| Title | Roles of PI3K and JAK Pathways in Viability of Retinal Ganglion Cells after Acute Elevation of Intraocular Pressure in Rats with Different Autoimmune Backgrounds. | | Author(s) | Huang Y, Li Z, Wang N, van Rooijen N, Cui Q | | Source | BMC Neurosci 2008 Aug 11; 9(1):78. | | Abstract | ABSTRACT:
BACKGROUND: We recently showed that PI3K/akt and JAK/STAT pathways play different roles in retinal ganglion cell (RGC) surviving after optic nerve (ON) injury and intraocular pressure (IOP) elevation, and autoimmune background modulates responses of macrophages and RGCs to ON injury and IOP elevation. In this study we investigated whether autoimmune background influences PI3K/akt and JAK/STAT functions following IOP elevation in Fischer 344 (F344) and Lewis rats that are of different autoimmune profiles. IOP elevation was performed at 110mmHg for 2 hours. Pathway inhibitors were applied intravitreally to block respective pathway signal transduction. To examine the role of these pathways independent of macrophages, phagocytic cells in the retina were removed by intravitreal application of clodronate liposomes.
RESULTS: We found that significantly more RGCs were lost in Lewis than F344 rats 3 weeks after IOP elevation. Inhibition of PI3K/akt or JAK/STAT pathway resulted in significant loss of RGCs in both rat strains. More macrophages were seen in Lewis than in F344 eyes after IOP elevation, and removal of macrophages in the eye by clodronate liposomes protected RGCs in both strains.
CONCLUSIONS: This study thus demonstrates that PI3K/akt and JAK/STAT pathways mediate RGC surviving after IOP elevation in both strains, and autoimmune background does not influence the functions of these two pathways. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 18691439 |
|
