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© 1993 Oxford University Press

research-article

Gap junctional intercellular communication of primary and asbestos-associated malignant human mesothelial cells

K. Linnainmaa 1 4, K. Pelin 1, E. Vanhala 1, T. Tuomi 1, C. Piccoli 2, D.J. Fitzgerald 2 3 and H. Yamasaki 2

1Institute of Occupational Health, Departments of Industrial Hygiene and Toxicology and Occupational Medicine Helsinki, Finland
2Unit of Multistage Carcinogenesis, International Agency for Research on Cancer Lyon, France
3Environmental Health Branch, South Australian Health Commission Adelaide, Australia

4To whom reprint requests should be addressed at: Institute of Occupational Health, Topeliuksenkatu 41 a A, SF-00250 Helsinki, Finland

We examined gap junctional intercellular communication (GJIC) of primary human mesothelial cells and cell lines of asbestos-associated human pleural mesotheliomas, and the effect of asbestos and other mineral fibres on these cells. In homologous cultures, the GJIC capacity of six out of seven tumour cell lines was markedly less than for primary mesothelial cells. This defect in GJIC appeared not to be at the expression level of mRNA and protein of the gene encoding the 43 kDa gap junction protein. In heterologous cocultures of tumour cells and primary mesothelial cells, however, 80–90% of the tumour cell/normal cell contacts were functional. Exposure of primary mesothelial cells to TPA, a phorbol ester tumour promoter, resulted in marked inhibition of GJIC, being an action common to numerous tumour promoters. Such an effect though was not observed with the carcinogenic mesothelioma-inducing mineral fibres chrysotile and amosite, neither with glass wool. These results suggest that a permanent defect in GJIC capacity is a common feature of human mesothelioma cells, but how mineral fibres are involved in the process of mesotheliomagenesis is still unclear.


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