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Differential expression of type I cytokeratins in hamster cheek pouch epithelium following treatment with dimethylbenzanthracene
Author(s) -
Shearer B. H.,
McMillan M. D.,
Jenkinson H. F.
Publication year - 1997
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.1997.tb00018.x
Subject(s) - cheek pouch , in situ hybridization , dmba , hamster , epithelium , cytokeratin , biology , microbiology and biotechnology , cheek , immunohistochemistry , pathology , messenger rna , anatomy , immunology , medicine , biochemistry , gene , carcinogenesis , genetics
Cytokeratin (CK) expression in untreated, paraffin‐treated or dimethylbenzanthracene (DMBA)‐treated hamster cheek pouch epithelium was investigated utilizing monoclonal antibodies AE1 or AE3, which react with type I or type II CKs, respectively, and by in situ hybridization utilizing type I CK‐specific probes. The latter were isolated from a cDNA library of hamster cheek pouch mRNA and designated CK 13 and CK 10 based on their respective homologies (>95% amino acids) with murine CK 13 and human CK 10. Treatment of hamster cheek pouch epithelium with DMBA resulted in increased expression of type I CK, detected immunohistochemically with monoclonal AE1, but decreased expression of type II CKs detected with AE3. Despite an overall increase in type I CKs, in situ hybridization demonstrated differential expression of type I CKs with altered distribution of CK 13 mRNA and reduced expression of CK 10 mRNA, providing additional sensitive markers for DMBA‐associated changes in CKs. These changes were constant at 2 to 22 weeks in the pre‐neoplastic and neoplastic epithelium following the initial application of DMBA.