Enhanced expression of SLC4A11 by tert-Butylhydroquinone is mediated by direct binding of Nrf2 to the promoter of SLC4A11.

Background: SLC4A11, a Na + dependent OH transporter, is highly expressed in the epithelium and endothelium of the cornea. Mutations in SLC4A11 cause congenital hereditary endothelial dystrophy (CHED), a progressive disease with gradual loss of vision and characterized by degeneration and dysfunction of corneal endothelial cells. SLC4A11 expression is also responsive to oxidative stress.

Determination of Oxidative Stress Markers in the Aqueous Humor and Corneal Tissues of Patients With Congenital Hereditary Endothelial Dystrophy.

Purpose: The aim of this study is to determine the presence of oxidative stress markers in the aqueous humor (AH) and corneal tissues of patients with congenital hereditary endothelial dystrophy (CHED).

Methods: Interventional prospective study was undertaken to quantify levels of ascorbic acid and glutathione in the AH of patients with CHED. AH was collected from patients undergoing keratoplasty and levels of ascorbic acid and glutathione were determined using biochemical assays and measured spectrophotometrically.

Differential expression of antimicrobial peptides in corneal infection and regulation of antimicrobial peptides and reactive oxygen species by type III secretion system of Pseudomonas aeruginosa.

Pseudomonas aeruginosa is an opportunistic pathogen and is the major cause of corneal infection worldwide that secret several virulent toxins through its type III secretion system (T3SS). In defense against pathogenic insults, epithelial cells and macrophages express antimicrobial peptides (AMPs) that are essential components of host immune response. In this study, we have determined the expression of several AMPs in patients with P.

SLC4A11 depletion impairs NRF2 mediated antioxidant signaling and increases reactive oxygen species in human corneal endothelial cells during oxidative stress.

Corneal endothelial dystrophy is a progressive disease with gradual loss of vision and characterized by degeneration and dysfunction of corneal endothelial cells. Mutations in SLC4A11, a Na dependent OH transporter, cause congenital hereditary endothelial dystrophy (CHED) and Fuchs' endothelial corneal dystrophy (FECD), the two most common forms of endothelial degeneration. Along with genetic factors, oxidative stress plays a role in pathogenesis of several corneal diseases.