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Manuscript from project group Prof. Ana Zenclussen published

Monday, 21. January 2013

Mast cells rescue implantation defects caused by c-kit deficiency

Katja Woidacki1, Milan Popovic1, Martin Metz2, Anne Schumacher1, Nadja Linzke1, Ana Teles1, Francoise Poirier3, Stefan Fest4, Federico Jensen1, Gabriel A. Rabinovich5#, Marcus Maurer2#, Ana Claudia Zenclussen1#

1Experimental Obstetrics and Gynecology, Medical Faculty, Otto-von-Guericke University, Magdeburg, Germany.
2Department of Dermatology and Allergology, Charité – Universitätsmedizin Berlin, Germany.
3Institut Jacques Monod, CNRS UMR 7592, Paris-Diderot University, France
4Department of Paediatrics Haematology and Oncology, Universitätsmedizin Leipzig, Germany.
5Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental (IByME) and Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.
#: shared authorship

PubMed link:


Various physiologically relevant processes are regulated by the interaction of the receptor tyrosine kinase (c-Kit) and its ligand stem cell factor (SCF), being SCF known to be the most important growth factor for mast cells (MCs). In spite of their traditional role in allergic disorders and innate immunity, MCs have lately emerged as versatile modulators of a variety of physiologic and pathologic processes. Katja Woidacki, a member of Prof. Ana Zenclussen’s working group demonstrated that MCs are critical for pregnancy success. Recently, this work was published in ‘Cell Death and Disease’. Uterine MCs presented a unique phenotype, accumulated during receptivity and expanded upon pregnancy establishment. KitW-sh/W-sh mice, whose MC-deficiency is based on restricted c-Kit gene expression, exhibited severely impaired implantation, which could be completely rescued by systemic or local transfer of wild-type bone marrow-derived MCs. Transferred wild type MCs favored normal implantation, induced optimal placentation as well as spiral artery remodeling and promoted the expression of MC proteases, transforming growth factor-β and connective tissue growth factor. MCs contributed to trophoblast survival, placentation and fetal growth through secretion of the glycan-binding protein galectin-1. Our data unveil unrecognized roles for MCs at the feto-maternal interface with critical implications in reproductive medicine.

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