PRL-1, a protein tyrosine phosphatase, is expressed in neurons and oligodendrocytes in the brain and induced in the cerebral cortex following transient forebrain ischemia.

Abstract

Protein tyrosine phosphorylation is thought to play an important role in the regulation of neural function. We reported previously that CL100, a cytoplasmic type protein tyrosine phosphatase (PTP), was induced after transient forebrain ischemia. In the present study, changes in the mRNA levels after ischemia of PRL-1, a cytoplasmic type PTP and immediate-early gene similar to CL100, was examined. In situ hybridization histochemistry showed that PRL-1 mRNA was expressed in normal adult rats in neurons and oligodendrocytes in widespread regions including the cerebral cortex, hippocampus and cerebellum. PRL-1 mRNA was expressed in the developing brains on embryonic days 15 and 19 and postnatal day 1. Northern blot analysis showed that PRL-1 mRNA was induced from 6 h to 9 h after reperfusion in the cerebral cortex of postischemic rats. These findings suggest that PRL-1 plays a role in neurons and oliogodendrocytes, and that expression of PRL-1 mRNA is regulated by a mechanism different from those of other immediate-early genes such as c-fos and c-jun.