Activation of cGMP/PKG/p65 signaling associated with PDE5-Is downregulates CCL5 secretion by CD8 ⁺ T cells in benign prostatic hyperplasia.

ABSTRACT:

Background

Benign prostatic hyperplasia (BPH) is the most common urological disease in elderly men, but the underlying pathophysiological mechanisms are complex and not fully understood. Phosphodiesterase type 5 inhibitors (PDE5-Is) used to treat BPH could upregulate the cyclic guanosine monophosphate (cGMP)-dependent protein kinase G (PKG) signaling, which was shown to blunt inflammation in the prostate. Our previous findings indicate that CD8⁺ T cells promote the proliferation of BPH epithelial cells (BECs) in low androgen conditions through secretion of CCL5; however, the role of the cGMP/PKG pathway in the process is unclear.

Methods

Paraffin-embedded tissues were used for expression quantity of CD8⁺ T cells, CCL5, cyclin D1, and PDE5 protein by imm

SUBMITTER: Jin S 

PROVIDER: S-EPMC6593656 | biostudies-literature | 2019 Jun

REPOSITORIES: biostudies-literature