Upregulation of Dpysl2 and Spna2 gene expression in the rat brain after ischemic stroke.
Ischemia activates the synthesis of potentially damaging and protective proteins in the central nervous system. Dihydropyrimidinase-like 2 (Dpysl2), a protein involved in neuronal differentiation and axonal guidance, and alpha-spectrin 2 (Spna2), a protein involved in maintaining neuronal membrane integrity, were found altered in various nervous system diseases. Modifications of Dpysl2 and Spna2 proteins have been reported in focal ischemic stroke, but their significance is not yet established. Therefore, this study was aimed to investigate the temporal expression of Dpysl2 and Spna2 genes in normal and stroke rat brain and to characterize stroke brains for cell areas, apoptosis, and microglia cells. The middle cerebral artery of rat brain was occluded and the brain tissue was sectioned for in situ hybridization of Dpysl2 and Spna2 genes, TUNEL, and OX-42 immunofluorescence staining. Dpysl2 and Spna2 mRNA expression was quantified by real-time RT-PCR. Characterization of stroke brain for apoptosis and microglia cells showed apoptotic cells and activated microglia, mainly in the infarct core of ipsilateral cortex and striatum of stroke brain. Significant upregulation of Dpysl2 and Spna2 mRNA expression in the penumbra region after stroke was observed predominantly in injured swollen cells in the cortex and striatum. Upregulation of Dpysl2 and Spna2 expression in hypertrophic cells in the penumbra regions of cortex and striatum of stroke brain indicates an early neuronal defense mechanism involving active neuronal repair, regeneration and development, as these genes are known to be involved in neurite outgrowth and plasticity.
Indraswari
Fransisca
F
Department of Anatomy, Yong Loo Lin School of Medicine, National University Health System, National University of Singapore, Singapore.
Wong
Peter T H
PT
Yap
Elgin
E
Ng
Y K
YK
Dheen
S Thameem
ST
D000818:Animals; D017209:Apoptosis / Q000235:genetics; D001921:Brain / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002545:Brain Ischemia / Q000235:genetics* / Q000378:metabolism* / Q000503:physiopathology; D004195:Disease Models, Animal; D005786:Gene Expression Regulation / Q000235:genetics*; D005911:Gliosis / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D020287:In Situ Nick-End Labeling; D020244:Infarction, Middle Cerebral Artery / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics*; D008297:Male; D008840:Microfilament Proteins / Q000235:genetics*; D017628:Microglia / Q000378:metabolism / Q000473:pathology; D009410:Nerve Degeneration / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D009416:Nerve Regeneration / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000235:genetics*; D009473:Neuronal Plasticity / Q000235:genetics; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020521:Stroke / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D015854:Up-Regulation / Q000235:genetics; D033921:Vesicular Transport Proteins / Q000235:genetics*
D036341:Intercellular Signaling Peptides and Proteins; D008840:Microfilament Proteins; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; C422208:Sptan1 protein, rat; D033921:Vesicular Transport Proteins; C095114:collapsin response mediator protein-2