Immunohistochemical expression of Napsin A in normal human fetal lungs at different gestational ages and in acquired and
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ORIGINAL ARTICLE
Immunohistochemical expression of Napsin A in normal human fetal lungs at different gestational ages and in acquired and congenital pathological pulmonary conditions Giovanna Giordano 1
&
Nicoletta Campanini 1 & Elena Varotti 1
Received: 29 August 2019 / Revised: 18 March 2020 / Accepted: 25 March 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Surfactant protein B (SP-B) is a key component of pulmonary surfactant. SP-B is processed to a mature, surface-active protein from a pro-peptide by two distinct cleavage events in its N-terminal and C-terminal regions. Napsin A, a protease expressed in type II pneumocytes, is responsible for the N-terminal cleavage event. Here, for the first time, we have evaluated the expression of Napsin A in normal fetal lungs at different gestational ages and in lungs from fetuses and neonates with congenital and acquired pathological pulmonary conditions. Lung samples were collected from fetal and neonatal autopsies at the Department of Medicine and Surgery’s Pathology Unit of Parma University (Italy). Immunohistochemical analysis was performed using a primary anti-Napsin A (clone IP64 clone) monoclonal antibody. A section of lung adenocarcinoma was used as an external positive control. Napsin A was expressed early in normal fetal lungs throughout the epithelium of the distal pseudoglandular tracts. In fetuses at 30 weeks of gestation and term newborns, Napsin A was already expressed only in isolated cells within the alveolar epithelium, similar to adult subjects. Furthermore, increased expression of Napsin A compared with a control group was observed in lung tissue from fetuses and a newborn with pathological conditions (inflammatory diseases and pulmonary hypoplasia). In conclusion, this study demonstrates that Napsin A is produced early in fetal life, and that its production is increased in many diseases, presumably in an effort to remedy functional pulmonary failure. Keywords Napsin A . Immunohistochemical expression . Fetal lung . Neonatal lung
Introduction Pulmonary surfactant is a lipoprotein complex produced by type II pneumocytes of the alveolar epithelium. By increasing pulmonary compliance and reducing surface tension at the air/ liquid interface, this substance may prevent alveolar collapse at end-expiration. Thus, pulmonary surfactant is of paramount importance in lung function. The lipid component of pulmonary surfactant is dipalmitoylphosphatidylcholine (DPPC), and maintaining an interface rich in DPPC during lung expansion and This article is part of the Topical Collection on Quality in Pathology * Giovanna Giordano [email protected] 1
Department of Medicine and Surgery, Pathology Unit, University of Parma, Viale A. Gramsci, 14, 43126 Parma, Italy
contraction is crucial to preventing alveolar collapse. In addition to DPPC, pulmonary surfactant contains four proteins (“surfactant-associated proteins,” or SPs) that act synergistically to maintain high levels of DPPC. Surfactant protein B (SP-B) is a critical comp
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