ARCHIV. - ISSN 0945-6317. - 473:Suppl1(2018), pp. S309-S309. [10.1007/s00428-018-2422-1]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11381/2849840
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