E-cadherin expression is inversely correlated with aging and inflammation in the prostate

Benign prostatic hyperplasia (BPH) is a prostatic disease that is significantly associated with aging. However, it is not well understood how aging contributes to BPH pathogenesis. Several factors associated with an increased risk of BPH are also associated with increasing age, including chronic inflammation and declining epithelial barrier function. Thus, this study explored the potential associations between aging, loss of adherens junction protein E-cadherin and the presence of inflammatory mediators in prostate tissue specimens from healthy young donor and BPH patients.

Serial prostate sections from a cohort of five donors aged 15-26 years and 13 BPH patients aged 50-77 years were immunostained with E-cadherin, COX-2, CD4, CD8, CD20 and CD68. E-cadherin and COX-2 H-Scores and the number of inflammatory cells were calculated for the same area in donor, normal adjacent prostate to BPH (NAP) and BPH specimens. Quantification and statistical correlation analyses were performed for comparisons between groups.

E-cadherin was decreased in aged NAP tissues and in BPH compared to young donor tissue. E-cadherin was inversely correlated with age and infiltration of inflammatory cells in NAP compared to young healthy donor prostate. Stromal COX-2 was positively correlated with age and inflammation. E-cadherin was further down-regulated in BPH, while COX-2 H-Scores were not significantly altered in BPH compared to NAP.

These findings suggest that aging is associated with down-regulation of E-cadherin and up-regulation of stromal COX-2 immunostaining in the prostate. E-cadherin immunostaining was inversely associated with age and inflammation, while stromal COX-2 immunostaining was positively associated with age and inflammation in the prostate. These findings suggest that the prostate epithelial barrier is altered and inflammation is increased with age in the prostate. These changes are further exacerbated in BPH, and may be involved in BPH pathogenesis.