Pax2+ astrocytes in the fish optic nerve head after optic nerve crush
Abstract The transcription factor Pax2 actively participates in the development of the vertebrate visual system. In adults, Pax2 expression persists in a subpopulation of Müller cells and/or astrocytes in the retina and optic nerve head (ONH), although its function remains elusive. In a previous wor...
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Veröffentlicht in: | Brain research 2013-01, Vol.1492 (25), p.18-32 |
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Zusammenfassung: | Abstract The transcription factor Pax2 actively participates in the development of the vertebrate visual system. In adults, Pax2 expression persists in a subpopulation of Müller cells and/or astrocytes in the retina and optic nerve head (ONH), although its function remains elusive. In a previous work we showed that the pax2 gene expression is modified and the Pax2+ astrocyte population in the ONH strongly reacted during the regeneration of the retina after a lesion in goldfish. In the present work we have analyzed Pax2 expression in the goldfish ONH after optic nerve (ON) crush. At one week post-injury, when the regenerating axons arrive at the ONH, the pax2 gene expression level increases as well as the number of Pax2+ astrocytes in this region. These Pax2+ astrocytes show a higher number of Cytokeratin (Ck)+ /GFAP+ processes compared with control animals. In contrast, a different S100+ astrocyte population is not modified and persists similar to that of controls. Furthermore, we find a ring that surrounds the posterior ONH that is formed by highly reactive astrocytes, positive to Pax2, GFAP, Ck, S100, GS and ZO1. In this region we also find a source of new astrocytes Pax2+ /PCNA+ that is activated after the injury. We conclude that Pax2+ astrocytes constitute a subpopulation of ONH astrocytes that strongly reacts after ON crush and supports our previous results obtained after retina regeneration. Altogether, this suggests that pax2 gene expression and Pax2+ astrocytes are probably directly involved in the process of axonal regeneration. |
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ISSN: | 0006-8993 1872-6240 |
DOI: | 10.1016/j.brainres.2012.11.014 |