Human PTGS1 blocking peptide

Ankylosing spondylitis (AS) is the most common form of spondyloarthritis and is characterized by both inflammation and new bone formation. Despite many years of arduous efforts, we still do not clearly understand the pathogenesis of AS. The mechanisms behind new bone formation have been especially challenging to decipher due to the difficulty in obtaining tissue from spinal joints. The link between inflammation and bone formation looks obvious, but how inflammation drives spinal fusion is not evident. There are now two genes linked to prostaglandins (PG) that could be involved in AS pathogenesis. The first one is PTGER4 that codes for the EP4 receptor for PGE2 and the other one is PTGS1 that codes for prostaglandin-endoperoxide syntase 1 or cyclogenase 1. The bone morphogenic protein and Wnt signaling pathways could be important in signaling increased bone formation in AS. The disease-modifying potential of anti-inflammatories and tumor necrosis factor alpha inhibitors is discussed.

The aim of this study was to evaluate the occurrence and the activity of prostaglandin-endoperoxide synthase 1 (PTGS1), PTGS2, and endothelial, neuronal, and inducible nitric oxide synthase (e-, n-, and iNOS) in early, mid, late, and regressive corpora lutea (CL) of bovines during diestrus. PTGS1 immunoreactivity was localised mainly in the cytoplasm of small luteal cells, whereas PTGS2 was detected in the cytoplasm of large luteal cells during early, mid, and late stages. The immunoexpression of all NOS isoforms was observed in the nuclei of luteal cells in the CL stages examined. PTGS1 enzyme activity was higher in late CL and lower in regressive ones; PTGS2 increased from early to late CL and lowered in regressive ones. Constitutive NOS enzymatic activity (eNOS plus nNOS) was higher in late CL and lower in regressive ones; iNOS was lower in regressive CL. These results support the idea that PTGSs and NOSs regulate the bovine CL life span mainly during the transition from the luteotrophic to the luteolytic phase. (Folia Morphol 2013; 72, 1: 36-40)