Acute spinal cord injury (SCI) results in immediate tissue damage, followed by long-lasting secondary injury associated to the release of inflammatory molecules, including nucleotides, which may contribute to damage development by activating specific membrane receptors. In this respect, the pathological over-activation of the new purinergic receptor GPR17 has been recently proposed to participate to brain ischemia (Ciana et al., 2006. EMBO J 25:4615). In this study we aimed at evaluating GPR17 expression in the spinal cord and its possible role in SCI-associated damage. Adult mice were subjected to extradural SCI with an aneurysm clip after T6-T9 laminectomy and injected with bromodeoxyuridine to evaluate cell proliferation. GPR17 expression was evaluated by immunohistochemistry 24h, 72h and 1 week after injury. In sham-operated mice, GPR17 was expressed by many III-tubulin-positive neurons and CC1-positive oligodendrocytes, but not by GFAP-positive astrocytes. Ependymal cells and the 29.8±2.1% of cells expressing the neuroprogenitor marker NG2 also expressed GPR17. After SCI, cell proliferation strongly increased in parallel with the total number of GPR17-expressing cells. In fact, despite the massive death of GPR17-positive neurons and oligodendrocytes, a proliferating population of GPR17- and IB4-positive microglia/macrophages emerged. GPR17 was never found in Nestin- and GFAP double-positive reactive astrocytes. Taken together, in a similar way to brain ischemia, our data show an increase in GPR17 expression that may contribute to acute SCI damage. On the other hand, presence of GPR17 on neuroprogenitor-like cells also suggests a potential role of this receptor in the long-term reparative changes associated to SCI.

GPR17 expression in healthy and injured spinal cord / G. Villa, S. Ceruti, T. Genovese, E. Mazzon, P. Bramanti, S. Cuzzocrea, M.P. Abbracchio. - In: PURINERGIC SIGNALLING. - ISSN 1573-9538. - 4:suppl. 1(2008), pp. S45-S45. ((Intervento presentato al convegno Purines tenutosi a Copenhagen nel 2008 [10.1007/s11302-008-9116-0].

GPR17 expression in healthy and injured spinal cord

G. Villa
Primo
;
S. Ceruti
Secondo
;
M.P. Abbracchio
Ultimo
2008

Abstract

Acute spinal cord injury (SCI) results in immediate tissue damage, followed by long-lasting secondary injury associated to the release of inflammatory molecules, including nucleotides, which may contribute to damage development by activating specific membrane receptors. In this respect, the pathological over-activation of the new purinergic receptor GPR17 has been recently proposed to participate to brain ischemia (Ciana et al., 2006. EMBO J 25:4615). In this study we aimed at evaluating GPR17 expression in the spinal cord and its possible role in SCI-associated damage. Adult mice were subjected to extradural SCI with an aneurysm clip after T6-T9 laminectomy and injected with bromodeoxyuridine to evaluate cell proliferation. GPR17 expression was evaluated by immunohistochemistry 24h, 72h and 1 week after injury. In sham-operated mice, GPR17 was expressed by many III-tubulin-positive neurons and CC1-positive oligodendrocytes, but not by GFAP-positive astrocytes. Ependymal cells and the 29.8±2.1% of cells expressing the neuroprogenitor marker NG2 also expressed GPR17. After SCI, cell proliferation strongly increased in parallel with the total number of GPR17-expressing cells. In fact, despite the massive death of GPR17-positive neurons and oligodendrocytes, a proliferating population of GPR17- and IB4-positive microglia/macrophages emerged. GPR17 was never found in Nestin- and GFAP double-positive reactive astrocytes. Taken together, in a similar way to brain ischemia, our data show an increase in GPR17 expression that may contribute to acute SCI damage. On the other hand, presence of GPR17 on neuroprogenitor-like cells also suggests a potential role of this receptor in the long-term reparative changes associated to SCI.
Settore BIO/14 - Farmacologia
2008
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/57787
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