FGF2 Deficiency Modulates Early Microglial Responses Without Affecting Photoreceptor Survival in a Retinitis Pigmentosa Mouse Model.

Fibroblast growth factor 2 (FGF2) is expressed in retinal Müller glia cells, and its expression increases in response to photoreceptor degeneration. To investigate the physiological relevance of FGF2, we analyzed retinal morphology and cellular responses in Fgf2-deficient (Fgf2(-/-)) mice. Loss of FGF2 did not affect photoreceptor survival, retinal vasculature, or retinal pigment epithelium (RPE) integrity. To further understand its role in retinal degeneration, Fgf2(-/-) mice were crossed with Pde6b(STOP/STOP) mice, a model of retinitis pigmentosa (RP). We then analyzed outer nuclear layer thickness, cone number, rod outer segments length, RPE morphology, and microglia number in Fgf2(-/-)Pde6b(STOP/STOP) and Pde6b(STOP/STOP) mice. Although FGF2 was upregulated in degenerating photoreceptor cells in the Pde6b(STOP/STOP) retina, its absence did not accelerate photoreceptor loss in Fgf2(-/-)Pde6b(STOP/STOP) mice. Interestingly, microglia numbers were significantly changed at early disease stages in Fgf2(-/-)Pde6b(STOP/STOP) retinas compared with Pde6b(STOP/STOP) controls, suggesting that FGF2 modulates inflammatory signaling. Together, these results show that loss of FGF2 does not alter photoreceptor degeneration kinetics or retinal morphology, but may contribute to the regulation of early microglial accumulation during degeneration.