|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Laboratoire de Physiologie de la Reproduction et des Comportements,4 UMR 6175 INRA-CNRS-Université de Tours-Haras Nationaux, Centre de Recherches de Tours, 37380 Nouzilly, France
Sechenov Institute of Evolutionary Physiology and Biochemistry,5 Russian Academy of Sciences, 194223 St. Petersburg, Russia
Institut de Physiologie et Biologie Cellulaire,6 UMR 6187 CNRS, 86022 Poitiers, France
ABSTRACT
Transferrin is well known as an iron transport glycoprotein. Dimeric or tetrameric transferrin forms have recently been reported to modulate phagocytosis by human leukocytes. It is mainly synthesized by the liver, and also by other sources, such as Sertoli cells of the testis. Sertoli cells show a strong phagocytic activity toward apoptotic germ cells and residual bodies. Here, we provide evidence that purified human dimeric transferrin from commercial sources decreased residual body phagocytosis, unlike monomeric transferrin. The presence of iron appeared essential for dimeric transferrin inhibitory activity. Importantly, dimeric transferrin could be visualized by immunoblotting in Sertoli cell lysates as well as in culture media, indicating that dimeric transferrin could be physiologically secreted by Sertoli cells. By siRNA-mediated knockdown, we show that endogenous transferrin significantly inhibited residual body ingestion by Sertoli cells. These results are the first to identify dimeric transferrin in Sertoli cells and to demonstrate its implication as a physiological modulator of residual body phagocytosis by Sertoli cells.
phagocytosis, residual bodies, Sertoli cells, testis, transferrin
3These authors contributed equally to this work.
1Supported by the Institut National de la Santé et de la Recherche Médicale (INSERM). M.G.Y. is funded by the Institut National de Recherche Agronomique (INRA). A.S. is funded by a fellowship from the Région Centre.
Correspondence: 2FAX: 33 2 47 42 77 43; e-mail: guillou{at}tours.inra.fr
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |