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Does Aspirin Affect Platelet Count

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Does Aspirin Affect Platelet Count

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Synergistic Effect Of Gbe50 & Aspirin Against Platelet Aggre

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Molecular Targets of Aspirin and Prevention of Preeclampsia and Potential Combination with Extracellular Vehicle Circulation During Pregnancy

By Suchismita Dutta Suchismita Dutta Scilit Preprints.org Google Scholar View Publications 1, Sathish Kumar Sathish Kumar Scilit Preprints.org Google Scholar View Publications 2, Jon Hyett Jon Hyett Scilit Preprints.org Google Scholar View Publications 3 and Carlos Salomon Carlos Salomon Scilit Preprints. org Google Scholar View Publications 1, 4, 5, *

A List Of New Platelet Function Tests.

Exosome Biology Laboratory, Clinical Diagnostics Centre, University of Queensland Clinical Research Centre, Royal Brisbane and Women’s Hospital, University of Queensland, Brisbane, QLD 4029, Australia

Received: 19 May 2019 / Revised: 30 July 2019 / Accepted: 26 August 2019 / Published: 5 September 2019

A healthy, uncomplicated pregnancy is the result of successful fertilization, embryo implantation, trophoblast development, and adequate placement. Any event in this series of events can lead to pregnancy complications such as preeclampsia (PE). Currently, the incidence of PE in all pregnancies worldwide is 2-8%, which results in high maternal and perinatal mortality and morbidity rates. In several randomized controlled clinical trials, an association was found between low-dose aspirin (LDA) treatment in early pregnancy and a significant reduction in the incidence of PE in high-risk pregnant women. However, there is a large knowledge gap regarding the identification of aspirin’s specific mechanism of action versus the placebo effect. It has been demonstrated that placenta-derived exosomes (PdE) are present in the maternal circulation as early as 6 weeks of gestation, and that bioactive molecules such as proteins, lipids, and RNA are the “fingerprint” of the cell from which the exosomes originate. Interestingly, exosome levels in PE are higher compared with normal pregnancies, and changes in PdE levels during the first trimester can be used to classify women at risk for PE. The aim of this review is to discuss the mechanisms of action of LDA on intestinal and maternal physiological systems including the role of PdE in these phenomena. This review article will contribute to an in-depth understanding of LDA-induced PE inhibition.

Pregnancy is an important event that brings significant changes to the mother’s physiology. A successful pregnancy requires that a series of processes from conception to the formation of the placental connection and the blood vessels of the mother and fetus are involved in the correct sequence. Adequate placement is one of the prerequisites for maintaining a healthy and normal pregnancy. New insights into placental processes include migration, invasion, attachment, proliferation, and differentiation of the main cellular components of the placenta, namely: extravillous trophoblasts (EVT), and then their interactions with the blood vessels, glands, and lymphatics of the decasualized maternal uterus [1]. Placement progresses further through digestion of the extracellular matrix where the EVT receives circulating oxidative stress from the surrounding mother and the effects of soluble cytokines [1]. However, allogeneic EVT also interacts with maternal decidual immune cells to confer immune competence [2]. Any deviation in these events can cause pathological pregnancy, namely preeclampsia (PE). The broad concept of the pathophysiology of PE includes defects in trophoblast invasion and inadequate remodeling of the uterine spiral arteries in the first trimester leading to decreased uteroplacental perfusion [3]. This in turn leads to poor perforation of the placental syncytiotrophoblast and stress which releases various mediators leading to endothelial dysfunction and clinical manifestations of PE [3]. Additionally, as a result of such abnormal placentation, abnormal levels of anti-angiogenic and inflammatory proteins are released that enter the maternal systemic circulation and affect maternal systemic vascular function, leading to clinical PE manifestations. Because PE and its clinical signs subside rapidly after delivery (removal of the placenta), the intestine must play a central or initiating role in this pregnancy disorder.

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New pharmacological interventions to prevent PE have not been developed for many years, as the development of complex pathology, the variable clinical picture of the disease and the difficulty in conducting drug discovery studies in pregnant women have been hampered. Low-dose aspirin (LDA) is considered the most effective prophylactic therapy to reduce disease prevalence in women at high risk for early-onset PE. The use of LDA in pregnant women is generally considered safe because it does not have a negative impact on the pregnant woman and/or the fetus she is carrying. It has been suggested that the main mechanism of action of LDA in providing its effects is through inhibiting thromboxane production which causes inhibition of platelet aggregation. In addition, LDA has a direct positive effect on villous trophoblasts [4]. However, recent evidence suggests that LDA prevents the development of PE by promoting trophoblast invasion and migration to the uterine arteries, influencing cytokine production and stimulating production of the proangiogenic protein placental growth factor (PlGF); therefore, preventing apoptosis and premature uterine artery remodeling [5].

A recent meta-analysis showed that LDA (≥100 mg/day) in early pregnancy (before 16 weeks) is beneficial in preventing common pregnancy complications; namely PE, fetal growth restriction, preterm birth [6, 7, 8, 9], suggesting that aspirin may have an effect on early implantation and placentation [10]. Low-dose aspirin has been used for many years to prevent PE [11, 12, 13]. A recent meta-analysis of individual patient data noted that LDA can reduce the risk of developing PE by 10% and small-for-gestational-age (SGA) births by 24% [14] without posing major safety risks to the mother or fetus other than the placenta. suddenly. in some cases [15]. Another study reported that low-dose aspirin is generally well tolerated in the prenatal and early pregnancy period [16].

In normal healthy pregnancy, placental sycytiotrophoblasts release extracellular vesicles (EVs) including exosomes into the maternal bloodstream containing several pieces of information (i.e., micro-RNA, mRNA, protein) for transport from origin cells to target cells over a very long time. maternal immune cells to adapt to the physiological changes associated with pregnancy [17]. The release of these EVs is increased from the preeclamptic gut due to oxidative stress, causing widespread systemic endothelial dysfunction, leading to maternal hypertension, impaired feto-placental circulation and damage to various maternal organs [ 17 ]. Several recently published reports suggest that LDA can influence the release of platelet-derived EVs; however, the effect of LDA on the regulation of placental EV release is unknown. Therefore, in this review, we will discuss the possible mechanisms of action of aspirin in the context of PE prevention and the possible role of extracellular vesicles released from the placenta in this phenomenon (Figure 1).

Pregnancy causes several changes in the mother’s physiology to maintain the correct course of pregnancy and involves a series of processes starting from fertilization to the establishment of feto-maternal communication and cross-communication through the placenta. Pre-implantation, vascular conditions, invasion of embryonic cells into the maternal uterine wall and oxidative stress are important regulators of the function of pregnancy events [18]. Before implantation, there is an increase in progesterone levels in the postovulatory circulation that inhibits estrogen-dependent proliferation of the uterine epithelium and promotes secretory transformation of the uterine glands. In the early stages of development, namely ~ day 6 of fertilization, the blastocyst microvilli interact with the pinopods of the uterine luminal endometrial epithelium to establish function, which becomes stabilized through increased adhesion of the trophectoderm and uterine luminal. epithelium. During these interactions, a number of molecules are secreted from activated immune cells including mucins, selectins, integrins and cadherins [ 18 , 19 ]. Soon after, invasion begins and the trophectoderm penetrates the uterine epithelium, invading the uterine artery wall where they interact with cells of the maternal circulatory immune system and mediate remodeling of the uterine spiral arteries supplied by the placenta. The aggregates containing the transcription material are then removed.

Randomized Clinical Trials That Compared The Effect Of Aspirin In The…

There is direct evidence that platelets are involved in the deposition process. During placentation, trophoblasts invade the decidual stroma including the uterine glands and migrate to the maternal uterine spiral arteries replacing the fine blood vessels.

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