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

• Autorzy: Grycz K. , Gajewska-Wozniak O. , Ji B. , Czarkowska-Bauch J. , Skup M.
• Języki publikacji: EN

Abstrakty

EN

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.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2017
• Tom: 77
• Numer: Suppl.1
• Opis fizyczny: p.101

Twórcy

autor

Grycz K.

• Department of Neurophysiology, Laboratory of Restorative Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland

autor

Gajewska-Wozniak O.

• Department of Neurophysiology, Laboratory of Restorative Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland

autor

Ji B.

• Department of Neurophysiology, Laboratory of Restorative Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland

autor

Czarkowska-Bauch J.

• Department of Neurophysiology, Laboratory of Restorative Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland

autor

Skup M.

• Department of Neurophysiology, Laboratory of Restorative Neurobiology, Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland