Polycystic ovary syndrome (PCOS) is a common endocrine disease of child-bearing period women and one of the main causes of infertility in women. Pentraxin 3 (PTX3) is a multifunctional protein with a series of biological activities. PTX3 participates in the regulation of insulin secretion and glucose metabolism, ovarian cumulus cell function, inflammatory factor activity, androgen metabolism, lipid absorption and transport, and endothelial cell function, thereby improving insulin resistance, promoting follicular development and ovulation, reducing chronic inflammation, inhibiting androgen levels, improving lipid metabolism abnormalities and preventing atherosclerosis and cardiovascular diseases, thus participating in the occurrence of PCOS and its complications. This article reviews the mechanism of PTX3 in PCOS and its complications, trying to provide new ideas and directions for the study of PCOS pathogenesis and its clinical diagnosis and treatment.
C-Reactive Protein/metabolism* ; Child ; Female ; Humans ; Insulin Resistance ; Polycystic Ovary Syndrome/physiopathology* ; Serum Amyloid P-Component/metabolism*

<p>BACKGROUNDAcute aortic dissection is a life-threatening cardiovascular emergency. Pentraxin-3 (PTX3) is proposed as a prognostic marker and found to be related to worse clinical outcomes in various cardiovascular diseases. This study sought to investigate the association of circulating PTX3 levels with in-hospital mortality in patients with acute Type A aortic dissection (TAAD).p><p>METHODSA total of 98 patients with TAAD between January 2012 and December 2015 were enrolled in this study. Plasma concentrations of PTX3 were measured upon admission using a high-sensitivity enzyme-linked immunosorbent assay system. Patients were divided into two groups as patients died during hospitalization (Group 1) and those who survived (Group 2). The clinical, laboratory variables, and imaging findings were analyzed between the two groups, and predictors for in-hospital mortality were evaluated using multivariate analysis.p><p>RESULTSDuring the hospital stay, 32 (33%) patients died and 66 (67%) survived. The patients who died during hospitalization had significantly higher PTX3 levels on admission compared to those who survived. Pearson's correlation analysis demonstrated that PTX3 correlated positively with high-sensitivity C-reactive protein (hsCRP), maximum white blood cell count, and aortic diameter. Multivariate logistic regression analysis demonstrated that PTX3 levels, coronary involvement, cardiac tamponade, and a conservative treatment strategy are significant independent predictors of in-hospital mortality in patients with TAAD. The receiver operating characteristic curve analysis further illustrated that PTX3 levels on admission were strong predictors of mortality with an area under the curve of 0.89. A PTX3 level ≥5.46 ng/ml showed a sensitivity of 88% and a specificity of 79%, and an hsCRP concentration ≥9.5 mg/L had a sensitivity of 80% and a specificity of 69% for predicting in-hospital mortality.p><p>CONCLUSIONHigh PTX3 levels on admission are independently associated with the in-hospital mortality in patients with TAAD.p>
Adult ; Aged ; Aneurysm, Dissecting ; blood ; mortality ; Aortic Aneurysm ; blood ; mortality ; C-Reactive Protein ; metabolism ; Female ; Hospital Mortality ; Humans ; Logistic Models ; Male ; Middle Aged ; Serum Amyloid P-Component ; metabolism

PURPOSE: To evaluate plasma pentraxin 3 (PTX3) in patients with retinal vein occlusion (RVO), and investigate the possibility of its role as a predictive biomarker. METHODS: Nested case-control study. The study included 57 patients with RVO and 45 age- and gender-matched subjects without RVO as controls. Plasma PTX3 and C-reactive protein concentration were measured in both groups a posteriori from frozen samples by using an enzyme-linked immunosorbent assay kit. RESULTS: The measured PTX3 value for the RVO group was 1,508 +/- 1,183 pg/mL (mean +/- standard deviation) and 833 +/- 422 pg/mL for the controls (p < 0.001). There was no significant difference in PTX3 levels between patients with central retinal vein occlusion and branched retinal vein occlusion (1,468 +/- 1,300 vs. 1,533 +/- 1,121 pg/mL; p = 0.818). CONCLUSIONS: Our data seems to support the role of chronic inflammation and ischemia in the development of RVO. It is possible that PTX3 can be used as a diagnostic biomarker of RVO.
Acute-Phase Proteins/metabolism ; Adult ; Aged ; Aged, 80 and over ; Biomarkers/*blood ; C-Reactive Protein/*metabolism ; Case-Control Studies ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Male ; Middle Aged ; Retinal Vein Occlusion/*blood/diagnosis ; Serum Amyloid P-Component/*metabolism

<p>BACKGROUNDEsophageal cancer is the sixth leading cause of cancer-related death worldwide. Pentraxin-3 (PTX3) is a member of the PTX superfamily. Here, we investigated the role of PTX3 in esophageal squamous cell carcinoma (ESCC).p><p>METHODSThe effect of PTX3 on ESCC cell proliferation, colony formation, apoptosis, migration, and invasion was investigated using cell viability assays, colony formation assays, flow cytometry, and migration and invasion assays. The effect of PTX3 on the tumorigenicity of ESCC in vivo was investigated with xenograft studies in nude mice.p><p>RESULTSPTX3 overexpression in ESCC cells reduced cellular proliferation and colony formation (P < 0.05) and increased the rate of apoptosis (P < 0.05). PTX3 expression had no significant effect on the migratory or invasive potential of ESCC cells. In our mouse model of human ESCC, we achieved 100% successful tumor establishment. Compared with the control and empty vector-expressing groups, the PTX3-expressing group formed significantly smaller tumors (P < 0.05).p><p>CONCLUSIONSThis study indicates that PTX3 might play an inhibitory role in ESCC.p>
Animals ; Apoptosis ; genetics ; physiology ; C-Reactive Protein ; genetics ; metabolism ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; genetics ; physiology ; Cell Survival ; genetics ; physiology ; Esophageal Neoplasms ; metabolism ; pathology ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Serum Amyloid P-Component ; genetics ; metabolism ; Xenograft Model Antitumor Assays

PURPOSE: To investigate the production of long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmic reticulum (ER) stress and its role in ER stress-associated cell death, PTX3 expression was evaluated in the human retinal pigment epithelial cell line, ARPE-19. METHODS: PTX3 production in ARPE-19 cells was analyzed in the absence or presence of tunicamycin treatment by enzyme-linked immunosorbent assay. PTX3 protein and mRNA levels were estimated using western blot analysis and real-time reverse transcription-polymerase chain reaction, respectively. Protein and mRNA levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and ARPE-19 cell viability were measured in the presence of tunicamycin-induced ER stress in control or PTX3 small hairpin RNA (shRNA)-transfected ARPE-19 cells. RESULTS: The protein and mRNA levels of PTX3 were found to be significantly increased by tunicamycin treatment. PTX3 production was significantly decreased in inositol-requiring enzyme 1α shRNA-transfected ARPE-19 cells compared to control shRNA-transfected cells. Furthermore, pretreatment with the NF-κB inhibitor abolished tunicamycin-induced PTX3 production. Decreased cell viability and prolonged protein and mRNA expression of CHOP were observed under tunicamycin-induced ER stress in PTX3 shRNA transfected ARPE-19 cells. CONCLUSIONS: These results suggest that PTX3 production increased in the presence of tunicamycin-induced ER stress. Therefore, PTX3 could be an important protector of ER stress-induced cell death in human retinal pigment epithelial cells. Inositol-requiring enzyme 1α and the NF-κB signaling pathway may serve as potential targets for regulation of PTX3 expression in the retina. Therefore, their role in PTX3 expression needs to be further investigated.
Anti-Bacterial Agents/pharmacology ; Apoptosis ; Blotting, Western ; C-Reactive Protein/biosynthesis/*genetics ; Cells, Cultured ; Endoplasmic Reticulum Stress/*drug effects/genetics ; Enzyme-Linked Immunosorbent Assay ; *Gene Expression Regulation ; Humans ; Polymerase Chain Reaction ; RNA, Messenger/*genetics ; Retinal Pigment Epithelium/*metabolism/pathology ; Serum Amyloid P-Component/biosynthesis/*genetics ; Tunicamycin/*pharmacology

<p>OBJECTIVETo investigate the regulatory effects of Shenfu Injection (SFI, ) on hemodynamic parameters and serum proteins in rats with post-infarction chronic heart failure (CHF).p><p>METHODSForty-five healthy Wistar rats were randomized into three groups: sham, heart failure (model) and SFI group. The CHF was induced by left coronary artery ligation. Seven days after the surgical operation, animals in the sham group and the model group received saline (6.2 mL/kg/d), while animals in the SFI group received SFI (6.2 mL/kg d) intraperitoneally. Four weeks later, cardiac hemodynamic parameters were measured via the carotid route. The expression of serum proteins was analyzed by two-dimensional electrophoresis and matrix-assisted laser desorption/ionization time-of-flight mass spectrometer (MALDI-TOF MS).p><p>RESULTSRecording of hemodynamic parameters showed that left ventricular systolic pressure (LVSP), maximum rate of left ventricular pressure (+dp/dtmax) rise, and maximum rate of left ventricular pressure (-dp/dtmax) decrease, while the left ventricular end diastolic pressure (LVEDP) rose in the model group compared to those in the sham group (P <0.05). The results of the MALDI-TOF MS indicated that haptoglobin (HP), pentraxin 3 (PTX3) and alpha-1-antitrypsin were up-regulated, while serum albumin and 40S ribosomal protein were down-regulated in the model group (P <0.05). Compared with the model group, LVSP, +dp/dtmax and -dp/dtmax were higher, while LVEDP was lower in the SFI group (P<0.05). Expression levels of HP and PTX3 were lower than in the model group (P<0.05).p><p>CONCLUSIONSFI could improve hemodynamic function and decrease inflammatory reactions in the pathophysiology of CHF. The serum proteins HP and PTX3 could be potential biomarkers for chronic ischemic heart failure, and they could also be the serum protein targets of SFI.p>
Animals ; Blood Proteins ; metabolism ; C-Reactive Protein ; metabolism ; Chronic Disease ; Drugs, Chinese Herbal ; therapeutic use ; Electrophoresis, Gel, Two-Dimensional ; Haptoglobins ; metabolism ; Heart Failure ; blood ; complications ; drug therapy ; physiopathology ; Heart Function Tests ; Hemodynamics ; Hydrogen-Ion Concentration ; Imaging, Three-Dimensional ; Inflammation ; complications ; drug therapy ; Male ; Myocardial Ischemia ; blood ; complications ; drug therapy ; physiopathology ; Phytotherapy ; Proteome ; metabolism ; Rats, Wistar ; Serum Amyloid P-Component ; metabolism ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization