Louisiana Via Research Day Book 2026

Biomedical Research: Section 2

Biomedical Research: Section 2

Krishna Patel, BS 1 ; Veronica Chang, OMS-II 1 ; Nektarios Barabutis, PhD 2 ; Stephen DiGiuseppe, PhD 1 , Rebekah Morrow, PhD 1 1 VCOM-Louisiana; 2 ULM College of Pharmacy 21 CHANGES IN INFLAMMATORY RESPONSE IN CORNEAL ENDOTHELIAL CELLS TREATED WITH GROWTH HORMONE RELEASING HORMONE ANTAGONISTS

Background: Original Research Changes in Inflammatory Response in Corneal Endothelial Cells Treated with Growth Hormone-Releasing Hormone Antagonists Context: Corneal endothelial dysfunction (CED) is an important cause of vision loss and can occur when inflammation damages the cells that maintain corneal clarity. Bacterial toxins such as lipopolysaccharide (LPS) can disrupt the endothelial barrier by altering the cell cytoskeleton and the tight junctions that normally hold cells together, leading to increased permeability and inflammation. Growth hormone–releasing hormone antagonists (GHRHAnt) have been shown to reduce inflammation and help preserve endothelial barrier function, suggesting they may have therapeutic potential in inflammatory corneal injury. Objective: Bovine corneal endothelial cells were treated with LPS alone or in combination with a GHRH antagonist to examine how GHRHAnt influence inflammatory changes at both the structural level and through secreted inflammatory signals.

Methods: Immunofluorescence imaging was used to visualize tight junctions and actin organization. To evaluate inflammatory signaling at the cellular level, culture supernatants were collected and analyzed using enzyme-linked immunosorbent assay (ELISA) to measure the release of pro-inflammatory mediators. Results: Immunofluorescence microscopy revealed that LPS treatment disrupted normal cell–cell contacts, produced irregular or ruffled cell borders, and increased actin stress fiber formation. Cells treated with both LPS and GHRHAnt showed partial preservation of monolayer organization. ELISA results showed no measurable differences in inflammatory mediator secretion at early time points, despite clear structural changes observed in the cells. Conclusions: These findings suggest that inflammatory signaling may begin within the cell before measurable cytokine release occurs. Future studies using longer exposure times may help determine when inflammatory mediators are released and whether GHRH antagonists reduce corneal endothelial inflammation over time.

33

32

2026 Research Recognition Day