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      PTX3 Gene 3’UTR polymorphism and its interaction with environmental factors are correlated with the risk of preeclampsia in a Chinese Han population

      research-article
      , MD, , MD
      Medicine
      Wolters Kluwer Health
      gene-environment interaction, pentraxin 3, preeclampsia, single nucleotide polymorphism

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          Abstract

          To investigate the interaction between the single nucleotide polymorphism of the 3’ untranslated region (3’UTR) of the pentraxin 3 ( PTX3) gene, as well as environmental factors and the preeclampsia risk in a Chinese Han population.

          Sanger sequencing was used to analyze rs5853783 and rs73158510 loci of the PTX3 gene 3’UTR from 235 patients with preeclampsia and 235 control subjects. The plasma PTX3 protein level was measured by enzyme-linked immunosorbent assay (ELISA).

          The risk of preeclampsia in the PTX3 gene rs5853783 locus D allele carriers was 0.72 times higher than that of the I allele carriers (95% CI: 0.60–0.84, P < .001). The risk of preeclampsia in the PTX3 gene rs73158510 locus A allele carriers was 1.36 times higher than in the G allele carriers (95% CI: 1.16–1.55, P < .001). The area under the ROC curve (AUC) for the diagnosis of preeclampsia by plasma PTX3 protein levels was 0.906 ( P < .001). The PTX3 gene rs5853783 and rs73158510 single nucleotide polymorphisms (SNPs) were associated with plasma PTX3 protein levels. The AUC of plasma PTX3 protein level diagnosis of preeclampsia in PTX3 gene rs5853783 locus II genotype subjects was up to 0.9371, followed by the ID genotype (AUC = 0.8586); the DD genotype was the lowest (AUC = 0.8154). The AUC of plasma PTX3 protein level diagnosis of preeclampsia in rs73158510 locus GG genotype subjects was 0.9102, GA genotype was 0.8766, and AA genotype was 0.8750.

          The rs5853783 and rs73158510 SNPs in the 3’UTR region of the PTX3 gene are associated with the risk of preeclampsia in a Chinese Han population.

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          Most cited references16

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          Pentraxins at the crossroads between innate immunity, inflammation, matrix deposition, and female fertility.

          C reactive protein, the first innate immunity receptor identified, and serum amyloid P component are classic short pentraxins produced in the liver. Long pentraxins, including the prototype PTX3, are expressed in a variety of tissues. Some long pentraxins are expressed in the brain and some are involved in neuronal plasticity and degeneration. PTX3 is produced by a variety of cells and tissues, most notably dendritic cells and macrophages, in response to Toll-like receptor (TLR) engagement and inflammatory cytokines. PTX3 acts as a functional ancestor of antibodies, recognizing microbes, activating complement, and facilitating pathogen recognition by phagocytes, hence playing a nonredundant role in resistance against selected pathogens. In addition, PTX3 is essential in female fertility because it acts as a nodal point for the assembly of the cumulus oophorus hyaluronan-rich extracellular matrix. Thus, the prototypic long pentraxin PTX3 is a multifunctional soluble pattern recognition receptor at the crossroads between innate immunity, inflammation, matrix deposition, and female fertility.
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            PTX3, A prototypical long pentraxin, is an early indicator of acute myocardial infarction in humans.

            Inflammation is an important component of ischemic heart disease. PTX3 is a long pentraxin whose expression is induced by cytokines in endothelial cells, mononuclear phagocytes, and myocardium. The possibility that PTX3 is altered in patients with acute myocardial infarction (AMI) has not yet been tested. Blood samples were collected from 37 patients admitted to the coronary care unit (CCU) with symptoms of AMI. PTX3 plasma concentrations, as measured by ELISA, higher than the mean+2 SD of age-matched controls (2.01 ng/mL) were found in 27 patients within the first 24 hours of CCU admission. PTX3 peaked at 7.5 hours after CCU admission, and mean peak concentration was 6.94+/-11.26 ng/mL. Plasma concentrations of PTX3 returned to normal in all but 3 patients at hospital discharge and were unrelated to AMI site or extent, Killip class at entry, hours from symptom onset, and thrombolysis. C-reactive protein peaked in plasma at 24 hours after CCU admission, much later than PTX3 (P 64 years old and women had significantly higher PTX3 concentrations at 24 hours (P<0.05). PTX3 was detected by immunohistochemistry in normal but not in necrotic myocytes. PTX3 is present in the intact myocardium, increases in the blood of patients with AMI, and disappears from damaged myocytes. We suggest that PTX3 is an early indicator of myocyte irreversible injury in ischemic cardiomyopathy.
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              Multimer formation and ligand recognition by the long pentraxin PTX3. Similarities and differences with the short pentraxins C-reactive protein and serum amyloid P component.

              PTX3 is a prototypic long pentraxin consisting of a C-terminal 203-amino acid pentraxin-like domain coupled with an N-terminal 178-amino acid unrelated portion. The present study was designed to characterize the structure and ligand binding properties of human PTX3, in comparison with the classical pentraxins C-reactive protein and serum amyloid P component. Sequencing of Chinese hamster ovary cell-expressed PTX3 revealed that the mature secreted protein starts at residue 18 (Glu). Lectin binding and treatment with N-glycosidase F showed that PTX3 is N-glycosylated, sugars accounting for 5 kDa of the monomer mass (45 kDa). Circular dichroism analysis indicated that the protein consists predominantly of beta-sheets with a minor alpha-helical component. While in gel filtration the protein is eluted with a molecular mass of congruent with900 kDa, gel electrophoresis using nondenaturing, nonreducing conditions revealed that PTX3 forms multimers predominantly of 440 kDa apparent molecular mass, corresponding to decamers, and that disulfide bonds are required for multimer formation. The ligand binding properties of PTX3 were then examined. As predicted based on modeling, inductive coupled plasma/atomic emission spectroscopy showed that PTX3 does not have coordinated Ca2+. Unlike the classical pentraxins CRP and SAP, PTX3 did not bind phosphoethanolamine, phosphocholine, or high pyruvate agarose. PTX3 in solution, bound to immobilized C1q, but not C1s, and, reciprocally, C1q bound to immobilized PTX3. Binding of PTX3 to C1q is specific and saturable with a Kd 7.4 x 10(-8) M as determined by solid phase binding assay. The Chinese hamster ovary cell-expressed pentraxin domain bound C1q when multimerized. Thus, as predicted on the basis of computer modeling, the prototypic long pentraxin PTX3 forms multimers, which differ from those formed by classical pentraxins in terms of protomer composition and requirement for disulfide bonds, and does not recognize CRP/SAP ligands. The capacity to bind C1q, mediated by the pentraxin domain, is consistent with the view that PTX3, produced in tissues by endothelial cells or macrophages in response to interleukin-1 and tumor necrosis factor, may act as a local regulator of innate immunity.
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                Author and article information

                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MEDI
                Medicine
                Wolters Kluwer Health
                0025-7974
                1536-5964
                17 January 2020
                January 2020
                : 99
                : 3
                : e18740
                Affiliations
                Department of Obstetrics, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
                Author notes
                []Correspondence: Wei Zhang, Department of Obstetrics, Affiliated Hangzhou First People's Hospital, Zhejiang University School of Medicine, No. 261, Huansha Road, Hangzhou, Zhejiang, China (e-mail: zhangweihz1983@ 123456163.com ).
                Article
                MD-D-19-05873 18740
                10.1097/MD.0000000000018740
                7220431
                32011454
                9a59100b-d4b7-47fd-bbcc-d5d374dfdcfa
                Copyright © 2020 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial License 4.0 (CCBY-NC), where it is permissible to download, share, remix, transform, and buildup the work provided it is properly cited. The work cannot be used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc/4.0

                History
                : 30 July 2019
                : 8 December 2019
                : 14 December 2019
                Funding
                Funded by: Health Science and Technology Plan Medical Key Specialty Disease Project of Hangzhou
                Award ID: 20150733Q03
                Award Recipient : Ning Xu
                Categories
                5600
                Research Article
                Observational Study
                Custom metadata
                TRUE

                gene-environment interaction,pentraxin 3,preeclampsia,single nucleotide polymorphism

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