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Yingqian Li, Kin-Sang Cho, Dong Feng Chen; Regulation of neurite growth by IGFBP family members. Invest. Ophthalmol. Vis. Sci. 2017;58(8):2593.
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Activation of axonal growth program is a critical step in successful nerve regeneration following injury. As a standard model of CNS neurons, retinal ganglion cells (RGCs) shut down the intrinsic axon growth program during the perinatal period in mice. We found previously that insulin-like growth factor binding protein like protein-1 (IGFBPL1) functions as a secretory factor that positively regulates RGC axonal outgrowth in vitro through mediating IGF-1 signaling pathways. This prompts us to examine the roles of other IGFBPs in IGF-1-mediated neurite growth in neurons, particularly RGCs.
The expression levels of IGFBP family members were quantatively assessed in purified RGCs of wild type and Igfbpl1 deficient mice at different ages: embryonic day 16 (E16), postnatal day 0 (P0) and P10 by q-PCR. These ages are before and after RGCs lose their ability to regenerate axons. In addition, we studied the capacity of these binding proteins in mediating neurite outgrowth in NGF-induced PC12 cell cultures. Percentage of cell bearing neurite, cell survival rate and average neurite length were quantified under a masked fashion.
We found that the levels of IGFBP7 changed drastically before and after RGCs lose their ability to regenerate axons. Interestingly, the expression levels of many IGFBP family members showed dramatic changes in Igfbpl1 KO mice when compared with wild type mice, including IGFBP7. Addition of IGFBP7 to PC12 cell cultures inhibited neurite outgrowth in a dose-dependent manner, without affecting cell survival.
Our results suggest that IGFBP family members are important players, acting as either a negative or positive regulator, in mediating RGC neurite outgrowth.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.
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