Premium
Desquamation takes center stage at the origin of proliferative inflammatory atrophy, epithelial–mesenchymal transition, and stromal growth in benign prostate hyperplasia
Author(s) -
Ferrucci Danilo,
Biancardi Manoel F.,
Nishan Umar,
RosaRibeiro Rafaela,
Carvalho Hernandes F.
Publication year - 2017
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10867
Subject(s) - stromal cell , desquamation , hyperplasia , prostate , epithelium , pathology , mesenchymal stem cell , epithelial–mesenchymal transition , atrophy , biology , cancer research , medicine , cancer , metastasis
In this commentary, we propose a relationship between desquamation, initially described as the collective detachment and deletion of epithelial cell in the prostate gland after castration, and proliferative inflammatory atrophy (PIA) and stromal growth in benign prostate hyperplasia (BPH). First, in response to diverse stimuli, including inflammatory mediators, epithelial cells desquamate and leave a large surface of the luminal side of the basement membrane (BM) exposed. Basal cells are activated into intermediate‐type cells, which change morphology to cover and remodel the exposed BM (simple atrophy) to a new physiological demand (such as in the hypoandrogen environment, simulated by surgical and/or chemical castration) and/or to support re‐epithelialization (under normal androgen levels). In the presence of inflammation (that might be the cause of desquamation), the intermediate‐type cells proliferate and characterize PIA. Second, in other circumstances, desquamation is an early step of epithelial‐to‐mesenchymal transition (EMT), which contributes to stromal growth, as suggested by some experimental models of BPH. The proposed associations correlate unexplored cell behaviors and reveal the remarkable plasticity of the prostate epithelium that might be at the origin of prostate diseases.