Increased COX-2 after ureter obstruction attenuates fibrosis and is associated with EP₂ receptor upregulation in mouse and human kidney.

ABSTRACT:

Aim

Cyclooxygenase-2 (COX-2) activity protects against oxidative stress and apoptosis early in experimental kidney injury. The present study was designed to test the hypothesis that COX-2 activity attenuates fibrosis and preserves microvasculature in injured kidney. The murine unilateral ureteral-obstruction (UUO) model of kidney fibrosis was employed and compared with human nephrectomy tissue with and without chronic hydronephrosis.

Methods

Fibrosis and angiogenic markers were quantified in kidney tissue from wild-type and COX-2^-/- mice subjected to UUO for 7 days and in human kidney tissue. COX-enzymes, prostaglandin (PG) synthases, PG receptors, PGE₂ , and thromboxane were determined in human tissue.

Results

COX-2 immunosignal was observed in

SUBMITTER: Tofteng SS 

PROVIDER: S-EPMC9542224 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature