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1

AAV5-mediated overproduction of LUCAM down-regulates perineuronal nets encapsulating motoneurons and their phosphacan component after complete spinal cord transection in the rat

100%
Grycz K., Platek R., Czrkowska-Bauch J., Skup M.
Acta Neurobiologiae Experimentalis
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2015
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tom 75
|
nr Supl.
BACKGROUND AND AIMS: The motoneurons (MNs) of the spinal cord are surrounded by perineuronal nets (PNNs) that restrict plasticity, maintain synapses and compartmentalize the neuronal surface. One of the PNN components, inhibitory to axonal growth in the injured spinal cord, is phosphacan (Pho), a chondroitin sulfate proteoglycan which binds to cell surface adhesion molecules such as L1CAM. Because L1CAM overexpression was found to promote recovery of spinal networks after injury we hypothesized that the mechanism may be through providing signals to downregulate Pho and PNNs. To evaluate the expression of Pho and response of PNNs encapsulating MNs to the injury and L1CAM overexpression in a chronic phase (5 weeks) after complete spinal cord transection. METHODS: Two groups of spinal rats (transected at Th9–10), injected with AAV5 vector carrying L1CAM or EGFP reference transgene and intact group were compared at the transcript (RTPCR) and protein (Pho immunofluorescence) level. PNNs were visualized with Wisteria floribunda agglutinin (WFA). Image analysis was performed on the longitudinal sections from the L1–2 segments acquired in confocal microscope. When analyzing PNN and Pho thickness, the perimeter of the net was taken as the point at which the most intense staining around the MN ended. Next, to focus on area of nerve terminals abutting on MNs, staining intensity of both markers was quantified in a rim around MNs limited to 2.1 mm. RESULTS: Pho around MNs formed the inner rim of PNN, occupying <50% of PNN thickness. Spinalization led to up-regulation of pho mRNA (2-fold, P<0.05) in L1–2 segments, and increased Pho protein (3-fold, P<0.05) in a rim. AAV-L1 injection decreased Pho towards controls (P<0.05) and reduced PNN thickness (by 45%), not modifying lesion-upregulated pho mRNA. CONCLUSION: L1 overexpression in spinal rats may promote MN reinnervation reducing PNNs involving Pho down-regulation. Support: NCN grants: 2013/09/B/NZ4/03306, Preludium12/05/N/ NZ4/02241.
2

Early changes in gene expression of spinal perineuronal nets components in rats after complete spinal cord transection

88%
Grycz K., Gajewska-Wozniak O., Ji B., Czarkowska-Bauch J., Skup M.
Acta Neurobiologiae Experimentalis
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2017
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tom 77
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nr Suppl.1
INTRODUCTION: Perineuronal nets (PNNs), which restrict axonal regeneration in the glial scar and limit synaptic plasticity, are composed of chondroitin sulfate proteoglycans (CSPGs) and Crtl1/Hapln1 link protein essential for PNN formation. Spinal cord transection (SCT) leads to changes of various CSPG proteins differently distributed between 2nd– 8th postlesion weeks. This raises the question if shortly after SCT when glial scar is formed, processes induced by tissue damage alter expression of genes coding for these proteins. AIM(S): To characterize gene expression levels of the selected CSPGs (brevican, neurocan, aggrecan, phosphacan), and of Crtl1/Hapln1 in the spinal cord of the intact rats and to quantify their changes at the second week after SCT at low-thoracic segments. METHOD(S): The CSPGs and Crtl1/Hapln1 gene transcripts were quantified in rats after complete SCT in fragments of the spinal cord: Th 9/10 (lesion site), its vicinity and in L1–L2. To quantify gene expression qRT-PCR was carried out and expression levels were presented relative to internal control gene (GAPDH) as the CT. RESULTS: In intact rats mRNA level of brevican was the highest among all tested CSPGs and Crtl1/Hapln1. Its level exceeded that of neurocan by 5-fold and the rest of CSPGs by at least 10‑fold. SCT caused significant, 4‑fold increase of neurocan and 5-fold decrease of Hapln1 transcripts in the lesion site, comparing to controls, and did not affect phosphacan and brevican transcripts. SCT caused weaker effects in L1–L2 segments where only neurocan and brevican transcripts significantly increased (by 160% and 30% respectively) whereas Crtl1/Hapln‑1 decreased by 40%. CONCLUSIONS: Increased transcript levels of neurocan in the lesion site indicate stimulation of its gene expression in astrocytes. A decrease in Crtl1/Hapln1 transcript may point to potential disturbances in postlesion PNN formation. FINANCIAL SUPPORT: NCN 2013/09/B/NZ4/03306, Preludium (K.G.) and Statutory for the Nencki Institute.
3

L1 overexpression in rats with complete spinal cord transection downregulates phosphacan and upregulates synaptophysin, GAP43 and Adcy1 expression

76%
Platek R., Grycz K., Wieckowska K., Czarkowska-Bauch J., Kugler S., Schachner M., Skup M.
Acta Neurobiologiae Experimentalis
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2013
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tom 73
|
nr Suppl.1
Recovery after spinal cord injury requires neuronal remodeling which is regulated by cell adhesion molecules (CAMs) and chondroitin sulfate proteoglycans (CSPGs). CSPG may be potentially both inhibitory and supportive of regenerative plasticity. To verify whether chronic (5 weeks) L1 CAM overexpression in transected spinal cord of the rat, proven to promote recovery in mice, affects CSPG phosphacan and markers of synaptic plasticity, adeno-associated viral vector encoding L1 protein (AAV5-L1) was injected into L1 lumbar segment, immediately after transection at Th10/11. Control group received AAV5-EGFP. AAV5-L1 transduced neurons and astrocytes below the lesion, resulting in 170-fold increase in L1 mRNA level at low thoracic segments (Th
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