Journal: Pharmaceutics

Article Title: Development of an Ophthalmic Hydrogel to Deliver MG53 and Promote Corneal Wound Healing †

doi: 10.3390/pharmaceutics17040526

Figure Lengend Snippet: rhMG53 inhibits vascular endothelial cell migration and tube formation. ( A ) rhMG53 did not induce cellular toxicity in HUVEC up to 100 μg/mL ( n = 5; ** p = 0.01). ( B ) Representative photomicrographs 24 h after scratch wounding, HUVEC treated with 50 μg/mL rhMG53 had significantly less migration and proliferation compared to control ( n = 9). Magnification 4×. ( C ) Quantification of the scratch area remaining at 24 h (**** p < 0.0001). ( D ) Representative photomicrographs and quantification of tube formation when HUVEC was seeded on Matrigel, followed by treatment with VEGF (10 ng/mL) with or without rhMG53 (50 μg/mL) for 18 h. rhMG53 significantly reduced tube length in VEGF-treated HUVEC ( n = 4; ** p = 0.0029). Magnification 4×. ( E ) HUVEC treated with IL-1B (10 ng/mL) with or without rhMG53 have decreased pSTAT3 protein expression; when normalized to total STAT3 expression, rhMG53 significantly (** p = 0.0084) decreased pSTAT3 ( n = 4). Statistical significance was assessed with the Kruskal–Wallis nonparametric test.

Article Snippet: For cell culture, KGM-2 culture media was purchased from Lonza (Walkersville, MD, USA), human corneal endothelial cell culture media from Celprogen (Torrance, CA, USA), Dulbecco’s modified Eagle’s media (DMEM), F-12K media, antibiotic, and fetal bovine serum (FBS) were purchased from Gibco (Carlsbad, CA, USA), endothelial cell growth supplement from Fisher Scientific (Waltham, MA, USA), and Matrigel from Corning Inc. (Corning, NY, USA).

Techniques: Migration, Control, Expressing