Endocrine Abstracts

Introduction: The (GH) gene, identical to that in the pituitary, is expressed in retinal ganglion cells (RGCs) in chickens, rats, mice and humans. Retinal GH is a neuroprotective factor, as it promotes RGC survival and, in humans, the concentration of GH in vitreous fluid may be a marker for ocular disease. Increasing retinal GH expression could thus have therapeutic potential. The factors regulating retinal GH expression are, however, unknown. The possibility that GH-releasing hormone (GHRH) might be involved in the expression of retinal GH was therefore investigated.

Methodology: The possible presence of GHRH was determined by immunohistochemistry, using retinal sections from embryonic chicks and fixed QNR/D cells (a commercial quail neuroretinal cell line). The possible GH-releasing activity of GHRH was determined by the in vitro culture of QNR/D cells with exogenous GHRH and by the measurement of mRNA, using of quantitative PCR.

Results: GHRH immunoreactivity was abundantly present in the cytoplasm of chick retinal RGCs and in QNR/D cells and in both cases was co-localized with GH immunoreactivity. After a 24 h incubation in exogenous GHRH (at 10–6 M) GH mRNA in the QNR/D cells was significantly increased.

Conclusion: These results demonstrate, for the first time, that GHRH is present in retinal RGCs and that exogenous GHRH promotes retinal GH expression. The co-localization of GH and GHRH also suggests that retinal GH regulation occurs locally by autocrine or paracrine mechanisms. Increased GHRH signaling might therefore be utilized therapeutically to increase retinal GH secretion.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.