Immunolocalization of Smad4 protein in the testis of domestic fowl (Gallus domesticus) during postnatal development
The transforming growth factor beta (TGF-β) superfamily exerts a wide range of effects on biological events, including spermatogenesis. Smad proteins are downstream signal mediators, which transduce TGF-β signals from the cell surface to the nucleus. Smad4 protein is the common transducer of the TGF...
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Published in | Acta histochemica Vol. 114; no. 5; pp. 429 - 433 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Germany
Elsevier GmbH
01.09.2012
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Subjects | |
Online Access | Get full text |
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Summary: | The transforming growth factor beta (TGF-β) superfamily exerts a wide range of effects on biological events, including spermatogenesis. Smad proteins are downstream signal mediators, which transduce TGF-β signals from the cell surface to the nucleus. Smad4 protein is the common transducer of the TGF-β superfamily that participates in the signaling of all the members of TGF-β superfamily. Smad4 is expressed in the mammalian testis and is believed to play an important role during testicular development and spermatogenesis. Information about Smad4 distribution and function in the testis of birds, including the domestic fowl, is still unclear. In the current study, our objective was to clarify the signal transduction pathway of the TGF-β superfamily in the regulation of testicular development and spermatogenesis by investigating the expression of Smad4 protein in the testis of newborn, prepuberty, puberty and adult domestic fowl. Cellular localization of Smad4 was determined by immunohistochemistry. Our study revealed that the Smad4 was widely expressed in the fowl testis, mainly immunolocalized in the cytoplasm of Sertoli cells, Leydig cells and germ cells. The presence of Smad4 protein in these testicular cells provides molecular and morphological evidence for TGF-β signal transduction during testicular development and spermatogenesis. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0065-1281 1618-0372 |
DOI: | 10.1016/j.acthis.2011.08.003 |