The expression of
platelet-derived growth factor (PDGF) and
PDGF receptors was studied in human normal and malignant mesothelial cells in vitro and in vivo. Staining with anti-
cytokeratin and ME1
antibodies and ultrastructural analysis confirmed the mesothelial nature of the cell lines used to study PDGF and
PDGF receptor expression in vitro. Using
antibodies,
mesothelioma cell lines were found to express PDGF and both the PDGF alpha- and the
PDGF beta-receptor, whereas cultured normal mesothelial cells expressed PDGF and
PDGF alpha-receptor. This PDGF and
PDGF receptor staining pattern largely reflects the earlier described
mRNA expression in these cell lines. The only exception was the immunocytochemical detection of PDGF alpha-receptors in the
mesothelioma cell lines, which is different from the inability to detect alpha-receptor transcripts on Northern blots. Expression was also investigated in mesothelial cells in vivo. Expression of PDGF was observed in
malignant mesothelioma cells on frozen tissue sections. In
pleural effusions, a double immunofluorescence staining procedure for PDGF and
epithelial membrane antigen (EMA) revealed PDGF expression by EMA-positive
malignant mesothelioma cells. PDGF beta-receptors and occasionally PDGF alpha-receptors were detected in frozen tissue sections of
malignant mesotheliomas, whereas
mesothelioma cells in effusions showed faint expression of only the
PDGF beta-receptor. In contrast, in effusions containing non-malignant mesothelial cells, only a very low level of
PDGF alpha-receptor could be detected. Taken together, these results indicate that the pattern of PDGF and
PDGF receptor expression in mesothelial cells in vivo largely corresponds to expression of PDGF and its receptors in vitro.
Malignant mesothelioma cell lines thus constitute a good model system for studies on the role of PDGF in this
malignancy. Furthermore, the data reported in this paper are consistent with the idea that an autocrine growth stimulatory effect of PDGF via
PDGF receptors may play a role in the pathogenesis of
malignant mesothelioma.