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Macrophage migration inhibitory factor in the human prostate: Identification and immunocytochemical localization
Author(s) -
Arcuri Felice,
del Vecchio Maria Teresa,
de Santi Maria Margherita,
Lalinga Anna Vittoria,
Pallini Vitaliano,
Bini Luca,
Bartolommei Sabrina,
Parigi Sabrina,
Cintorino Marcella
Publication year - 1999
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19990515)39:3<159::aid-pros3>3.0.co;2-m
Subject(s) - macrophage migration inhibitory factor , prostate , immunoelectron microscopy , immunohistochemistry , macrophage , population , hyperplasia , biology , western blot , immunocytochemistry , prostate cancer , pathology , medicine , immunology , endocrinology , cytokine , cancer , in vitro , biochemistry , environmental health , gene
BACKGROUND Macrophage migration inhibitory factor (MIF) is a lymphokine originally identified for its capacity to inhibit the random migration of macrophages. Recent data have further extended knowledge of the physiological role of this protein, showing that MIF is produced by several human organs and tissues. The present study was intended to evaluate the expression and tissutal localization of MIF in the human prostate. METHODS Prostate tissues were obtained from patients undergoing surgical adenomectomy for benign prostatic hyperplasia and were analyzed by Western blot, reverse transcriptase‐polymerase chain reaction, immunohistochemistry, and immunoelectron microscopy. RESULTS The presence of both MIF protein and mRNA was demonstrated in the prostate. Immunocytochemical studies localized MIF protein in the secretory luminal epithelial and basal layer cells. CONCLUSIONS The present study demonstrated that the human prostate is a site of MIF synthesis. Macrophages populate the human prostate and represent an important mechanism of defense of integrity and functionality of the gland. It is speculated that MIF might play a role in preserving prostate physiological activity by maintaining its macrophage population. Prostate 39:159–165, 1999. © 1999 Wiley‐Liss, Inc.