Potential Role of Protein Disulfide Isomerase in Metabolic Syndrome-Derived Platelet Hyperactivity

被引:12
|
作者
Gaspar, Renato Simoes [1 ]
Trostchansky, Andres [2 ,3 ,4 ]
de Andrade Paes, Antonio Marcus [1 ,4 ]
机构
[1] Univ Fed Maranhao, Dept Physiol Sci, Lab Expt Physiol, Sao Luis, MA, Brazil
[2] Univ Republica, Dept Bioquim, Montevideo, Uruguay
[3] Univ Republica, Fac Med, Ctr Free Rad & Biomed Res, Montevideo, Uruguay
[4] Univ Fed Maranhao, Hlth Sci Grad Program, Biol & Hlth Sci Ctr, Sao Luis, MA, Brazil
关键词
VASCULAR SMOOTH-MUSCLE; TRANSIENT ISCHEMIC ATTACK; NADPH-OXIDASE; NITRIC-OXIDE; OXIDATIVE STRESS; CARDIOVASCULAR RISK; THROMBUS FORMATION; INSULIN-RECEPTOR; NAD(P)H OXIDASE; ACTIVATION;
D O I
10.1155/2016/2423547
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Metabolic Syndrome (MetS) has become a worldwide epidemic, alongside with a high socioeconomic cost, and its diagnostic criteria must include at least three out of the five features: visceral obesity, hypertension, dyslipidemia, insulin resistance, and high fasting glucose levels. MetS shows an increased oxidative stress associated with platelet hyperactivation, an essential component for thrombus formation and ischemic events in MetS patients. Platelet aggregation is governed by the peroxide tone and the activity of Protein Disulfide Isomerase (PDI) at the cell membrane. PDI redox active sites present active cysteine residues that can be susceptible to changes in plasma oxidative state, as observed in MetS. However, there is a lack of knowledge about the relationship between PDI and platelet hyperactivation under MetS and its metabolic features, in spite of PDI being a mediator of important pathways implicated in MetS-induced platelet hyperactivation, such as insulin resistance and nitric oxide dysfunction. Thus, the aim of this review is to analyze data available in the literature as an attempt to support a possible role for PDI in MetS-induced platelet hyperactivation.
引用
收藏
页数:10
相关论文
共 50 条
  • [31] Endothelium but Not Platelet-Derived Protein Disulfide Isomerase Is Required for Fibrin Generation during Thrombus Formation in Vivo.
    Jasuja, Reema
    Cho, Jaehyung
    Furie, Bruce
    Furie, Barbara
    BLOOD, 2008, 112 (11) : 257 - 257
  • [32] Expression and Release of Platelet Protein Disulfide (PDI) Isomerase Is Increased in Patients with Hemophilia a
    Langer, Florian
    Voigtlaender, Minna
    Holstein, Katharina
    Spath, Brigitte
    Fiedler, Walter
    Bokemeyer, Carsten
    BLOOD, 2015, 126 (23)
  • [33] Platelet protein disulfide isomerase is restricted to the dense tubular system and not associated with the cell surface
    Pannerden, van Nispen Tot H. E.
    van Dijk, S. M.
    Du, V
    Heijnen, H. F. G.
    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2009, 7 : 330 - 330
  • [34] Attenuation of Platelet Activation and Thrombus Formation by Tannic Acid: Inhibition of Protein Disulfide Isomerase
    Li, Qing
    You, Tao
    Zhu, Li
    ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2019, 39
  • [35] The transmembrane protein disulfide isomerase TMX1 negatively regulates platelet responses
    Zhao, Zhenzhen
    Wu, Yi
    Zhou, Junsong
    Chen, Fengwu
    Yang, Aizhen
    Essex, David W.
    BLOOD, 2019, 133 (03) : 246 - 251
  • [36] Role of Protein Disulfide Isomerase during vascular repair after injury
    Tanaka, Leonardo Yuji
    Araujo, Haniel Alves
    Csordas, Andre Alcantara
    Hironaka, Gustavo Ken
    Takimura, Celso Kiyochi
    Martins Laurindo, Francisco Rafael
    FASEB JOURNAL, 2012, 26
  • [37] Role of protein disulfide isomerase pdi in von Willebrand factor dimerization
    Brehm, M. A.
    Lippok, S.
    Kolsek, K.
    Eggert, D.
    Obser, T.
    Schneppenheim, R.
    Graeter, F.
    Baldauf, C.
    Raedler, J.
    JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2015, 13 : 223 - 223
  • [38] LOCALIZATION OF PROTEIN DISULFIDE-ISOMERASE TO THE EXTERNAL SURFACE OF THE PLATELET PLASMA-MEMBRANE
    ESSEX, DW
    CHEN, K
    SWIATKOWSKA, M
    BLOOD, 1995, 86 (06) : 2168 - 2173
  • [39] Juglone prevents human platelet aggregation through inhibiting Akt and protein disulfide isomerase
    Kao, Ching-Chieh
    Kung, Po-Hsiung
    Tai, Chi-Jung
    Tsai, Meng-Chun
    Cheng, Yuan-Bin
    Wu, Chin-Chung
    PHYTOMEDICINE, 2021, 82
  • [40] Nitric oxide (NO) reacts with platelet-surface protein disulfide isomerase (PDI) and inhibits platelet function.
    Zai, A
    Rudd, MA
    Loscalzo, J
    FASEB JOURNAL, 1998, 12 (04): : A80 - A80