Pterygium, which is a fibrovascular overgrowth tissue of the conjunctiva, is a common ocular surface disorder worldwide, especially in China. 1 It is commonly triangular in shape and encroaches into the cornea, and originates from the degenerated conjunctiva and the underlying Tenon's capsule, resulting in abnormal fibrovascular tissue proliferation. 2 Many risk factors, such as sunny, hot, dry, windy, dusty climate, and smoky and tropical regions, are related to the pterygium. 1,2 Ultraviolet radiation is a major factor, that damages cell proliferation and induces abnormal cell proliferation, goblet cell hyperplasia, squamous metaplasia fibrosis, inflammation, angiogenesis and extracellular matrix breakdown. 3 The pathogenesis of pterygium still needs to be elucidated and deeply studied. To date, many surgical treatments have been performed on the pterygium including primary conjunctival closure, conjunctival autografts (CAs), limbal conjunctival autografts (LCAs), leaving bare sclera and amniotic membrane transplantation (AMT). [3][4][5] The main postoperative complication is recurrence; therefore, every effort should be directed in reducing the recurrence rate. However, no gold standard treatment for surgical procedures to completely prevent recurrence has been confirmed.

PurposeThe irreversible death of retinal ganglion cells (RGCs) plays an important role in the pathogenesis of glaucoma. Cellular repressor of E1A-stimulated genes (CREG), a secreted glycoprotein involved in cellular proliferation and differentiation, has been shown to protect against myocardial and renal ischemiareperfusion damage. However, the role of CREG in retinal ischemia-reperfusion injury (RIRI) remains unknown. In this study, we aimed to explore the effect of CREG on RGCs apoptosis after RIRI. MethodsWe used male C57BL/6J mice to establish the RIRI model. Recombinant CREG was injected at 1 day before RIRI. The expression and distribution of CREG were examined by immuno uorescence staining and western blotting. RGCs survival was assessed by immuno uorescence staining of at-mounted retinas. Retinal apoptosis was measured by the staining of TdT-mediated dUTP nick-end labeling and cleaved caspase-3. Electroretinogram analysis and optomotor response (ERG) were conducted to evaluate retinal function and visual acuity. The expressions of Akt, phospho-Akt (p-Akt), Bax, and Bcl-2 were analyzed by western blotting to determine the signaling pathways of CREG. ResultsWe found that CREG expression was decreased after RIRI, and intravitreal injection of CREG attenuated RGCs loss and retinal apoptosis. Besides, there was a signi cant recovery of the ERG a-and b-wave amplitudes and visual function after treatment with CERG. Furthermore, intravitreal injection of CREG upregulated p-Akt and Bcl-2 expression and downregulated Bax expression. ConclusionOur results demonstrated that CREG protected RGCs from RIRI and alleviated retinal apoptosis by activating Akt signaling. In addition, CREG also improved retinal function and visual acuity.

Purpose The irreversible death of retinal ganglion cells (RGCs) plays an important role in the pathogenesis of glaucoma. Cellular repressor of E1A-stimulated genes (CREG), a secreted glycoprotein involved in cellular proliferation and differentiation, has been shown to protect against myocardial and renal ischemia‐reperfusion damage. However, the role of CREG in retinal ischemia-reperfusion injury (RIRI) remains unknown. In this study, we aimed to explore the effect of CREG on RGCs apoptosis after RIRI.Methods We used male C57BL/6J mice to establish the RIRI model. Recombinant CREG was injected at 1 day before RIRI. The expression and distribution of CREG were examined by immunofluorescence staining and western blotting. RGCs survival was assessed by immunofluorescence staining of flat-mounted retinas. Retinal apoptosis was measured by the staining of TdT-mediated dUTP nick-end labeling and cleaved caspase-3. Electroretinogram analysis and optomotor response (ERG) were conducted to evaluate retinal function and visual acuity. The expressions of Akt, phospho-Akt (p-Akt), Bax, and Bcl-2 were analyzed by western blotting to determine the signaling pathways of CREG.Results We found that CREG expression was decreased after RIRI, and intravitreal injection of CREG attenuated RGCs loss and retinal apoptosis. Besides, there was a significant recovery of the ERG a- and b-wave amplitudes and visual function after treatment with CERG. Furthermore, intravitreal injection of CREG upregulated p-Akt and Bcl-2 expression and downregulated Bax expression.Conclusion Our results demonstrated that CREG protected RGCs from RIRI and alleviated retinal apoptosis by activating Akt signaling. In addition, CREG also improved retinal function and visual acuity.

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