Expression of PECAM-1/CD31 isoforms in human brain gliomas

Microvascular proliferation is a histopathological hallmark of glioblastoma s and anaplastic oligodendrogliomas. Platelet endothelial cell adhesion mol ecule 1 (PECAM-1/CD31) is involved in angiogenesis. PECAM-1 mediates homoph ilic and heterophilic interactions (with glycosaminoglycans and alpha V bet a 3), but deletion of exon 14 results in a loss of heterophilic adhesion. E xpression of various PECAM-1 isoforms was searched for in brain gliomas, sh owing microvascular proliferation (glioblastomas and anaplastic oligodendro gliomas) or not (oligodendrogliomas). In addition, expression of alpha V be ta 3 in some tumors was studied by immunohistochemistry. Various tissues an d the HUVEC primary cell line were used as controls. Immunohistochemistry showed that PECAM-1 was expressed by all endothelial c ells in all tissues and by some tumor cells in glioblastomas and anaplastic oligodendrogliomas. Microvascular proliferation always expressed alpha V b eta 3. In addition, some tumor cells in anaplastic oligodendroglioma and gl ioblastomas expressed it. In all samples examined, PECAM-1 exists under at least two transcriptional isoforms: the whole length molecule and an isofor m made by the splicing of exon 14. Western blot analysis revealed in all ca ses 130 and 110 kDa bands corresponding to the mature form and its precurso r respectively. These results suggest that splicing of exon 14 occurs in vivo in various no rmal and tumoral tissues and may modulate PECAM-1 adhesion according to the presence or not of other PECAM-1 ligands such as alpha V beta 3. Expression of PECAM-1 by tumor cells in glioblastomas and anaplastic oligod endrogliomas may favour angiogenesis by specific PECAM-1 interactions betwe en glial and endothelial cells.