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*

BACKGROUND AND OBJECTIVES: As shown in previous studies, pentraxin 3 (PTX3) can be a useful inflammatory marker for metabolic syndrome and central obesity. Serum PTX3 levels are also an independent factor associated with visceral fat area. The aim of this study was to assess the role of PTX3 as an inflammatory maker in patients with central obesity undergoing primary percutaneous coronary intervention (PCI) following an ST-segment elevation myocardial infarction (STEMI). SUBJECTS AND METHODS: From December 2007 to June 2008, 40 subjects (mean age: 61+/-11 years, M : F=34 : 6) with STEMI who underwent primary PCI were enrolled. We determined waist circumference, waist/hip ratio, body mass index (BMI), and visceral and total fat area via fat computed tomography (FAT-CT), and compared them with serum PTX3 concentrations. RESULTS: The serum PTX3 concentration was closely related to FAT-CT-estimated visceral fat area (r=0.41, p<0.01) and total fat area (r=0.38, p=0.01), respectively. The serum PTX3 concentration was not related to waist circumference (r=0.27, p=0.20), waist circumference/hip ratio (r=0.25, p=0.16), BMI (r=0.04, p=0.80) and lipid profiles, respectively. Among the parameters determining metabolic syndrome, an increasing visceral fat area had the strongest association with PTX3 concentrations. CONCLUSION: In patients with STEMI, PTX3 is associated with central obesity and it is significantly and independently correlated with visceral fat area. FAT-CT-estimated visceral fat area is the most reliable factor associated with serum PTX3 levels in patients with STEMI and central obesity.
Body Mass Index ; C-Reactive Protein ; Humans ; Intra-Abdominal Fat ; Myocardial Infarction ; Obesity, Abdominal ; Percutaneous Coronary Intervention ; Serum Amyloid P-Component ; Waist Circumference

<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

BACKGROUND AND OBJECTIVES: Pentraxin 3 (PTX3) was shown to be elevated in the acute phase of acute myocardial infarction (AMI) and to have prognostic significance in AMI patients. The aim of this study was to estimate whether the value of PTX3 could be used as a prognostic biomarker, with the global registry of acute coronary events (GRACE) risk assessment tool, in patients with acute coronary syndrome (ACS). SUBJECTS AND METHODS: Between July 2007 and June 2008, 137 patient subjects (mean age : 61+/-12 years, M : F=108 : 29) with ACS who underwent coronary intervention, but did not have a prior percutaneous coronary intervention (PCI) and/or follow-up coronary angiogram, were enrolled. We estimated the all-cause mortality or death/MI, in-hospital and to 6 months, using the GRACE risk scores and compared these estimates with serum PTX3 concentrations. RESULTS: The serum PTX3 concentration showed a significant increase in ST segment elevation myocardial infarction (STEMI) greater than the unstable angina pectoris (UAP) group (2.4+/-2.1 ng/mL vs. 1.3+/-0.9 ng/mL, p= 0.017, respectively), but did not show a significant difference between non-ST segment elevation myocardial infarction (NSTEMI) and the UAP group (1.9+/-1.4 ng/mL vs. 1.3+/-0.9 ng/mL, p=0.083, respectively). The serum PTX3 concentration was closely related to death/MI in-hospital (r=0.242, p=0.015) and death/MI to 6 months (r=0.224, p=0.023), respectively. The serum PTX3 concentration was not related to all-cause mortality in-hospital (r=0.112, p=0.269) and to 6 months (r=0.132, p=0.191), respectively. Among the parameters determining the GRACE risk scores, the degree of Killip class in congestive heart failure (CHF) was independently associated with the supramedian PTX3 concentration [odds ratio: 2.229 (95% confidence interval: 1.038-4.787), p=0.040]. CONCLUSION: The serum PTX3 level provides important information for the risk stratification of CHF among the parameters determining the GRACE risk scores in subjects with ACS.
Acute Coronary Syndrome ; Angina, Unstable ; C-Reactive Protein ; Estrogens, Conjugated (USP) ; Follow-Up Studies ; Heart Failure ; Humans ; Myocardial Infarction ; Percutaneous Coronary Intervention ; Risk Assessment ; Serum Amyloid P-Component

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

Diabetic nephropathy (DN) is currently the most common complication of diabetes. It is considered to be one of the leading causes of end-stage renal disease (ESRD) and affects many diabetic patients. The pathogenesis of DN is extremely complex and has not yet been clarified; however, in recent years, increasing evidence has shown the important role of innate immunity in DN pathogenesis. Pattern recognition receptors (PRRs) are important components of the innate immune system and have a significant impact on the occurrence and development of DN. In this review, we classify PRRs into secretory, endocytic, and signal transduction PRRs according to the relationship between the PRRs and subcellular compartments. PRRs can recognize related pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs), thus triggering a series of inflammatory responses, promoting renal fibrosis, and finally causing renal impairment. In this review, we describe the proposed role of each type of PRRs in the development and progression of DN.
Alarmins/physiology* ; C-Reactive Protein/physiology* ; Diabetic Nephropathies/etiology* ; Endocytosis ; Humans ; Immunity, Innate ; Mannose-Binding Lectin/physiology* ; Pathogen-Associated Molecular Pattern Molecules ; Receptors, Pattern Recognition/physiology* ; Serum Amyloid P-Component/physiology* ; Signal Transduction

<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 study the value of Pentraxin 3 (PTX3) in diagnosing the severity and cardiovascular function of the critically ill children. Method A total of 178 patients who were older than 28 days, with acute infection of respiratory or neurological system, excluding chronic or special disease, and admitted to the pediatric intensive care unit (PICU) of Hunan Children's Hospital from October 1, 2013 to April 30, 2014 were enrolled, including 102 male cases and 76 female cases. The ages ranged from 1 month to 13 years and 1 month, 78 of them were less than 1 year old ; 58 cases were between 1 to 3 years old; 42 cases were above 3 years old; 101 cases were diagnosed as respiratory system diseases, 77 cases had nervous system diseases. PTX3 was detected with enzyme-linked immunosorbent assay (ELISA) within 1 d after enrollment, at 3 days and 7 days, meanwhile, troponin, myocardial enzyme, brain-type natriuretic peptide (BNP), C-reactive protein (CRP), plasma calcitonin (PCT) and WBC etc. Were measured. According to the plasma PTX3 value which were measured within 24 h after enrollment the patients were divided into three groups: mildly elevated group (< 44 µg/L) 41 cases; moderately elevated group (44 - < 132 µg/L) in 66 cases; severely elevated group 71 cases (132 µg/L or higher). Those 178 patients were divided into 3 groups according to the degree of infection: non-sepsis group (78 cases), sepsis group (70 cases), severe sepsis group (30 cases), and in each group, those with heart failure were respectively 19 cases, 28 cases, 17 cases. Analysis of the plasma PTX3 expression changes in different clinical manifestations, different condition, different degrees of organ damages and prognosis for the patient. The continuous variables were analyzed with t-test, F-test, H-test, the categorical variables were analyzed with Chi-square test, and the correlation analysis was performed to calculate Pearson coefficients.p><p>RESULTThe PTX3 value measured within 24 h after enrollment increased with the degree of infection (50. 4(35. 2,70. 4) µg/L; 175. 8 (99. 6, 309. 9) µg/L;419. 9 (168. 3, 468. 6) µg/L; H = 88. 345, P = 0. 000). PTX3 level gradually declined, while in severe sepsis group decreased slowly (P <0. 05); the area under the ROC curve of Plasma PTX3 was larger than that of other inflammatory markers such as CRP and PCT, white blood cells and neutrophils in the diagnosis of sepsis; while the former three are PTX3, PCT and CRP (the sensitivity and specificity respectively were 0. 77, 0. 68; 0. 66, 0. 6; 0. 47, 0. 55); the PTX3 value of the severely elevated group was significantly higher than those of the mildly and moderately elevated groups (P <0. 05). The proportion of having 3 or more organs failure increased as the PTX3 rising among the groups of mildly elevated group, moderately elevated group and severely elevated group (1(2. 4%), 4(6. 1%), 14(19. 7%) χ2 =16. 16,P = 0. 000); and in each group, the proportion of having good and poor prognosis for these three groups were different (33 (80.5%) and 8 (19. 5%), 35 (53%) and 31 (47%), 28 (39.4%) and 43 (60.6%), χ = 17. 663, P = 0. 000). The K-M curve for these three groups had statistically significant difference (χ2 = 7. 086, P = 0. 029). Those with heart failure had higher PTX3 value than those in non-heart failure at the same degree of infection. PTX3 value increased with myocardial enzyme (troponin, creatine kinase isoenzyme, BNP) levels. In the diagnosis of heart failure, the area under the ROC curve were respectively PTX3 0. 824; BNP 0. 772; CM-KB 0. 643; CNTIO. 671, the sensitivity and specificity were PTX3 0. 8, 0. 58; CK-MB 0. 56,0. 79; CTNI 0. 60,0. 69; BNP 0. 73, 0. 58. In terms of predicting the prognosis of sepsis with heart failure complications, the PTX3 value's area under ROC curve was larger than that of BNP (respectively 0. 844, 0. 472).p><p>CONCLUSIONThe PTX3 is an objective biochemical marker in diagnosis of sepsis; it is helpful in assessment of severity and prognosis of sepsis; it also has a certain clinical value in the assessment of sepsis cardiovascular function damage.p>
Adolescent ; Biomarkers ; blood ; C-Reactive Protein ; analysis ; Calcitonin ; blood ; Cardiovascular System ; physiopathology ; Child ; Child, Preschool ; Creatine Kinase ; blood ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Infant ; Intensive Care Units, Pediatric ; Leukocyte Count ; Male ; Natriuretic Peptide, Brain ; blood ; Prognosis ; Protein Precursors ; blood ; ROC Curve ; Sensitivity and Specificity ; Sepsis ; diagnosis ; physiopathology ; Serum Amyloid P-Component ; analysis ; Troponin ; blood

Pentraxin 3 (PTX3) was identified as a marker of the inflammatory response and overexpressed in various tissues and cells related to cardiovascular disease. Honokiol, an active component isolated from the Chinese medicinal herb Magnolia officinalis, was shown to have a variety of pharmacological activities. In the present study, we aimed to investigate the effects of honokiol on palmitic acid (PA)-induced dysfunction of human umbilical vein endothelial cells (HUVECs) and to elucidate potential regulatory mechanisms in this atherosclerotic cell model. Our results showed that PA significantly accelerated the expression of PTX3 in HUVECs through the IkappaB kinase (IKK)/IkappaB/nuclear factor-kappaB (NF-kappaB) pathway, reduced cell viability, induced cell apoptosis and triggered the inflammatory response. Knockdown of PTX3 supported cell growth and prevented apoptosis by blocking PA-inducted nitric oxide (NO) overproduction. Honokiol significantly suppressed the overexpression of PTX3 in PA-inducted HUVECs by inhibiting IkappaB phosphorylation and the expression of two NF-kappaB subunits (p50 and p65) in the IKK/IkappaB/NF-kappaB signaling pathway. Furthermore, honokiol reduced endothelial cell injury and apoptosis by regulating the expression of inducible NO synthase and endothelial NO synthase, as well as the generation of NO. Honokiol showed an anti-inflammatory effect in PA-inducted HUVECs by significantly inhibiting the generation of interleukin-6 (IL-6), IL-8 and monocyte chemoattractant protein-1. In summary, honokiol repaired endothelial dysfunction by suppressing PTX3 overexpression in an atherosclerotic cell model. PTX3 may be a potential therapeutic target for atherosclerosis.
Apoptosis/drug effects ; Atherosclerosis/chemically induced/*drug therapy/immunology/pathology ; Biphenyl Compounds/chemistry/isolation & purification/*pharmacology ; C-Reactive Protein/*genetics/immunology ; Down-Regulation/drug effects ; Drugs, Chinese Herbal/chemistry/isolation & purification/*pharmacology ; Human Umbilical Vein Endothelial Cells ; Humans ; I-kappa B Kinase/*immunology ; Lignans/chemistry/isolation & purification/*pharmacology ; Magnolia/chemistry ; Palmitic Acid ; Protein-Serine-Threonine Kinases/*immunology ; Serum Amyloid P-Component/*genetics/immunology ; Signal Transduction/drug effects