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Plasminogen mRNA induction in the mouse brain after kainate excitation: codistribution with plasminogen activator
Ronit Sharon1, Rene Abramovitz, Ruth Miskin
1Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel.
Abstract:
Plasminogen (Plg), which can be converted to the active protease plasmin by plasminogen activators, has been previously implicated in brain plasticity and in toxicity inflicted in hippocampal pyramidal neurons by kainate. Here we have localized Plg. mRNA through in situ hybridization in brain cryosections derived from normal adult mice or after kainate injection (i.p.). The results indicated that Plg mRNA was undetectable in the normal brain, but after kainate injection it was induced in neuronal cells in multiple, but specific areas, including layers II-III of the neocortex; the olfactory bulb, anterior olfactory nucleus, and the piriform cortex; the caudate/putamen and accumbens nucleus shell; throughout the amygdaloid complex; and in the CAI/CA3 subfields of the hippocampus. Interestingly, this distribution pattern coincided with what we have recently described for the plasminogen activator inhibitor-2 (PAI-2) mRNA, however differing from that of the plasminogen activator inhibitor-1 (PAI-1) mRNA, as also shown here. These results suggest that enhanced Plg gene expression could be involved in events associated with olfactory, striatal, and limbic structures. Furthermore, because PAI-2 is thought to intracellularly counteract cytotoxic events, our results raise the possibility that PAI-2 can act in the brain as an intracellular neuroprotector against potential plasmin-mediated toxicity.
Insights
Plasminogen mRNA is absent in normal brains but induced by kainate in specific regions. This suggests plasminogen
Area of Science:
- Neuroscience
- Molecular Biology
- Gene Expression
Background:
- Plasminogen (Plg) and its activator, plasmin, are implicated in brain plasticity and kainate-induced neurotoxicity.
- Previous research suggests a role for Plg in neuronal function and dysfunction.
Purpose of the Study:
- To investigate the localization and induction patterns of Plg mRNA in the mouse brain following kainate administration.
- To compare the expression profile of Plg mRNA with plasminogen activator inhibitors (PAI-1 and PAI-2).
Main Methods:
- In situ hybridization was employed to detect Plg mRNA in brain cryosections.
- Experiments were conducted on normal adult mice and mice injected with kainate.
Main Results:
- Plg mRNA was undetectable in the normal adult mouse brain.
- Kainate injection induced Plg mRNA expression in specific neuronal populations, including the neocortex, olfactory bulb, piriform cortex, caudate/putamen, amygdala, and hippocampus.
- The distribution of induced Plg mRNA overlapped with PAI-2 mRNA but differed from PAI-1 mRNA.
Conclusions:
- Enhanced Plg gene expression following kainate suggests its involvement in olfactory, striatal, and limbic system processes.
- The co-localization with PAI-2 raises the possibility of PAI-2 acting as an intracellular neuroprotector against plasmin-mediated toxicity in the brain.
