Prox1 expression in rod precursors and Müller cells
The transcription factor Prox1 acts in rodent retinogenesis, at least in promoting cell cycle withdrawal and horizontal cell production. In the mature retina, this protein is detected at the inner nuclear layer of all vertebrate groups. We have made a neurochemical characterisation of Prox1 + cell t...
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Veröffentlicht in: | Experimental eye research 2010-02, Vol.90 (2), p.267-276 |
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Zusammenfassung: | The transcription factor Prox1 acts in rodent retinogenesis, at least in promoting cell cycle withdrawal and horizontal cell production. In the mature retina, this protein is detected at the inner nuclear layer of all vertebrate groups. We have made a neurochemical characterisation of Prox1
+ cell types in two different vertebrate groups: mammals and fish. As well as Prox1
+ horizontal cells, we have observed Prox1
+/PKC-α
+ rod bipolar cells in mouse and cone ON and mixed b bipolar cells in goldfish. In mouse, only some CB
+ and CR
+ amacrine cells are Prox1
+ and the TH
+ and CR
+ amacrine cells are Prox1
−. However, in goldfish all CR
+ amacrine cells and TH
+ interplexiform cells are Prox1
+ and in the GCL displaced amacrine cells are also Prox1
+. Besides its expression in different interneuron subpopulations, we demonstrate, for the first time, the presence of Prox1 in the GS
+ and CRALBP
+ Müller cells in the retina of adult mammals and in developing and mature retina of fish. The presence of Prox1 in these cells appears to be related to survival or maintenance of their phenotype. We also demonstrate that in fish, where retinal formation persists into adulthood, Prox1 is expressed in dividing PCNA
+ cells at the peripheral growing zone, in rod progenitors at the inner and outer nuclear layers as well as in early progenitors during a retinal regeneration process after cryo-lesion of the peripheral growing zone. Therefore, Prox1 functions in vertebrate retinogenesis may be more complex than previously expected. |
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ISSN: | 0014-4835 1096-0007 |
DOI: | 10.1016/j.exer.2009.10.015 |