Regulated Expression of PTPRJ by COX-2/PGE2 Axis in Endothelial Cells

Abstract

BackgroundThis study was designed to examine a novel role of COX-2/PGE2 signaling as a regulator of PTPRJ expression in endothelial cells.MethodsA bioinformatics analysis of a whole genome array was carried out to search for regulators of PTPRJ expression in endothelial cells. PTPRJ expression was also measured in endothelial cells derived from a balloon injury-induced neointimal hyperplasia model in male New Zealand Rabbits. Changes in PTPRJ expression in HUVEC cells was examined by RT-PCR and western blotting after transfection of COX-2 plasmids or treatment with varying concentrations of a COX-2 inhibitor.ResultsA significant correlation was identified between COX-2 and PTPRJ in GSE39264 (Pearson correlation coefficient = −0.87; n = 22; P<0.01, two-tailed). PTPRJ expression was reduced during the progression of neointimal hyperplasia after balloon injury, which correlated with an increase in COX-2 expression. In HUVECs, after transfection with 1 µg/ml, 0.5 µg/ml, or 0.25 µg/ml COX-2 plasmids, PTPRJ protein expression was reduced to 0.60- (±0.08), 0.75- (±0.09), and 0.88- (±0.04) fold, respectively, while mRNA expression was reduced to 0.15- (±0.03), 0.26- (±0.05), and 0.47- (±0.09) fold, respectively. After treatment of HUVECs with 10 µmol/L or 20 µmol/L celecoxib, the reduction in PTPRJ expression induced by COX-2 over-expression was not only rescued but in fact increased by 2.05-fold (±0.28) and 3.34-fold (±0.37), respectively, compared with control.ConclusionsOur results suggest that COX-2/PGE2 signaling may function as a negative regulator of PTPRJ expression in endothelial cells both in vivo and vitro.

SdrG gene activated joint surface membrane protein PTPRJ to induce periprosthetic joint infection after total hip arthroplasty

“…It is a member of the protein tyrosine phosphatase family with tumour suppressor activity. 18,19 PTPRJ is downregulated in a variety of cancer tissues and cell lines and inhibits tumour activity by negatively regulating the expression of several proteins involved in proliferation signalling. 20,21 The platelet adhesion rate in PJI group was markedly larger compare to aseptic loosening and simple wound infection group, and the rate in simple wound infection group was larger than aseptic loosening group.…”

“…The expression of protein tyrosine phosphatase receptor J (PTPRJ) in PJI group was much higher than that in simple wound infection group, and the difference was statistically significant. It is a member of the protein tyrosine phosphatase family with tumour suppressor activity 18,19 . PTPRJ is downregulated in a variety of cancer tissues and cell lines and inhibits tumour activity by negatively regulating the expression of several proteins involved in proliferation signalling 20,21 .…”