Effects of LAR and PTP-BL phosphatase deficiency on adult mouse retinal cells activated by lens injury.

Using intact and lens-lesioned wildtype, leucocyte common antigen-related phosphatase deficient (LARDeltaP) and protein tyrosine phosphatase (PTP)-BAS-like phosphatase deficient (PTP-BLDeltaP) mice, we have evaluated the role of LAR and PTP-BL in retinal ganglion cell survival and neuritogenesis, and survival of activated retinal glia in vitro. There were no differences in in vitro retinal ganglion cell neuritogenesis and survival, as well as in activated retinal glia survival between intact wildtype and intact LARDeltaP or PTP-BLDeltaP mutant mice. In wildtype, LARDeltaP, and PTP-BLDeltaP retinal cultures, pre-conditioning by lens injury significantly increased retinal ganglion cell neuritogenesis and activated retinal glia numbers. However, in retinal cultures from lens-lesioned LARDeltaP and PTP-BLDeltaP mice, significantly smaller percentages of retinal ganglion cells grew neurites compared to lens-lesioned wildtype cultures. Significantly increased numbers of retinal ganglion cells survived in retinal cultures from lens-lesioned LARDeltaP mice compared to lens-lesioned wildtypes. PTP-BL phosphatase deficiency did not affect retinal ganglion cell survival in retinal cultures from lens-lesioned mice, though activated retinal glia numbers were significantly reduced in cultures from lens-lesioned PTP-BLDeltaP mice compared to lens-lesioned wildtypes. In summary, a functional phenotype was found in LARDeltaP and PTP-BLDeltaP mice, that was only obvious in lens lesion-stimulated retinal cultures. These observations suggest that LAR enhances retinal ganglion cell neurite initiation whilst suppressing retinal ganglion cell survival, and that PTP-BL facilitates both retinal ganglion cell neurite initiation and survival of activated retinal glia.