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FGF2 stimulates SDF‐1 expression through the Erm transcription factor in Sertoli cells
Author(s) -
Yoon KyungAe,
Chae YoungMi,
Cho JeYoel
Publication year - 2009
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.21759
Subject(s) - sertoli cell , transcription factor , gene knockdown , biology , stromal cell , microbiology and biotechnology , gene , endocrinology , spermatogenesis , cancer research , genetics
Ets‐related molecule ( Erm ) is a member of the Ets transcription factor family. Erm is known to be an important factor for the self‐renewal of Spermatogonial stem cells (SSCs) and the maintenance of spermatogenesis. We investigated the molecular mechanism of Erm regulation on SDF‐1 in TM4 Sertoli cells. Erm and Sdf‐1 levels were up‐regulated after FGF2 treatment in TM4 cells, whereas these levels were significantly decreased by FGF2 in ST2 bone marrow stromal cells. Knockdown of Erm by siRNA in the presence of FGF2 decreased the Sdf‐1 levels in TM4 cells. The expression levels of Erm were similar and Erm overexpression increased the Sdf‐1 in both TM4 and ST2 cells. FGFR subtype analysis revealed that FGFR4 was expressed in TM4 cells but not in ST2 cells. A blocking experiment also confirmed that FGFR4 is partly responsible for the up‐regulation of Erm and SDF‐1 induced by FGF2 stimulation in TM4 cells. FGF2 and ERM increased the activity of Sdf‐1 gene promoter region in a dose‐dependent manner. EMSA revealed that ERM strongly binds to the −846 to −851 nucleotide region of the potential Ets binding site (EBS) in the Sdf‐1 promoter. In addition, CXCR4, the SDF‐1 receptor, was expressed in spermatogonia and Sertoli cells in the seminiferous tubules of the mouse testis. Our results indicate that ERM directly regulates Sdf‐1 gene expression by interacting with its cis ‐acting element in response to FGF2 stimulation in TM4 cells. J. Cell. Physiol. 220: 245–256, 2009. © 2009 Wiley‐Liss, Inc.