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      Altered Expression of TXNIP in the peripheral leukocytes of patients with coronary atherosclerotic heart disease

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          Abstract

          Background:

          Coronary atherosclerotic heart disease (CAD) is mainly caused by atherosclerosis, an inflammatory disease characterized by plaque formation in arteries. Reactive oxygen species caused structural damage and dysfunction of arterial endothelial cells. Thioredoxin-interacting protein ( TXNIP) is the endogenous inhibitor and regulator of thioredoxin, a major cellular antioxidant and antiapoptotic system. In order to explore the role of TXNIP in the occurrence and development of CAD, we detected the TXNIP expression and discussed its molecular mechanisms in CAD.

          Methods:

          The mRNA levels of TXNIP gene in peripheral leucocytes were detected in CAD and healthy controls (CTR) by quantitative real-time polymerase chain reaction. And TXNIP proteins were detected by western blotting.

          Results:

          TXNIP gene expression levels in patients with unstable angina pectoris (UAP, n = 96) were significantly increased compared with those of CTR (n = 192, P < .05). However, the situation is different in acute myocardial infarction (n = 96, P > .05). Logistic regression analysis showed that TXNIP levels were significantly positive correlated with UAP (OR = 1.728, P < .05).

          Conclusions:

          TXNIP gene expression in the peripheral leucocytes was increased in patients with UAP, indicating that TXNIP in circulating leucocytes may be involved in the pathogenesis of UAP.

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          Most cited references26

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          Obesity, inflammation, and atherosclerosis.

          Understanding of the pathophysiology of atherogenesis has evolved substantially during the last few decades. Atherosclerosis was once identified as a lipid-storage disease, but is now recognized as a subacute inflammatory condition of the vessel wall, characterized by infiltration of macrophages and T cells, which interact with one another and with cells of the arterial wall. The pathological mechanisms of obesity recapitulate many features of the inflammatory processes at work in atherosclerosis. Our current appreciation of the similarities between obesity and atherosclerosis has already fostered innovations for the diagnosis, prognosis, and prevention of these two conditions.
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            Neutrophil infiltration of culprit lesions in acute coronary syndromes.

            Neutrophils in unstable atherosclerotic lesions have not received much consideration, despite accumulating evidence suggesting a link between systemic inflammation and acute coronary syndromes. Coronary artery segments were obtained at autopsy from 13 patients with acute myocardial infarction (AMI); 8 had a ruptured and 5 an eroded plaque. Patients (n=45) who had died of noncardiovascular diseases served as reference. Atherectomy specimens were obtained from 35 patients with stable angina pectoris (SAP) and from 32 patients with unstable angina pectoris (UAP). Antibodies against CD66b, elastase, myeloperoxidase, and CD11b identified neutrophils; CD10 identified neutral endopeptidase (NEP). CD66b-positive and NEP-positive neutrophils were counted and expressed as a number per square millimeter of tissue. All specimens with plaque rupture or erosion showed distinct neutrophil infiltration; the number did not differ between ruptured and eroded plaques. However, the number of NEP-positive neutrophils was significantly higher (P<0.0001) in ruptured plaques than in eroded plaques. UAP patients showed neutrophils in 14 of 32 culprit lesions; in SAP only 2 of 35 lesions contained neutrophils. The number of neutrophils and NEP-positive cells in patients with UAP was significantly higher (neutrophils, P<0.0005; NEP-positive cells, P<0.005) than in patients with SAP. The observations suggest that neutrophil infiltration is actively associated with acute coronary events. The high number of NEP-positive neutrophils in ruptured plaques, compared with eroded plaques, may reflect differences in the underlying pathophysiological mechanisms.
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              Vitamin D3 up-regulated protein 1 mediates oxidative stress via suppressing the thioredoxin function.

              As a result of identifying the regulatory proteins of thioredoxin (TRX), a murine homologue for human vitamin D3 up-regulated protein 1 (VDUP1) was identified from a yeast two-hybrid screen. Cotransfection into 293 cells and precipitation assays confirmed that mouse VDUP1 (mVDUP1) bound to TRX, but it failed to bind to a Cys32 and Cys35 mutant TRX, suggesting the redox-active site is critical for binding. mVDUP1 was ubiquitously expressed in various tissues and located in the cytoplasm. Biochemical analysis showed that mVDUP1 inhibited the insulin-reducing activity of TRX. When cells were treated with various stress stimuli such as H2O2 and heat shock, mVDUP1 was significantly induced. TRX is known to interact with other proteins such as proliferation-associated gene and apoptosis signal-regulating kinase 1. Coexpression of mVDUP1 interfered with the interaction between TRX and proliferation-associated gene or TRX and ASK-1, suggesting its roles in cell proliferation and oxidative stress. To investigate the roles of mVDUP1 in oxidative stress, mVDUP1 was overexpressed in NIH 3T3 cells. When cells were exposed to stress, cell proliferation was declined with elevated apoptotic cell death compared with control cells. In addition, c-Jun N-terminal kinase activation and IL-6 expression were elevated. Taken together, these results demonstrate that mVDUP1 functions as an oxidative stress mediator by inhibiting TRX activity.
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                Author and article information

                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MEDI
                Medicine
                Wolters Kluwer Health
                0025-7974
                1536-5964
                December 2017
                08 December 2017
                : 96
                : 49
                : e9108
                Affiliations
                [a ]Department of Cardiology, Jining No. 1 People's Hospital
                [b ]Central Laboratory, Affiliated Hospital of Jining Medical University
                [c ]Department of Traditional Chinese Medicine, Jining No. 1 People's Hospital, Shandong, China.
                Author notes
                []Correspondence: Zixiu Wei, Department of Cardiology, Jining No. 1 People's Hospital, 6 Jiankang Road, Jining, Shandong 272000, China (e-mail: jnsyyw01163.com, wzix@ 123456sina.com ).
                Article
                MD-D-17-02525 09108
                10.1097/MD.0000000000009108
                5728958
                29245343
                7ce585ca-aee6-4739-8807-40e53bdbf94d
                Copyright © 2017 the Author(s). Published by Wolters Kluwer Health, Inc.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. http://creativecommons.org/licenses/by-nc-sa/4.0

                History
                : 23 April 2017
                : 17 September 2017
                : 14 November 2017
                Categories
                3400
                Research Article
                Clinical Trial/Experimental Study
                Custom metadata
                TRUE

                coronary atherosclerotic heart disease,gene expression,leucocytes,txnip

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