Expression of angiogenic factor with G patch and FHA domains 1 (AGGF1) in placenta from patients with preeclampsia.

INTRODUCTION: Preeclampsia (PE) is a major contributor to maternal and foetal morbidity and mortality worldwide. It manifests as high blood pressure and proteinuria in women at more than 20 weeks of gestation. Abnormal levels of anti- and pro-angiogenesis factors are known to be associated with PE. In the present study, we aimed to determine the localisation of angiogenic factor with G patch and FHA domains 1 (AGGF1) in the placenta and to compare the expression levels of AGGF1 in the third-trimester placentas of preeclamptic and normotensive pregnancies. MATERIALS AND METHODS: Placental tissue samples were collected from women with PE (n = 28) and without PE (n = 28). The normotensive controls without PE were matched for gestational age at delivery with the patients with PE. The expression levels of AGGF1 in the placental tissues were evaluated using immunohistochemistry, quantitative reverse transcription polymerase chain reaction and Western blot. RESULTS: The immunoexpression of AGGF1 was localised in the syncytiotrophoblast tissue. Notable, the mRNA and protein expression levels of AGGF1 were decreased in preeclamptic placentas as compared with the normotensive control group (P < 0.05). DISCUSSION: Our results suggest that the decreased AGGF1 in preeclamptic placentas may be related to the pathogenesis of preeclampsia.

NLRP3 inflammasome activation by estrogen promotes the progression of human endometrial cancer.

BACKGROUND: Activation of NLPR3 inflammasome is associated with the development and progression of some types of malignant tumors, but its role in endometrial cancer is unclear. This study aimed to investigate the expression and function of NLRP3 inflammasome in endometrial cancer. MATERIALS AND METHODS:  The expression levels of NLRP3, its inflammasome components and estrogen receptor ß in endometrial cancer and paired non-tumor tissues were detected. The effects of NLPR3 silencing or overexpression on the proliferation, migration, and invasion of Ishikawa and HEC-1A cells were determined. The impact of NLPR3 silencing on the growth of implanted tumors was determined in vivo. The effects of estrogen on NLPR3 inflammasome activation and Ishikawa cell proliferation were determined. RESULTS: The upregulation of NLRP3, ASC, caspase-1, and IL-1ß was associated with the progression of endometrial cancer and poor survival. NLPR3 silencing inhibited the proliferation, migration, and invasion of endometrial cancer cells while NLPR3 overexpression had opposite effects. NLPR3 silencing reduced IL-1ß and caspase-1 expression and the growth of implanted endometrial tumors, accompanied by decreased pro-IL-1ß maturation. Estrogen enhanced NLPR3, ERß, pro-IL-1ß, IL-1ß expression, and endometrial cancer cell proliferation, which were mitigated by treatment with ERß inhibitor but not ERα inhibitor. CONCLUSION: Our results suggest that estrogen acts through ERß to enhance the activation of NLPR3 inflammasome and promote the progression of endometrial cancer. NLPR3 inflammasome may be a new therapeutic target for endometrial cancer.