Anti-PTPRO (aa 151-284) polyclonal antibody

Preeclampsia is a serious complication of pregnancy and leads to maternal hypertension and proteinuria. It remains a major health problem for mothers and babies across the world due to high maternal and fetal morbidity and mortality. Accumulated data have implicated the critical role of microRNA in preeclampsia. However, to date, the role of miR-548c-5p in preeclampsia remains vaguely understood. In this study, we first elucidate the role of miR-548c-5p and its underlying molecular mechanism in preeclampsia. Compared with healthy controls, miR-548c-5p was obviously downregulated in serum exosomes and placental mononuclear cells in patients with preeclampsia. Nonetheless, PTPRO was significantly upregulated and negatively associated with miR-548c-5p in placental mononuclear cells in patients with preeclampsia. PTPRO was a target of miR-548c-5p. PTPRO was downregulated in the miR-548c-5p-overexpressed macrophages. In addition, miR-548c-5p could inhibit the proliferation and activation of LPS-stimulated macrophages, as evidenced by decreased levels of inflammatory cytokines (IL-12 and TNF-) and less nuclear translocation of pNF-B in pTHP1 cells. MiR-548c-5p acts as an anti-inflammatory factor in preeclampsia. The axis of miR-548c-5p/PTPRO/NF-B may provide novel targets for the diagnosis and treatment of preeclampsia.

Protein tyrosine phosphatase receptor type O (PTPRO), one of the receptor types of phosphotyrosine phosphatases (PTP), was recently described as a tumor suppressor in various kinds of cancers. We aimed to clarify the role of PTPRO in hepatocellular carcinoma (HCC). It was demonstrated in 180 pairs (120 male and 60 female) of clinical HCC specimens that the PTPRO level was significantly reduced, as compared with adjacent tissue, and the PTPRO level in male adjacent tissue was lower than in female. We further found that estrogen receptor alpha (ER alpha) could up-regulate PTPRO expression as a transcription factor. Moreover, an in vitro study showed that cell proliferation was inhibited and apoptosis was promoted in PTPRO-transduced HCC cell lines, whereas an in vivo study represented that tumor number and size was increased in ptpro(-/-) mice. As a result of its tumor-suppressive position, PTPRO was proved to down-regulate signal transducers and activators of transcription (STAT3) activity dependent on Janus kinase 2 (JAK2) and phosphoinositide 3-kinase (PI3K) dephosphorylation. Conclusions: PTPRO expression results in pathological deficiency and gender bias in HCC, which could be attributed to ERa regulation. The suppressive role of PTPRO in HCC could be ascribed to STAT3 inactivation. (HEPATOLOGY 2013;57:678-688)