Diabetes compromises tight junction protein claudin 14 in the urinary bladder

Area of Science:

• Urology
• Diabetology
• Cell Biology

Background:

• Diabetes increases infection risk and antibiotic resistance, necessitating alternative treatments.
• Compromised host conditions in diabetes favor disease progression.
• Cell junction proteins are crucial for epithelial barrier integrity against pathogens.

Purpose of the Study:

• Investigate the impact of high glucose on urinary bladder cell junction proteins.
• Examine the role of claudin 14 expression in diabetic urinary bladders.
• Explore the relationship between intracellular calcium and claudin 14 in high glucose conditions.

Main Methods:

• Analyzed claudin 14 expression in human urine exfoliated cells and type 2 diabetic mouse bladders.
• Conducted in vitro studies on high glucose-treated human uroepithelial cells.
• Assessed the effects of external calcium supplementation on cell migration and claudin 14 expression.

Main Results:

• Claudin 14 expression was compromised in diabetic human and mouse urinary bladders.
• Lower intracellular calcium levels correlated with reduced claudin 14 expression in high glucose.
• Calcium supplementation restored claudin 14 expression and improved cell migration via focal adhesion and β-1 integrins.

Conclusions:

• High glucose in diabetes compromises urinary bladder epithelial barrier function by downregulating claudin 14.
• Intracellular calcium levels are critical regulators of claudin 14 expression and epithelial integrity.
• Restoring epithelial barrier function through calcium supplementation may be a therapeutic strategy for diabetic complications.