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Altered expression of connexins 26 and 43 in Sertoli cells in seminiferous tubules infiltrated with carcinoma‐ in‐situ or seminoma
Author(s) -
Brehm Ralph,
Marks Alexander,
Rey Rodolfo,
Kliesch Sabine,
Bergmann Martin,
Steger Klaus
Publication year - 2002
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1140
Subject(s) - sertoli cell , spermatogenesis , seminoma , biology , immunostaining , seminiferous tubule , testicle , blood–testis barrier , cytokeratin , gap junction , endocrinology , medicine , immunohistochemistry , andrology , microbiology and biotechnology , intracellular , immunology , genetics , chemotherapy
The expression of connexins (cx) 26 and 43 in testis infiltrated with carcinoma‐ in‐situ (CIS) or seminoma was examined to gain insight into the relationship between aberrant gap junctional communication and spermatogenic impairment in the neoplastic testis. In uninvolved tubules with normal spermatogenesis, cx43 immunostaining was localized to the Sertoli–Sertoli junctional complex and cx26 was absent. In contrast, infiltrated tubules with spermatogonial arrest or CIS‐only were negative for cx43, but displayed strong intracytoplasmic Sertoli cell staining for cx26. The Sertoli cells in these tubules re‐expressed cytokeratin 18 (ck18), signifying a reversion to a less differentiated state. Western blot analysis for cx43 revealed a single immunoreactive band at 43 kD (normal spermatogenesis) and three bands at 43, 41, and 39 kD (impaired spermatogenesis with CIS or seminoma). For cx26, a doublet band at 26/28 kD (normal spermatogenesis) and an additional doublet band at 52/54 kD (impaired spermatogenesis with CIS or seminoma) were observed. The altered expression of cx26 and cx43 in Sertoli cells in testes infiltrated with CIS or seminoma suggests that a derangement in intercellular communication between Sertoli cells and between Sertoli cells and germ cells may play a role in the resulting spermatogenic impairment and possibly in the proliferation and neoplastic progression of CIS cells. Copyright © 2002 John Wiley & Sons, Ltd.