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A phosphatidylinositol transfer protein α‐dependent survival factor protects cultured primary neurons against serum deprivation‐induced cell death

Selective neuronal loss is a prominent feature in both acute and chronic neurological disorders. Recently, a link between neurodegeneration and a deficiency in the lipid transport protein phosphatidylinositol transfer protein α (PI‐TPα) has been demonstrated. In this context it may be of importance that fibroblasts overexpressing PI‐TPα are known to produce and secrete bioactive survival factors that protect fibroblasts against UV‐induced apoptosis. In the present study it was investigated whether the conditioned medium of cells overexpressing PI‐TPα (CMα) has neuroprotective effects on primary neurons in culture. We show that CMα is capable of protecting primary, spinal cord‐derived motor neurons from serum deprivation‐induced cell death. Since the conditioned medium of wild‐type cells was much less effective, we infer that the neuroprotective effect of CMα is linked (in part) to the PI‐TPα‐dependent production of arachidonic acid metabolites. The neuroprotective activity of CMα is partly inhibited by suramin, a broad‐spectrum antagonist of G‐protein coupled receptors. Western blot analysis shows that brain cortex and spinal cord express relatively high levels of PI‐TPα, suggesting that the survival factor may be produced in neuronal tissue. We propose that the bioactive survival factor is implicated in neuronal survival. If so, PI‐TPα could be a promising target to be evaluated in studies on the prevention and treatment of neurological disorders.